Podcasts about avnrt

Contributor: Taylor Lynch MD Supraventricular tachycardias (SVTs) arise above the bundle of His The term SVT includes AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia, atrial fibrillation, atrial flutter, and multifocal atrial tachycardia  AVNRT is the most common form of SVT Paroxysmal Spontaneous or provoked by exertion, coffee, alcohol, or thyroid disease More common in women (3:1 women:men ratio) HR 160-240 Narrow complex with a normal QRS Unstable patients receive synchronized cardioversion at 0.5-1 J/kg Valsalva maneuver is attempted before pharmaceutical interventions Increases vagal tone at the AV node to slow conduction and prolongs its refractory period to normalize the conduction Traditionally, patients are asked to bear down, but this only works in 17% of patients REVERT trial assessed a modified valsalva that worked in 43% of patients Adenosine Slows conduction at the AV node by activating potassium channels and inhibiting calcium influx Extremely uncomfortable for most patients Not commonly used anymore Nondihydropyridine calcium-channel blockers are preferred A 2009 RCT investigated low-infusion CCBs compared with adenosine bolus The study found a conversion rate of 98% in the CCB group vs. adenosine group at 86.5% The main adverse effect of CCB is hypotension, which a slow infusion rate can mitigate Diltiazem dose is 0.25 mg/kg/2min and repeat at 0.35 mg/kg/15 minutes or slow infusion at 2.5 mg/min up to a conversion or 50 mg total References 1. Appelboam A, Reuben A, Mann C, et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): A randomised controlled trial. Lancet. 2015;386(10005):1747-1753. doi:10.1016/S0140-6736(15)61485-4 Belz MK, Stambler BS, Wood MA, Pherson C, Ellenbogen KA. Effects of enhanced parasympathetic tone on atrioventricular nodal conduction during atrioventricular nodal reentrant tachycardia. Am J Cardiol. 1997;80(7):878-882. doi:10.1016/s0002-9149(97)00539-0 Lim SH, Anantharaman V, Teo WS, Chan YH. Slow infusion of calcium channel blockers compared with intravenous adenosine in the emergency treatment of supraventricular tachycardia. Resuscitation. 2009;80(5):523-528. doi:10.1016/j.resuscitation.2009.01.017 Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [published correction appears in Circulation. 2016 Sep 13;134(11):e234-5. doi: 10.1161/CIR.0000000000000448]. Circulation. 2016;133(14):e506-e574. doi:10.1161/CIR.0000000000000311 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

This week we will hear 2 lectures from the World Congress on ablation in children from two world authorities. In the first, Professor Jeff Kim of Texas Children's Hospital speaks about unusual accessory pathway connections and offers some insights into how to ablate them. Following Dr. Kim, Professor John Papagiannis, chief of cardiology at the Onassis Center in Greece offers us some insights into why some AVNRT is challenging to ablate and how to approach these rare but difficult cases. Why is ablation not 100% effective in children for 'simple' things like accessory pathways or AVNRT? Drs. Kim and Papagiannis provide a few insights into why there is no such thing as 'just AVNRT' or 'just a pathway'.

Take Home Points AVNRT is a common tachydysrhythmia that results from a reentrant loop within the AV node. Unstable patients with AVNRT should be considered for immediate synchronized electrical cardioversion. Stable patients with AVNRT can have a trial of vagal maneuvers followed by chemical cardioversion with adenosine or verapamil and synchronized electrical cardioversion if that ... Read more The post REBEL Core Cast 98.0 – AVNRT appeared first on REBEL EM - Emergency Medicine Blog.

In de aflevering van deze week wordt alles omtrent SVT's besproken. Een groep van hartritmestoornissen die we bijna elke dag in de acute zorg tegenkomen. We bespreken de herkenning, behandeling en oorzaken van verschillende SVT's om onze patiënten beter te kunnen helpen.De volgende onderwerpen komen aan bod:Wat is een SVT?Waarom zijn atriumfibrileren en sinustachycardie ook SVT's ?Waarom zijn betablokkers bij een sinustachycardie vaak geen goed idee?Waarom wordt de diagnose atriumflutter vaak gemist?Waarom helpt het omdraaien van een ECG om bepaalde SVT's te diagnosticeren?Hoe behandelen we atriumfibrileren het best?Wat is een AVNRT en is het schadelijk voor de patiënt?Kan een SVT ook brede QRS complexen hebben?Wanneer geven we adenosine bij een SVT?Wanneer moeten we een patiënt cardioverteren?Bronnen:https://pubmed.ncbi.nlm.nih.gov/29627355/ (treatment of Afib in the ICU)https://www.sciencedirect.com/science/article/pii/S1875213611003639 (SR + MA over Rate vs Rhythm control buiten de IC)https://journals.lww.com/ccmjournal/Abstract/2008/05000/Treatment_of_new_onset_atrial_fibrillation_in.35.aspx (SR over Rate vs Rhythm Control op de IC)https://pubmed.ncbi.nlm.nih.gov/33831963/ (SR over anticoagulatie therapie bij Afib op de IC)https://rebelem.com/svt-aberrancy-versus-vt/ (SVT of VT? #1)https://litfl.com/vt-versus-svt-ecg-library/ (SVT of VT? #2)https://litfl.com/supraventricular-tachycardia-svt-ecg-library/ (LITFL SVT)https://derangedphysiology.com/main/required-reading/cardiology/Chapter%20511/atrial-fibrillation (Deranged Physiology Afib)Bedankt voor het luisteren!Volg @intensiefdepodcast op InstagramVragen? intensiefdepodcast@gmail.com

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Daily Cardiology Symposium 1401: Arrhythmia

Take Home Points AVNRT is a common tachydysrhythmia that results from a reentrant loop within the AV node. Unstable patients with AVNRT should be considered for immediate synchronized electrical cardioversion. Stable patients with AVNRT can have a trial of vagal maneuvers followed by chemical cardioversion with adenosine or verapamil and synchronized electrical cardioversion if that ... Read more The post REBEL Core Cast 84.0 – AVNRT appeared first on REBEL EM - Emergency Medicine Blog.

In this episode, we review the approach to SVT with a focus on AVRT and AVNRT. We discuss the common clinical manifestations, etiology, investigations and management, with a special medicine minute on the REVERT trial. Written by: Dr. Chris Olesovsky (Internal Medicine Resident)Reviewed by: Dr. Sean Balmain (Cardiology) and Dr. Pete Wu (General Internal Medicine)Sound Editing by: Nafis Hossain (Internal Medicine Resident)Infographic by: Alison Lai

Supraventricular tachycardia can present very stable, but this patient rapidly declined.  In this episode we explain what exactly is happening with SVT, and go through all the different treatment modalities from vagal maneuvers, to medications, to synchronized cardioversion.

So in this episode we run through narrow complex tachycardias, not I hear you say a perfect visual topic for an audio platform like a podcast, but hold your horses… No matter what your level, or your depth of understanding of narrow complex tachycardias, we really hope this will offer some extra knowledge and contemplation for both those of you, like us, that have been treating patient with NCT for decades, right through to those of you that are completely new to the topic. We run through all the normal stuff like definitions, clinical context and electrical pathways. Then we have a think about those terms and concepts like node dependance, AVRT, AVNRT, WPW etc, and then we come back to the fundamentals of delivering excellent care and how we can use a structure of interpretation to decide how best to treat our patient both pre and in-hospital.  We've tried to really nail down and describe some of the concepts in a way that should make this topic a lot easier to understand and most importantly help us all deliver excellent care. Once again we'd love to hear any thoughts or feedback either on the website or via twitter @TheResusRoom. Enjoy! Simon, Rob & James

Welcome to our first episode of a 2-part series on arrhythmias! Here we discuss the highest-yield points on tachyarrhythmias, which include: A fib, AVRT, AVNRT, V tach, Torsades, and V fib. Hope you enjoy this HIGH-YIELD episode!

Pin-Up-Docs Innere Werte: Jeden Monat sezieren wir für euch ein Thema aus dem weiten Feld der Inneren Medizin, berichten von unseren Praxiserfahrungen, verknüpfen mit aktueller Forschung und möchten euch kurzweilig Handlungsempfehlungen für euren medizinischen Alltag vermitteln. In der sechsten Folge beschäftigen wir uns mit dem Thema ‚AV-Knoten-Reentry-Tachykardie‘. CME-Punkte könnt Ihr bis einschließlich 30. September 2021 erwerben. Um diese zu beantragen, […] Der Beitrag Innere Werte – September 2021 – AVNRT erschien zuerst auf pin-up-docs - don't panic.

CardioNerd (Amit Goyal), cardioobstetrics series co-chair Dr. Natalie Stokes, Cardionerds Duke University CardioNerds Ambassador and episode lead fellow, Dr. Kelly Arps, join Dr. Andrea Russo, Director of Electrophysiology and Arrhythmia Services at Cooper Medical School of Rowan University and immediate past president Heart Rhythm Society, for a discussion about pregnancy and arrhythmia. Stay tuned for a message from Dr. Sharonne Hayes about WomenHeart. Audio editing by Gurleen Kaur. Claim free CME for enjoying this episode! Dr. Russo's disclosures: Johnson and Johnson, Medtronic, Inc., Boston Scientific Corporation, Kestra, Medilynx, Up-to-Date, and ABIM. Abstract • Pearls Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Episode Abstract Pregnant patients may have exacerbation of underlying arrhythmic syndromes or unmasking of previously undiagnosed arrhythmic syndromes. Management of atrial and ventricular tachyarrhythmias should proceed with increased urgency in pregnant patients due to risk of adverse hemodynamic events in the mother and fetus. Cardioversion of atrial and ventricular arrhythmias is safe in pregnancy. Preferred antiarrhythmic agents in pregnant patients include metoprolol, propranolol, verapamil, flecainide, propafenone, sotalol, procainamide, and lidocaine. Management of arrhythmias in pregnancy should include collaboration with obstetrics and maternal-fetal medicine teams. Pearls Pre-conception counseling is a shared decision making process; include obstetrics and maternal-fetal medicine colleagues in challenging cases. Have a high sense of urgency for acute arrhythmias in pregnancy due to risk of impaired fetal perfusion. Goals of acute arrhythmic management should include rapid treatment while avoiding hypotension. In scenarios when beta blockers are indicated, metoprolol and propranolol are first choice. Avoid atenolol as this drug has the highest risk of fetal bradycardia and intra-uterine growth retardation in the class. Lidocaine or procainamide should be first line for ventricular arrhythmias in pregnancy. Amiodarone is potentially teratogenic and should not be used in pregnant patients unless all other options have been exhausted. Show notes 1. What are the expected electrophysiologic changes associated with pregnancy? Increase in resting heart rate which peaks in third trimesterPR shorteningECG axis shift leftward and upwardNon-specific ST and T wave changes These changes, along with increased cardiac output and volume with increased stretch in all chambers, increase the risk of re-entrant arrhythmias in those who are predisposed. ↑ atrial volume -> ↑ stretch -> ↑ ectopy -> ↑ risk for re-entrant arrhythmias 2. What is the approach to pre-conception counseling for patients with known arrhythmias or arrhythmic syndromes? Anticipate frequency and potential severity of adverse arrhythmic outcomes during pregnancy and post-partum periodConsider available options for rhythm control and anticoagulation therapy, as appropriate, during the pre-conception, pregnancy, and post-partum periodsConsider catheter ablation prior to pregnancy, particularly for curable arrhythmias such as Wolff-Parkinson-White (WPW) and AVNRT   Offer genetic counseling about hereditary risk to fetus for inherited arrhythmias such as Brugada syndrome and Long QT syndrome 3. What is the management of SVT in pregnancy? Consider the increased risk of tachyarrhythmias in pregnancy: Typically benign arrhythmias can lead to more rapid decompensation in mother due to increased baseline cardiac output. Typically benign arrhythmias can lead to rapid danger to the fetus due to maternal hypotension and shortened diastolic ...

In this episode, we tackle a group of tachyarrhythmias known as paroxysmal supraventricular tachycardias, or pSVTs. This family includes atrioventricular nodal re-entry tachycardia (AVNRT) and atrioventricular reciprocating tachycardia (AVRT), and is related to the Wolff-Parkinson-White syndrome. Learn how these arrhythmias come about in the first place, then how to recognize them and ultimately treat them. There's more to pSVTs than the buzzwords; come hear for yourself!

Supra ventricular Arrhythmia's

V tomto díle se zaměříme na AV nodální reentry tachykardii. Zejména pak na to, jak tuto arytmii řešit na urgentním interním příjmu.

OlguYabancı uyruklu 34 yaşında kadın hasta, acil servise dispne ile başvuruyor. Türkçe bilmeyen hastanın anamnezinden öğrenilebildiği kadarıyla primer AC hastalığı kaynaklı pulmoner hipertansiyon (PHT) öyküsü olduğu, evde 2 l/dk O2 desteği ile yaşadığı belirtiliyor. Yakın zamanda ise  yurt dışına AC transplantasyonu amacıyla çıkacağı ifade ediliyor. O zamana kadar yanında getirmediği oral bir preparata kullandığı belirtiliyor. Hasta ilk bakıda 10 lt/dk O2 ile hipoksik ve takipneik olarak görülüyor. Fizik muayenede alt extremite ödemi ve asit varlığı tespit ediliyor. Sizce ileri evre PHT olan bir hastanın tedavi yönetimi nasıl olmalıdır? Tanım PHT, dinlenme halinde sağ kalp kateterizasyonu ile ölçülen ortalama pulmoner arter basıncının >25 mmHg olması olarak tanımlanır. EKO'da ölçülen sağ ventrikül (RV) sistolik basıncı (>35 mmHg), PHT için oldukça yönlendirici fakat tanısal değildir (1). Sınıflama PHT, primer (grup 1) ve sekonder (grup 2-5) sebepler olarak ayırılabilir (2,3): Grup 1 Pulmoner arterial hipertansiyon:İdiyopatik veye kalıtsal olabilir.Bağ doku hastalığı (skleroderma), HIV, orak hücre hastalığına sekonder. Grup 2 Sol kalp ilişkili pulmoner venöz hipertansiyon:PHT'un en sık sebebi.Kardiyomyopati, diastolik disfonksiyon, MS, MY, AS, AY. Grup 3 Kronik hipoksemik AC hastalığı:KOAH, İAH, OSA Grup 4 Kronik tromboembolik hastalık Grup 5 Çeşitli:Sistemik bozukluklar (sarkoidoz, nörofibromatozis), hematolojik bozukluklar (miyeloproliferatif) PHT anatomik ve patofizyolojik sınıflama (PMID: 26226870) Patofizyoloji Net mekanizma bilinmemekle birlikte, endojen vazodilatörler (prostasiklin vb) ve vazokonstriktörler (endotelin-1) arasında dengenin bozulması ile ilişkili olduğu düşünülmektedir.  Pulmoner vasküler direnç arttığında, preload ve atım hacmini korumak için  RV zamanla genişler. RV genişlemesi ise, interventriküler septumu iterek sol ventrikül dolumu ve atım hacminin azalmasına neden olur. Ayrıca, RV genişlemesi triküspit yetmezliğine neden olur. Normalde, düşük RV duvar gerilimi nedeniyle, RV hem sistolde hem de diastolde beslenir. PHT varlığında ise RV beslenmesi sadece diastolde gerçekleşir. Bu durum da RV iskemisine ve RV yetmezliğine neden olur (4).  Başvuru Semptomlar nonspesifik olmakla birlikte, hem istirahat hem de egzersiz sırasında dispne en sık semptomdur. Diğerleri arasında göğüs ağrısı, yorgunluk, presenkop/senkop yer alır. Fizik Muayene Hastalığın ileri evrelerinde bulgular belirginleşir; JVD,Hepatomegali,Asit,Alt extremite ödemi veOskültasyonda artmış P2.  Olgunun devamıHastanın yapılan EKO'sunda sağ boşluklar geniş, ciddi TY, Sistolik PAB 120 mmHg olarak ölçülüyor. Toraks BT'de ise pulmoner trunkus çapı 35 mm ölçülürken, emboli bulgusuna rastlanmıyor. Kistik AC hastalığı ve bronşektazi ön planda raporlanıyor. Sizce bu hastada hangi testler daha değerlidir? Tetkik EKG En sık sağ aks deviasyonu.En sık aritmi AF, flutter, AVNRT.  AC grafi Genişlemiş RA, RV ve hiler pulmoner arterler. EKO Apikal 4 odacık pencerede RV dilatasyonu, RV:LV oranı >1.Parasternal kısa aksta D bulgusu.Subkostal pencerede, RV serbest duvar kalınlığının artması (>5mm) kronik PHT lehine.Diğer bulgular ise sağ atriyal genişleme, triküspit kaçağı, TAPSE < 15mm. Geniş sağ ventrikül ve duvar kalınlığı. D görünümü Lab Artmış troponin ve BNP. CT Pulmoner arter çapı >30mm (Pulmoner arter, aortadan geniş olmamalı). Geniş RV. Pulmoner arter çapı, çıkan aortadan geniş. Olgunun devamıHastanın takipnesi izlemde gerilememesi üzerine NİMV tedavisi başlanıyor. Bu süreçte hastada hipotansiyon gelişiyor ve sonrasında hipoksisi derinleşiyor. Dopamin tedavisi başlanıyor. Propofol ile sedasyon sonrası entübe edildikten kısa bir süre sonra hastada arrest gelişiyor. Sizce bu hastada hemodinamik instabilite nedeni nedir? Nasıl ve ne zaman entübe edilmelidir? Yönetim Hipoksi ve hiperkapniden kaçın

Video version https://youtu.be/abGsk9x7ax0Non-Invasive EPS – Fact or Fiction? We’ve already discussed the use of CRM devices to monitor and manage arrhythmias, but what about using the leads to gain more information about the root cause of the problem? We can use the information from the separate leads during, for example, a tachycardic event to analyse and really find out what’s happening to the patient. This is good for the patient as it can mean avoiding further invasive EP studies, and helpful for us because we can make a more informed and timely decision about treatment routes. One of the first things we’re taught when learning to interpret EKGs is not to trust the machine’s report without checking it out for ourselves (STEMI or LVH, anyone?); maybe we should take that a little further and make sure we agree with our CRM devices!Let’s start with an example – the arrhythmia report here tells us we’re looking at an episode of VT, but we notice that the atrial and ventricular rates are around the same rate – 144/145bpm. The A-sensed lead and V-sensed lead show that we start off with A-paced beats followed closely by V-paced beats… all good so far. Then we see that the episode of tachycardia starts with a premature atrial beat – and we know that VT typically starts with a ventricular premature beat. Is this really VT? Could it be SVT? Then we see a run of atrial premature beats, each followed – eventually – by a ventricular beat. So it looks like we’re seeing an atrial rhythm with a very – VERY – slow pathway. Our atrial premature beat did have a V-paced beat afterwards, but the conduction pathway is so slow… could the premature beat have blocked the fast pathway, forcing conduction through a slow pathway with retrograde fast pathway conduction? So we now have a slow-fast SVT; typical of atrio-ventricular nodal re-entry tachycardia (AVNRT). With AVNRT we have a re-entry circuit going round the AV nodeNow, this patient has a device with an atrial electrode and a ventricular electrode, and these devices have the capacity to do basic EP studies without any further invasive procedures. So we can use this device alone to further our understanding of the patient’s needs, with none of the risks or costs associated with traditional EPS. Wonderful!Here we have a report from a St. Jude’s dual chamber pacemaker in a female patient who was admitted to hospital with serious symptomatic palpitations and pre-syncope. We had been unable to catch one of these episodes on a 12-lead EKG, but they were convincingly cardiac, at high risk of causing injury to the patient, and so we really needed to consider treatment. Should we do EP studies with a view to finding a source of arrhythmia and ablating? Traditional EP studies, although generally very safe, are not without their risks. It’s an invasive procedure where we introduce tubes through a blood vessel into the heart. There’s a risk of bleeding at the insertion site, and a risk of trauma anywhere en route to or within the heart. Although they’re done in aseptic conditions we can’t rule out the possibility of infection, and in this case the patient had a known blood-borne virus which always increases the risks to the staff involved in her care.Luckily, we knew that this woman had a dual-chamber pacemaker, with an atrial and a ventricular lead. In this case we were able to use her pacemaker to do an atrial drive at 700milliseconds – we can see two beats conducted from the atrium to the ventricles… then we initiate a premature atrial beat which actually triggered 8 beats of SVT – supra-ventricular tachycardia. At this point the patient confirmed that this had reproduced her symptoms of palpitations and feeling pre-syncopal. So we were able to make a diagnosis, based only on EP studies conducted through her already implanted device, of AVNRT. We can see that her premature atrial beats took a long time to conduct, so we think they’re going down a slow pathway to the ventricle, then with a dual nodal pathology - following a refractory phase - are returning to the atrium via the fast pathway and looping round until terminated. We could also consider the possibility of an atrial tachycardia, but we know that atrial tachycardia doesn’t typically terminate in the atrium unless with an ectopic premature atrial beat. What we have here terminates with an normal atrial beat with a usual morphology complex - unlikely to be an atrial tachycardia.What could we do in the cath lab to help confirm our diagnosis and plan management? We need to reinduce the tachycardia and try pacing it from the ventricle slightly faster than the atrial tachycardia had been. Once we stop pacing the ventricle, we can see a V-beat… then an A-beat… then a V-beat. Such a V-A-V response, according to Morady in his famous paper is most likely to be AVNRT or AVRT – atrioventricular re-entry tachycardia involving an accessory pathway, such as in Wolff-Parkinson-White syndrome. If we’d been looking at atrial tachycardia we’d expect to see V-A then another A then V. We’d see the drive for the tachycardia coming truly from the atria so we’d see more atrial than ventricular beats sensed.How can we tell from this whether it’s an AVNRT or an AVRT’s accessory pathway? We need to measure the PPI – the post-pacing interval. If we take the time between the last paced beat in the ventricle to the next beat in the ventricle and subtract it from the tachycardia cycle length (TCL) we’ll see the distance our entrainment location is from the tachycardia. The distance of this PPI minus TCL tells us more about what we’re seeing: if it’s less than 110 milliseconds, it’s most likely an accessory pathway – the ventricle is involved in the tachycardia, close to the circuit in the accessory pathway. However if its above 110milliseconds, it’s likely to be AVNRT; we’re further from the tachycardia circuit as the circuit is within the atria/AV node so when we pace from the ventricle we’re waiting for the impulse from our pacemaker-initiated ventricular beat to penetrate the atrial-nodal circuit. In this example we have a PPI of 541, minus a TCL of 360 – well above the 110, and far away from the tachycardia circuit. When we paced from the ventricle we were entraining the tachycardia, but we were pacing from a point in the conduction system far away from the tachycardia initiation point.We also used a few other techniques to help our diagnosis: we did incrementally faster pacing from the ventricle, and also from the atrium, and we saw that the conduction from the atrium to the ventricle, and the conduction from the ventricle to the atrium, as we increased the speed, was decremental; both the AV delay AND the VA delay grew longer. This indicates that the patient is unlikely to have an accessory pathway – in an accessory pathway the conduction is not decremental as it’s the AV node that slows down the conduction from the atria to the ventricle and vice-versa. There are some other pathways which could be considered, and we’ll discuss these another time.This is a great example of getting some really sophisticated EPS and making a clear diagnosis using already-implanted dual chamber devices. We followed this with a typical AVNRT ablation which ended up being a really simple procedure based on the information we already had from her pacemaker.It’s uncommon, in our experience, to use already-implanted devices to perform fully diagnostic EP studies. Does your department use this method? If you have any experience or comments about this, if you have any thoughts about the benefits or limits of these methods, we’d love to hear from you!Here at EPme.me we love feedback; our aim is to help you learn so please do get in touch with ideas for sessions you’d like to see. Whether you work in electrophysiology, devices, both or neither, we want to hear from you. Follow our YouTube channel to keep up to date with leading cardiac electrophysiology from around the world. Sign up for our newsletter to receive our free ECG cheatsheet — you’ll wonder how you did without it.COMING UP: Next few weeks, we’re gonna be talking some great EP cases’ Fresh from the EP lab Part 1 - “4th time lucky”. Some really interesting case studies from the EP lab.Thank you so much!Website: https://epme.me/Instagram: http://instagram.com/cardiac_electrophysiologyTwitter: https://twitter.com/EPmedotmeFacebook: https://www.facebook.com/EPme.me/Pinterest: https://www.pinterest.com/epmedotme/YouTube channel:https://www.youtube.com/channel/UCism4RgECx2HYcn4x_IWhbA?sub_confirmation=1

Video version https://youtu.be/AKOdaRQe5zgVT or not?Cardiac Rhythm Management (CRM) devices are widely used to address heart rhythm disorders thanks to sophisticated algorithms. But can we always trust them?Let’s have a look at an interesting case study from our clinic.New_Fig1_eventThis is an event that happened to a 52-years old male patient with a defibrillator. What type of tachycardia could it be?Was it:· a ventricle tachycardia (VT)?· an atrial tachycardia (AT)?· an accessory pathway (AVRT)?· an AV node re-entry tachycardia (AVNRT)?Patient’s CRM device algorithm recognized it as a VT event.CRM device recognition:· a ventricle tachycardia (VT)· an atrial tachycardia (AT)· an accessory pathway (AVRT)· an AV node re-entry tachycardia (AVNRT)But can we trust this result?A closer look at the caseAs we can see in the case report, an average Atrial rate was faster than average Ventricle rate. However, the criteria for VT event is the opposite, isn’t it?And what about EGM?There are equal atrial and ventricle rates occurring in the event and the device recognizes it as VT in the marker channel.In consequence on this recognition, the device provides anti-tachycardia pacing (ATP) therapy in the ventricle to override the VT and stops it without having to give a shock to our patient.It helped, but was it really VT?How it startedAfter an A sensed and V sensed beat we can see a premature ventricular complex (PVC) that is correctly labeled in the marker channel as well.This premature ventricular beat is followed by an A paced and V paced beat, so obviously the premature ventricular beat had no connection/effect to the tachycardia.Nevertheless, the next A sensed beat is conducted down to the ventricle and THAT seems to be the start of the tachycardia.This is followed by a second A beat that goes down to the ventricle.And what is more interesting – AV delay changed!But VT doesn’t start with an atrial event! That means it was probably not VT and the CRM device was not right.New_Fig2_avg_rates_channels_PVC_start_ AV_delayWas it:· a ventricle tachycardia (VT)?· an atrial tachycardia (AT)?· an accessory pathway (AVRT)?· an AV node re-entry tachycardia (AVNRT)?Tachycardia morphologyWhat’s more, if we have a look at the shock EGM, we can see a wide complex QRS representing a contraction of the ventricle.A premature V beat has a very different shape from the tachycardia beat. That brings another point against VT because of the QRS morphology of the tachycardia looks like a normal sinus rhythm beat.VA intervalNot only did the tachycardia morphology prove that it’s probably not VT. A short VA interval could direct us to an AVNRT.A typical AVNRT generally conducts from the atrium to the ventricle down the slow pathway and back up the fast pathway. In other words, we can’t confirm it’s AVNRT, but it’s a likely option.TerminationThe event is terminating through ventricular pacing (ATP).The ventricles are being paced at a faster rate than the tachycardia and the tachycardia is still running in the atrium at its own rate, at the same time. That confirms it’s not an accessory pathway (AVRT) because otherwise, it would be running at the V pacing rate, as AVRT by definition involves both the A and V.New_Fig3_ channels_shape_shortVA_terminationIt has already been proven that it’s not a VT and it’s not an accessory pathway.Was it:· a ventricle tachycardia (VT)?· an atrial tachycardia (AT)?· an accessory pathway (AVRT)?· an AV node re-entry tachycardia (AVNRT)?The tachycardia terminated by itself. And it didn’t terminate in the ventricle but in the atrium. As you can see in the following strip from a similar event in the same patient (also recognized as VT).New_Fig4_term_inAIt’s very unlikely it was an atrial premature beat and it’s also unlikely that it is an atrial tachycardia because it wouldn’t just stop on an atrial beat if the atrium was running.Was it:· a ventricle tachycardia (VT)?· an atrial tachycardia (AT)?· an accessory pathway (AVRT)?· an AV node re-entry tachycardia (AVNRT)?Don’t trust solely in devicesBoston Scientific devices know how to detect the difference between SVT and VT. How does the devices work?The device reading is based on rhythm ID algorithm that correlates to the morphology. However, since the device is counting only what’s happening on the ventricular channel and not on the atrial channel, as it's marked in the Ventricle blanking period (the sensed atrial beats are recorded in brackets), that’s why it’s detecting the event as VT and not SVT.Thanks to the device our patient received a VT treatment and it helped him, even though it wasn’t a VT. We found out that the event was an SVT, most likely an AVNRT. Therapy treatment for this diagnosis is a simple ablation. Whereas the type of treatment for VT or AVNRT would be totally different.New_Fig5_key_factorsIn this case, the patient has undergone a successful SVT ablation in the EP lab, because he was symptomatic with this SVT, and we wanted to avoid more of these events being wrongly recognized as VT by mistake. In the future, his defibrillator might not just give him anti-tachycardia pacing, but an inappropriate electric shock. And that’s what we certainly didn't want.DiagnosingIn order to recognize heart rhythm disorders correctly, it’s important to constantly train our electrophysiology skills. Even though we work with modern devices, the algorithms are sometimes not reliable enough.With this in mind, there is a final key point to remember–when the device recognizes a VT event, always ask: is it really a VT or not?Here at EPme.me we love feedback; our aim is to help you learn so please do get in touch with ideas for sessions you’d like to see. Whether you work in electrophysiology, devices, both or neither, we want to hear from you. Follow our YouTube channel to keep up to date with leading cardiac electrophysiology from around the world. Sign up for our newsletter to receive our free ECG cheatsheet — you’ll wonder how you did without it.COMING UP: Next few weeks, we’re gonna be talking about using devices in arrhythmia diagnosis. Some really interesting case studies from devices, to explore further the effects and use of devices in EP.Thank you so much!Website: https://epme.me/Instagram: http://instagram.com/cardiac_electrophysiologyTwitter: https://twitter.com/EPmedotmeFacebook: https://www.facebook.com/EPme.me/Pinterest: https://www.pinterest.com/epmedotme/YouTube channel:https://www.youtube.com/channel/UCism4RgECx2HYcn4x_IWhbA?sub_confirmation=1

I episode 18 taler Morten og Karl om Valsalva manøvren, nærmere bestemt den modificerede valsalva manøvre. Denne manøvre er udviklet til at bremse en supra ventrikulær takykardi (SVT),  et emne der fylder meget lidt i uddannelse og instrukser. Vi  gennemgår fysiologien bag de gængse takyarytmier og hvilke rytmer man vil kunne have effekt af manøvren.  De fortæller om udførelse af selve manøvren og hvad der sker i kroppen under og efter den. Samt om hvilke patienter vi ikke skal forsøge os på. Hør hele podcasten og se vores video på bloggen, der viser hvordan den modificerede valsalva manøvre kan udføres i det præhospitale.  God fornøjelse.  Abonner eller hent via iTunes for iOS og for android via Stitcher. Nu også via TUNE IN Links, henvisninger og videoer   Proceduren https://youtu.be/CZP9peZQ9qY https://www.youtube.com/watch?v=8DIRiOA_OsA Video som forklarer AVNRT og AVRT - youtube Generelt om Valsalva: SGEM#67: Shock the monkey - Podcast om standart Valsalva Llifeinthefastlane om fysiologien bag ved Valsalva manøvren Information om REVERT trial Link til den fulde artikel Lancet 2015 SGEM#147: This is a SVT and om gonna REVERT it, using the modified Valsalva manoeuvre Kritisk analyse af REBEL:EM af Salem Rezaie Rick Body at St. Emlyn’s: JC The REVERT Trial – Dip or Doom for SVT in the Emergency Department Ryan Radecki at EMLit of Note: Valsalva 2.0 Steve Mathieu at The Bottom Line: Postural Modification to the Standard Valsalva Manoeuvre for Emergency Treatment of Supraventricular Tachycardias (REVERT) – A Randomised Controlled Trial Bøger Tim Phalen: the 12-lead ECG in myocardial infarction Andre relevante sager: Karls avancerede men dog hjemme producerede Valsalva device Kig forbi FOAMmedic Live og tilmeld dig Avanceret EKG eller Basal EKG. En unik mulighed for at lære noget kompliceret på en legende måde i selskab med det præhospitale fags bedste kollegaer. Støt FOAMmedics arbejde med 5 eller 10 kr pr. podcast. Hvis du har lyst til at støtte vores arbejde med at lave lækker lyd og skrift så klik ind på 10er.dk og støt os med 5,10 eller 15 pr. podcast episode, så bliver vi så sindsygt stolte og glade. Eller klik på 10'er logo her under og en pop-up løsning kommer frem.  

Paul Wang:         Welcome to the monthly podcast “On The Beat”, for Circulation: Arrhythmia and Electrophysiology. I am Dr. Paul Wang, Editor-in-Chief, with some of the key highlights from this month's issue. We'll also hear from Dr. Suraj Kapa, reporting on new research from the latest journal articles in the field.                                 In our first article, Adetola Ladejobi and associates studied 1,433 patients, between 2000 and 2012, who were discharged alive after sudden cardiac arrest. A reversible and correctable cause was identified in 792 patients, or 55%. A reversible cause for sudden cardiac arrest was defined as significant electrolyte or metabolic abnormality, evidence of acute myocardial infarction or ischemia, recent initiation of antiarrhythmic drug, or illicit drug use, or other reversible circumstances.                                 Of the 792 sudden cardiac arrest survivors, due to reversible or correctable cause, 207 or 26% of the patients received an ICD after their indexed sudden cardiac arrest. During a mean follow-up of 3.8 years, 319 or 40% of patients died. ICD implantation was highly associated with a lower all-cause mortality, p < 0.001, even after correcting for unbalanced baseline characteristics.                                 In subgroup analyses, only patients with sudden cardiac arrest, were not associated with myocardial infarction, extracted benefit from the ICD, p < 0.001.                                 The authors concluded that in survivors of sudden cardiac arrest, due to a reversible and correctable cause, ICD therapies associated with lower all-cause mortality, except if the sudden cardiac arrest was due to myocardial infarction.                                 Further prospect of multi-center randomized control trials will be needed to confirm this observation.                                 In our next study, Carlo Pappone and associates, studied 81 patients with persistent atrial fibrillation, randomized to undergo high density electrophysiological mapping, to identify repetitive regular activities, before modified circumferential pulmonary vein ablation, or modified circumferential pulmonary vein ablation alone. The primary endpoint was freedom from arrhythmia recurrence at one year.                                 In the 81 patients with persistent atrial fibrillation, there were 479 regions exhibiting repetitive regular activities in these patients, or 5.9 repetitive regular activities per patient. There were 232 regions in the mapping group, which consisted of 41 patients, and 247 regions in the control group, consisting of 40 patients. Overall, 39% of the repetitive regular activities were identified within pulmonary veins, whereas 61% were identified in non-pulmonary vein regions.                                 Mapping-guided ablation resulted in higher arrhythmia termination rate, as compared to conventional strategy, 61% vs. 30%, p < 0.007. Total RF duration, mapping, and fluoroscopy times were not significantly different between the groups. No major procedure related adverse events occurred.                                 After one year, 73% of the mapping group of patients were free of recurrences, compared to 50% of the control group, p = 0.03.                                 The authors concluded that targeted ablation of regions showing repetitive regular activities provided adjunctive benefit in terms of arrhythmia freedom at one year in treatment of patients with persistent atrial fibrillation. These findings should be confirmed by additional larger randomized multi-centered studies.                                 In the next article, Maciej Kubala and associates examine repolarization abnormalities in 40 patients with arrhythmogenic right ventricular cardiomyopathy, comparing extent and location of abnormal T-waves of one millimeter or greater in depth, downsloping elevated ST segment in two or more adjacent leads to the area and location of endocardial bipolar and unipolar, and epicardial bipolar voltage abnormalities. They found an abnormal unipolar right ventricular endocardial area of 33.4% with presence in eight patients without negative T-waves. Patients with negative T-waves extending beyond V3, seen in 20 patients, had larger low bipolar and unipolar endocardial areas, and larger epicardial low bipolar areas, compared to those with negative T-waves limited to leads V1 to V3.                                 ECG localization of negative T-waves regionalized to the location of substrate. Patients with downsloping elevated ST segment, all localized to leads V1, V2 had more unipolar endocardial abnormalities involving outflow in mid-right ventricle, compared to patients without downsloping elevated ST segment.                                 The authors concluded that in arrhythmogenic right ventricular cardiomyopathy, abnormal electric current areas were proportional to the extent of T-wave inversion on the 12 lead electrocardiogram. Marked voltage abnormalities can exist without repolarization changes. Downsloping elevated ST segment patterns in V1 and V2 occurs with more unipolar endocardial voltage abnormalities, consistent with more advanced trans neural disease.                                 In the next manuscript, Teresa Oloriz and associates examine the timing and value of program stimulation after catheter ablation for ventricular tachycardia. They performed 218 program ventricular stimulations six days after ablation in 210 consecutive patients, 48% with ischemic cardiomyopathy in the median left ventricular ejection fraction of 37%. After ablation, ICDs were programmed according to NIPS results. Class A were noninducible, Class B non documented inducible VT, and Class C documented inducible VT. Concordance between the programmed ventricular stimulation at the end of the procedure and at six days was 67%. The positive predictive value and negative predictive value were higher for the programmed ventricular stimulation at day six. Ischemic patients and those with preserved ejection fraction showed the highest negative predictive value.                                 Among noninducible patients at the end of the procedure, but inducible at day six, 59 patients had VT recurrence at one year follow-up. Recurrences were 9% when both studies were noninducible. There were no inappropriate shocks, incidents of syncope with 3%, none harmful. The rate of appropriate shocks per patient per month according to NIPS was significantly reduced, comparing the month before and after the ablation.                                 The authors concluded that programmed ventricular stimulation at day six predicts VT recurrence.                                 In the next study, Tor Biering-Sørensen and associates examined ECG global electrical heterogeneity, GEH, in its longitudinal changes, are associated with cardiac structure and function, in their Atherosclerosis Risk and Community study, ARIC, consisting of 5,114 patients, 58% which were female and 22% African Americans. Using the resting 12-lead ECGs, and echocardiographic assessments of left ventricular ejection fraction, global strain, left ventricular mass index, end diastolic volume index, end systolic volume index at visit five.                                 Longitudinal analysis included ARIC participants with measured GEH at visits one to four. GEH was quantified by spatial ventricular gradient, the QRST angle, and the sum of the absolute QRST integral. Cross sectional and longitudinal regressions were adjusted for manifest subclinical cardiovascular disease.                                 Having four abnormal GEH parameters was associated with a 6.4% left ventricular ejection fraction decline, a 24.2 gram/meter square increase in left ventricular mass index, a 10.3 milliliter/meter square increase in left ventricular end diastolic volume index, and a 7.8 milliliter/meter square increase in left ventricular end systolic index. All together, clinical and ECG parameters accounted for approximately one third of the left ventricular volume in 20% of the systolic function variability.                                 The associates were significantly stronger in patients with subclinical cardiovascular disease. The QRST integral increased by 20 millivolts/meter second for each three year period participants who demonstrated left ventricular dilatation at visit five. Sudden cardiac death victims demonstrated rapid GEH worsening, while those with left ventricular dysfunction demonstrated slow GEH worsening.                                 The authors concluded that GEH is a marker of subclinical abnormalities in cardiac structure and function.                                 In the next manuscript, Takumi Yamada and associates studied 19 patients with idiopathic ventricular arrhythmias, originating in the parietal band in 14 patients, in the septal band in 5 patients. Among 294 consecutive patients with right ventricular arrhythmia origins, parietal band and septal band ventricular arrhythmias exhibited a left bundle branch block, with left inferior in 12 patients', superior in 2 patients' axes, in left or right inferior axis pattern in four and one patients respectively.                                 In Lead 1, all parietal band ventricular arrhythmias exhibited R-waves, while septal band ventricular arrhythmias often exhibited S-waves. A QS pattern in lead AVR, in the presence of a knock in the mid QRS were common in all infundibular muscle ventricular arrhythmias. During infundibular muscle ventricular arrhythmias, a far-field ventricular electrogram, with an early activation, was always recorded in the His bundle region, regardless of the location of ventricular arrhythmia regions. With 9.2 radiofrequency applications in a duration of 972 seconds, catheter ablation was successful in 15 of the 19 patients. Ventricular arrhythmias recurred in four patients during a fallout period of 43 months.                                 In the next paper, Uma Mahesh Avula and associates examine the mechanisms underlying spontaneous atrial fibrillation, in an Ovine model of left atrial myocardial infarction. The left atrial myocardial infarction was created by ligating the atrial branch of the left anterior descending artery. ECG loop recorders were implanted to monitor atrial fibrillation episodes.                                 In seven sheep, Dantrolene, a Ryanodine receptor blocker, was administered in vivo, during the observation period. The left atrial myocardial infarction animals experienced numerous episodes of atrial fibrillation during the eight day monitoring period, that were suppressed by Dantrolene. Optical mapping showed spontaneous focal discharges originating through the ischemic/normal-zone border. These spontaneous focal discharges were calcium driven, rate dependent, and enhanced by isoproterenol, but suppressed by Dantrolene.                                 In addition, these spontaneous focal discharges initiated atrial fibrillation-maintaining reentrant rotors anchored by marked conduction delays at the ischemic/normal-zone border. Nitric oxide synthase one protein expression decreased in ischemic zone myocytes, or NADPA oxidase in xanthine oxidase enzyme activities in reactive oxygen species increased. Calmodulin aberrantly increased, Ryanodine binding to cardiac Ryanodine receptors in the ischemic zone. Dantrolene restored the physiologically binding of Calmodulin to the cardiac Ryanodine receptors.                                 The authors concluded that atrial ischemia causes spontaneous atrial fibrillation episodes in sheep, caused by spontaneous focal discharges that initiate re-entry. Nitroso redox imbalance in the ischemic zone is associated with intensive reactive oxygen species production, and altered the Ryanodine receptor responses to Calmodulin. Dantrolene administered normalize the Calmodulin response and prevents left atrial myocardial infarction, spontaneous focal discharges in atrial fibrillation initiation.                                 In the next study, Wouter van Everdingen and associates examine the use of QLV for achieving optimal acute hemodynamic response to CRT with a quadripolar left ventricular lead. 48 heart failure patients with left bundle branch block were studied. Mean ejection fraction 28%, mean QRS duration 176 milliseconds. Immediately after CRT implantation, invasive left ventricular pressure volume loops were recorded during biventricular pacing, with each separate electrode at four atrial ventricular delays.                                 Acute CRT response, measured as a change in stroke work compared to intrinsic conduction, was related to the intrinsic interval between the Q on the electrocardiogram and the left ventricular sensing delay, that is the QLV, normalized for the QRS duration, resulting in QLV over QRS duration in the electrode position.                                 QLV over QRS duration was 84% and variation between the four electrodes was 9%. The change in stroke work was 89% and varied by 39% between the electrodes. In univariate analysis, an anterolateral or lateral electrode position in a high QLV to QRS duration ratio had a significant association with a large change in stroke work, all P less than 0.01.                                 In a combined model, only QLV over QRS duration remained significantly associated with a change in stroke work, P less than 0.5. However, a direct relationship between QLV over QRS duration in stroke work was only seen in 24 patients, while 24 other patients had an inverse relation.                                 The authors concluded that a large variation in acute hemodynamic response indicates that the choice of stimulated electrode on the quadripolar electrode is important. Although QLV to QRS duration ratio was associated with acute hemodynamic response at a group level, it cannot be used to select the optimal electrode in the individual patient.                                 In the next study, Antonio Pani and associates conducted a multi-centered prospective study evaluating the determinance of zero-fluoroscopy ablation of supraventricular arrhythmias. They studied 430 patients with an indication for EP study and/or ablation of SVT. A procedure was defined as zero-fluoroscopy when no fluoroscopy was used. The total fluoroscopy time inversely was related to number of procedures previously performed by each operator since the study start. 289 procedures, or 67%, were zero-fluoro. Multi-variable analyses identified as predictors of zero-fluoro was the 30th procedure for each operator, as compared to procedures up to the ninth procedure, the type of arrhythmia, AVNRT having the highest probability of zero-fluoro, the operator, and the patient's age. Among operators, achievement of zero-fluoro varied from 0% to 100%, with 8 operators, or 23%, achieving zero-fluoro in 75% of their procedures. The probability of zero-fluoro increased by 2.8% as the patient's age decreased by one year. Acute procedural success was obtained in all cases.                                 The authors concluded that the use of 3D mapping completely avoided the use of fluoroscopy in most cases, with very low fluoro time in the remaining, and high safety and effectiveness profiles.                                 In the next paper, Demosthenes Katritsis and associates examine the role of slow pathway ablation from the septum as an alternative to right-sided ablation. Retrospectively, 1,342 undergoing right septal slow pathway ablation for AV nodal reentry were studied. Of these, 15 patients, 11 with typical and 4 with atypical AVNRT, had a left septal approach following unsuccessful right sided ablation, that is, the righted left group. In addition, 11 patients were subjected prospectively to a left septal only approach for slow pathway ablation, without previous right septal ablation, that is, left group. Fluoroscopy times in the right and left group, and the left groups were 30.5 minutes and 20 minutes respectively, P equals 0.6. The rate of [inaudible 00:18:24] current delivery time for comparable, 11.3 minutes and 10.0 minutes respectively.                                 There are no additional ablation lesions at other anatomical sites in either group, and no cases of AV block were encountered. Recurrence rate for arrhythmias in the right and left group was 6.7% and 0% in the left group, in the three months following ablation.                                 The authors concluded that the left septal anatomical ablation of the left inferior nodal extension is an alternative to ablation of both typical and atypical AV nodal reentry when ablation at the right posterior septum is ineffective.                                 In our next study, Mark Belkin and associates reported prior reports of new-onset device-detected atrial tachyarrhythmias. Despite the clear association between atrial fibrillation and the risk of thromboembolism, the clinical significance of new-onset device-detected atrial tachyarrhythmias and thromboembolism remains disputed.                                 The authors aim to determine the risk of thromboembolic events in these patients. Using the Ovid Medline, Cochrane, SCOPUS databases to identify 4,893 reports of randomized control trials, perspective or retrospective studies of pacemaker and defibrillator patients reporting the incidence of device detected atrial tachyarrhythmias.                                 The authors examine 28 studies, following a total of 24,984 patients. They had an average age of 69.9 years and a mean study duration of 21.8 months. New-onset device-detected atrial tachyarrhythmias was observed in 23% of patients. Among nine studies, consisting of 8,181 patients, reporting thromboembolism, the absolute incidence was 2.1%. Thromboembolic events were significantly greater among patients with new-onset device-detected arrhythmias, with a relative risk of 2.88, compared to those who had less than one minute of tachyarrhythmias, 1.77 risk ratio.                                 The authors concluded that new-onset device-detected atrial tachyarrhythmias is common, affecting close to one quarter of all patients with implanted pacemakers and defibrillators.                                 In our last paper, Sanghamitra Mohanty and associates performed a meta-analysis systematically evaluating the outcome of pulmonary vein isolation with and without thermoablation in patients with atrial fibrillation. For pulmonary vein ablation alone, only randomized trials conducted in the last three years reporting single procedure success rates, off antiarrhythmic drugs at 12 months or greater follow-up were included. In the PVI plus FIRM group, all public studies reporting a single procedure off antiarrhythmic drug success rate with at least one year follow-up were identified.                                 Meta-analytic estimates were derived, using the DerSimonian and Laird Random-effects Models, and pooled estimates of success rates. Statistical heterogeneity was assessed using the Cochran Q test and I-square. Study quality was assessed with the Newcastle-Ottawa Scale.                                 15 trials were included, 10 with PVI plus FIRM, with 511 patients, non-randomized perspective design, and 5 pulmonary vein isolation-only trials, consisting of 295 patients, all randomized.                                 All patients in the pulmonary vein only trials had 100% non paroxysmal atrial fibrillation, except for one study, and no prior ablations. About 24% of the PVI plus FIRM patients had paroxysmal atrial fibrillation.                                 After 15.9 months of follow-up, the off antiarrhythmic drug pooled success was 50% with FIRM plus PVI, compared to 58% in the PVI alone. The difference in the effect size between the groups was not statistically significant. No significant heterogeneity was observed in this meta-analysis.                                 The authors concluded that the overall pooled estimate did not show any therapeutic benefit of PVI FIRM over PVI alone.                                 That's it for this month, but keep listening. Suraj Kapa will be surfing all journals for the latest topics of interest in our field. Remember to download the podcast On The Beat. Take it away, Suraj. Suraj Kapa:          Thank you, Paul, and welcome back to “On The Beat”. Again, my name is Suraj Kapa and I'm here to review with you articles across the cardiac electrophysiology literature that were particularly hard hitting in the month of February.                                 To start, we review the area of atrial fibrillation, focusing on anticoagulation. Reviewing an article published in this past month's issue of the Journal of the American Heart Association, by Steinberg et al., entitled Frequency and Outcomes of Reduced Dose Non-Vitamin K Antagonist Anticoagulants, results from ORBIT AF II. The ORBIT AF II registry, also called the Outcomes Registry for Better Informed Treatment of Atrial Fibrillation, is a prospective national observational registry of AF patients.                                 The author sought to describe the frequency, appropriateness, and outcomes of patients prescribed reduced doses of NOACs in the community practice. They reviewed the records of almost 8,000 patients receiving NOACs and noted that the vast majority, nearly 84%, received a standard dose of NOACs, consistent with the U.S. FDA labeling. While only 16% received a reduced dose, only 43% of these were consistent with labeling instructions. Those who received reduced dose NOACs inappropriately more often tended to be younger and have, interestingly, lower overall bleeding risks scores.                                 Furthermore, compared with those appropriately receiving dosing, patients receiving inappropriately reduced dose NOACs had a higher unadjusted rates of thromboembolic events and death.                                 These data are important to understand, in that, discussion with patients, that inappropriate reduction of NOACs does not necessarily offer appropriate protection against long-term risk of thromboembolic events. Thus, close attention must be paid to consideration of the use cases and instructions for use.                                 While the registry cannot get into the details of why the dose was reduced in the spectrum of patients, it does highlight the fact that this continues to be a problem in general practice.                                 Further data is needed to understand what leads to inappropriate dose reduction, which could include factors such as patient preference, or physician education.                                 Staying within the realm of anticoagulation and understanding individual needs, we next review an article published in this past month's issue of Circulation, by Nielsen et al., entitled Female Sex Is a Risk Modifier Rather Than a Risk Factor for Stroke in Atrial Fibrillation. Should we use a CHA2DS2-VA score rather than CHA2DS2-VASc? In this review, the authors sought to evaluate whether female sex is truly an overall risk factor, as opposed to a risk modifier.                                 Using three nationwide registries, they identified patients with nonvalvular atrial fibrillation between 1997 and 2015, and they calculated two sets of scores. The first score, they termed a CHA2DS2-VA score, calculated for men and women with follow-up of one year in the Danish National Patient Registry. They wanted to calculate the risk based on this pseudo-value method. They then reviewed female sex as a prognostic factor by inclusion as an interaction term on the CHA2DS2-VA score, to calculate overall thromboembolic risk.                                 Amongst over 200,000 patients with atrial fibrillation, almost half of whom are women, they noted that the mean CHA2DS2-VA score, where sex is excluded, was a tad higher in women than men, namely 2.7 vs. 2.3. However, women had an overall higher one year thromboembolic rate of 7.3 vs. 5.7 per 100 person-years. Interestingly, with a CHA2DS2-VA score of zero, the absolute risk of thromboembolism was equal amongst men and women, around .5%. Once overall points increased above one, however, women exhibited a higher stroke risk. This interaction was statistically significant.                                 Thus, the authors indicated that female sex is a risk modifier for stroke in patients with atrial fibrillation, rather than a risk factor. The terminology is important to consider. Essentially, what they are noting is that at the lower risk level, female sex, in and of itself, is not something that necessarily puts somebody in the higher risk cohorts. Instead, at higher risk levels, because of other factors, a woman may have a higher overall risk of stroke than men. Thus, stroke risk is accentuated in women, who would have been eligible for oral anticoagulating treatment anyway, on the basis of a CHADS score above one.                                 These data highlight the importance of thinking about the fact that at the lower risk score level, female sex alone might not be sufficient to say that a patient has reached the CHA2DS2-VASc score of one and above. But, really, you need an overall CHA2DS2-VA score, or a risk score, inclusive of at least two other risk factors to indicate that now, being a female is going to modify the risk and further accentuate it.                                 Now, one thing to note is, these data are very consistent with the guidelines. The European guidelines indicates that female sex alone, which in the CHA2DS2-VASc score would confer a risk score of one, should not, by itself, construe the need to put somebody on anticoagulation.                                 However, it's important to highlight that these data show that at a CHA2DS2-VASc score of one in females, they should really be construed as equivalent to a CHA2DS2-VASc score of zero in men.                                 Using the CHA2DS2-VA score, where sex is excluded, but considering that women overall have a higher incidence of stroke at any given CHA2DS2-VA level above one, will help better counsel women about the importance of being on anticoagulants.                                 The next article we review relates to long-term risk related to atrial fibrillation, published in February's issue of Heart Rhythm, by Nishtala et al., entitled Atrial Fibrillation and Cognitive Decline in the Framingham Heart Study. While there's much out there about the potential long-term role of cognitive decline in atrial fibrillation patients, longitudinal research investigating the relationship is relatively sparse. Thus, the authors sought to investigate the association between atrial fibrillation and cognitive performance, cross-sectionally and longitudinally.                                 They chose patients within the Framingham study who are dementia and stroke-free at the time of baseline neuropsychological assessments. They evaluated atrial fibrillation status as a two level variable, namely prevalent atrial fibrillation vs. no atrial fibrillation in cross-sectional analyses. And they also separated into prevalent atrial fibrillation at baseline, interim development of atrial fibrillation, and those who didn't develop any atrial fibrillation in longitudinal analysis.                                 They studied 2,682 participants in the Framingham Heart study, including original and offspring cohorts. They noted that a baseline of about 4% had diagnosed atrial fibrillation. Prevalent AF was noted to be significantly associated with poorer attention. Interestingly, sex differences were noted, with men performing worse on test of abstract reasoning and executive function than women.                                 They noted that prevalent atrial fibrillation was significantly associated with the longitudinal decline in executive function, in both the original cohorts, as well as interim atrial fibrillation being significantly associated with longitudinal decline in executive function of the offspring cohorts. Thus, they noted that atrial fibrillation is associated with a profile of long-term change in cognitive function.                                 The importance of these data are to further highlight the potential contribution of atrial fibrillation to cognitive decline. While the exact mechanisms remain to be fully elucidated, the question of how to get ahead of the cognitive decline associated with atrial fibrillation is further put out by these data.                                 Whether the relationship between atrial fibrillation and cognitive decline is due to recurrent thromboembolic events vs. the therapies used vs. other factors such as humid anatomic factors resulting in poor brain perfusion, are relatively unclear.                                 Certainly it is also possible that atrial fibrillation simply reflects a process associated with other factors that might lead to cognitive decline. However, again, further mechanistic studies and potential treatment interventions to mitigate the risk of cognitive decline are still needed.                                 Speaking of this, we next review a paper published in the European Heart Journal this past month, by Friberg and Rosenqvist, entitled Less Dementia with Oral Anticoagulation in Atrial Fibrillation.                                 Speaking of treatments to avoid long-term cognitive decline, the authors sought to evaluate if oral anticoagulant treatment might offer protection against long-term dementia risk in atrial fibrillation.                                 These retrospective registry studies of patients with the hospital diagnoses of atrial fibrillation and no prior diagnosis of dementia in Sweden, including patients between 2006 and 2014. The study included a total of 444,106 patients over 1.5 million years. They noted that patients who were on anticoagulant treatment at baseline were associated with a 29% lower risk of dementia than patients without anticoagulant treatments. Thus, there is an overall 48% lower risk on treatments with the appropriate anticoagulation. There is no difference on whether Warfarin or the newer oral anticoagulants were used.                                 Thus, the authors concluded that the risk of dementia is higher without oral anticoagulant treatment in patients with atrial fibrillation, suggesting that early initiation of anticoagulant treatment in patients with atrial fibrillation could be of value to preserve long-term cognitive function.                                 This relates directly back to the previous paper, which focused more on the epidemiologic risk, while this paper focuses on elements that might construe mechanism or treatment options.                                 Many authors have concluded the incredible importance of early recognition of the need for anticoagulant initiation in patients with atrial fibrillation. While the exact mechanism of cognitive decline and dementia in atrial fibrillation remains to be completely elucidated, certainly recurrent thromboembolic events that might be relatively silent as they occur, but result in a long-term cumulative risk might be helped by placing patients on anticoagulants.                                 This becomes another reason to counsel patients on the importance of long-term anticoagulant therapy. Certainly, the limitations of these studies, however, are the retrospective nature and the fact that there might be some subtle differences that may not be otherwise able to be construed from retrospective registry data regarding the relative role of anticoagulants in truly protecting against long-term cognitive decline. However, the data are certainly provocative.                                 Continuing within realm and discussing outcomes associated atrial fibrillation, we next review an article by Leung et al., entitled The Impact of Atrial Fibrillation Clinical Subtype on Mortality, published in JACC: Clinical Electrophysiology this past month.                                 The author sought to investigate the prognostic implications of a subtype of atrial fibrillation, paroxysmal or persistent, on long-term prognosis. They sought to evaluate differences in mortality between paroxysmal or persistent atrial fibrillation amongst 1,773 patients. They adjusted for comorbid diseases associated with atrial fibrillation, as well as CHA2DS2-VASc score. In the study, a total of about 1,005 patients or about 57% had persistent atrial fibrillation. Over the follow-up period, about 10% of those with paroxysmal atrial fibrillation and 17% of those with persistent atrial fibrillation died.                                 They noted that persistent atrial fibrillation, after correcting for other comorbidities, was independently associated with worse survival. Thus, they concluded that persistent atrial fibrillation is independently associated with increased mortality in the long term.                                 These data are relevant in that they highlight that persistent atrial fibrillation in its nature might construe an overall higher risk cohort. It remains to be fully understood what are the true mechanistic differences between persistent and paroxysmal atrial fibrillation. Overall, however, the community grossly agrees that persistent atrial fibrillation likely suggests a higher degree of atrial myopathy. If we believe this, then it is reasonable to believe that the risk associated with this specific form of atrial fibrillation might result in higher long-term harm.                                 Of course, these data are subject to the same limitations of all retrospective data. Namely, these persistent atrial fibrillation patients might have received different therapies or been more sick to start with that cannot be construed by comorbidities alone.                                 Furthermore, these data do not necessarily get to the point of whether treating atrial fibrillation in the persistent patient more aggressively necessarily reduces the risk equivalent to that of paroxysmal patients. Thus, further understanding is needed to understand how to use these data to reduce this mortality difference.                                 Continuing within the realm of epidemiology of atrial fibrillation, we next review an article published in this past month's issue of Circulation, by Mandalenakis et al., entitled Atrial Fibrillation Burden in Young Patients with Congenital Heart Disease. It is assumed that patients with congenital heart disease are vulnerable to atrial fibrillation because of multiple factors. These include residual shunts, hemodynamic issues, atrial scars from previous heart surgery, valvulopathy and other factors.                                 However, there's limited data on the overall risk of developing atrial fibrillation and complications associated with it, especially in children and young adults with congenital heart disease. Furthermore, these children and young adults with congenital heart disease have never been compared with overall risk and control subjects.                                 The authors use the Swedish Patient and Cause of Death Registries to identify all patients with diagnoses of congenital heart disease born from 1970 to 1993. They then matched these patients with control subjects from the Total Population Register in Sweden. They noted amongst almost 22,000 patients with congenital heart disease and almost 220,000 matched control subjects that 654 patients amongst the congenital heart disease cohort developed atrial fibrillation, while only 328 amongst the larger control group developed atrial fibrillation. The mean follow-up overall was 27 years.                                 They noted the risk of developing atrial fibrillation was almost 22 times higher amongst patients with congenital heart disease than control subjects. They noted the highest risk with a hazard ratio of over 84 was noted in patients with conotruncal defects. Furthermore, at the age of 42 years, over 8% of patients with congenital heart disease had a recorded diagnosis of atrial fibrillation.                                 Interestingly, heart failure was a particularly important complication in patients with congenital heart disease and atrial fibrillation, with over 10% of patients developing atrial fibrillation and [inaudible 00:38:20] congenital heart disease developing a diagnosis of heart failure as well.                                 These data are important in that they help in counseling the importance of close follow-up of patients with congenital heart disease and their long-term risk of other complications. Even if patients might be perceivably well managed, incident atrial fibrillation might increase risk of stroke in these patients. It is further important to note that many of these patients cannot be evaluated according to traditional risk or evaluations. Thus, it is important to consider whether or not a patient should be treated with anticoagulation once they develop atrial fibrillation.                                 The high risk of overall atrial fibrillation incidents, particularly in patients with more complex congenital defects, needs to be taken into consideration when advising on the frequency of follow-up.                                 It is important to further note that we must think of this overall risk as the minimum possible risk, namely, counseling a congenital heart disease patient that up to one in ten of them may develop atrial fibrillation by the age of 42 years, is likely the minimum amount. The reason for this is many patients, due to either lack of follow-up or lack of sufficient monitoring, and the asymptomatic nature of atrial fibrillation in many patients might have not been diagnosed.                                 Implications or treatments remain to be seen, and whether or not there are methods to reduce the overall risk of atrial fibrillation is unclear. However, engaging congenital heart disease experts and advising patients, especially at younger ages, on the importance of close electrocardiographic monitoring for a potential atrial fibrillation risk is critical.                                 Next within the realm of atrial fibrillation, we switch to the topic of ablation. And review an article by Pallisgaard et al., published in this last month's issue of European Heart Journal, entitled Temporal Trends in Atrial Fibrillation Recurrence Rates After Ablation, between 2005 and 2014: a nationwide Danish cohort study.                                 Ablation has been increasingly used as a rhythm control strategy for patients with atrial fibrillation. Over this time, we have all noted evolution in both the experience and the techniques used. Thus, the authors sought to evaluate whether recurrence rate of atrial fibrillation has changed over the last decade. They included all patients with first-time AF ablation done between 2005 and 2014 in Denmark. They then evaluated recurrent atrial fibrillation based on a one year follow-up. They included a total of 5,425 patients undergoing first-time ablation.                                 They noted, interestingly, that the patient median age increased over time, and the median AF duration prior to ablation decreased over time. However, the rates of recurrent atrial fibrillation decreased from 45% in 2005 to 31% in the more recent years of 2013, 2014. With the relative risk of recurrent atrial fibrillation almost being cut in half.                                 They noted that female gender, hypertension, atrial fibrillation duration more than two years, and cardioversion with one year prior to ablation were all associated with an increased risk of recurrent atrial fibrillation, regardless of year.                                 These data, again, are retrospective and thus must be taken in the context of that consideration. However, they highlight that it is possible either our selection of appropriate patients for atrial fibrillation ablation or our techniques have improved overall success.                                 The fact that atrial fibrillation ablation is still a relatively young field, with evolving approaches and evolving techniques, needs to be taken into consideration when advising patients on success rates. Using data from many years prior to informed discussion today is fraught with potential error, especially as our catheter design and mapping system use and understanding of appropriate lesion set changes.                                 Of course, some criticism is required as well. While the patients included were relatively older in more recent years, the total AF duration prior to ablation decreased over the years. This suggests that patients are being ablated earlier than they were in the early days of atrial fibrillation ablation.                                 There is some data out there to suggest that earlier ablation for atrial fibrillation might result in a lower long-term recurrence rate. Thus, this might account for some of the difference. However, it is unlikely that it accounts for all of it, given the degree of reduction in overall risk of occurrence.                                 Staying within the trend of talking about changes in techniques for atrial fibrillation ablation, we next review an article published in this past month's issue of Heart Rhythm, by Conti et al., entitled Contact Force Sensing for Ablation of Persistent Atrial Fibrillation: A Randomized, Multicenter Trial. Contact force sensing is one of the newer techniques being used to optimize the success rates for atrial fibrillation ablation. It is generally felt that understanding when one is in contact will optimize atrial fibrillation ablation outcomes by ensuring the physician knows each time they are in contact, and also potentially reducing complications by avoiding excessive contact.                                 Thus, the authors designed the TOUCH AF trial to compare contact force sensing-guided ablation vs. contact force sensing-blinded ablation. They included a total of 128 patients undergoing first-time ablation for persistent atrial fibrillation, and thus randomized them to a situation where the operator was aware of the contact force vs. blinded to the contact force. While the force data was hidden in the blinded cohort, it was still recorded on the backend.                                 In all patients, wide antral pulmonary vein isolation plus a roof line was performed, and patients were followed at 3, 6, 9, and 12 months, with clinical visits, ECGs, and 48-hour Holter monitoring.                                 The primary endpoint was cumulative radio frequency time for procedures, and atrial arrhythmia is greater than 30 seconds after three months is considered a recurrence.                                 They noted that average force was higher in the contact force-guided arm than contact force-blinded arm, though not statistically significant, with an average of 12 grams in the latter and 14 grams in the former.                                 Interestingly, the total time of ablation did not differ between the two groups. Furthermore, there was no difference in the single procedure freedom from atrial arrhythmia, computing to about 60% in the contact force-guided arm vs. the 63% in the contact force-blinded arm. They did notice, however, that lesions with associated gaps were associated with significantly less force and less force-time integral.                                 The authors concluded from this, the contact force-guided ablation did not result in significant decrease in total radio frequency time or 12-month outcomes in terms of freedom from atrial arrhythmias.                                 These data are important to help guide us in terms of thinking about how the tools we use, as they change, actually alter outcomes. Sometimes we may perceive benefits based on logical thinking that's knowing more about what is happening when we are performing a procedure should optimize that procedure. However, this is not necessarily always the case, and thus highlights the importance of randomized trials to directly compare different situations, such as awareness of contact force vs. lack of awareness of contact force.                                 The relevance of these particular articles is that when we compare catheters with different designs, it does not necessarily highlight the importance of the force number itself. Namely, comparing a contact force catheter vs. non-contact force catheter implicates use of essentially two completely different catheters. To understand the incremental utility of force in making decisions, it is important to consider the same catheter, but simply with awareness or lack of awareness of the actual force number.                                 One of the limitations, however, is that individuals who might have been trained on using the same force sensing catheter might have some degree of tactile feedback and understanding of the amount of force being applied to the tip of the catheter, based on having been repeatedly exposed to contact force numbers during use of said catheter. Thus, there might be a difference in being blinded to contact force in early stage operators than in later stage operators who might have been trained based on repeated feedback.                                 Thus, it's difficult to conclude, necessarily, that contact force is not offering mental benefit. In fact, there's a fair chance that it does. However, offering a skeptical viewpoint to help guide the importance of continually evolving technology in actually improving outcomes is important.                                 Finally, within the realm of atrial fibrillation, we review an article published by Pathik et al., in this past month's issue of Heart Rhythm, entitled Absence of Rotational Activity Detected Using 2-Dimensional Phase Mapping and the Corresponding 3-Dimensional Phase Maps in Human Persistent Atrial Fibrillation.                                 Current clinically used phase mapping systems involve 2-dimensional maps. However, this process may affect accurate detection of rotors. The authors sought to develop 3-dimensional phase mapping technique that uses a 3D location of the same basket electrodes that are used to create the currently available 2-dimensional maps. Specifically, they wanted to determine whether the rotors detected in 2D phase maps were present in the corresponding time segments and anatomical locations in 3D phase maps.                                 They used one minute left atrial atrial fibrillation recordings obtained in 14 patients, using the basket catheter, and analyzed them offline, using the same phase values, based on 2-dimensional vs. 3-dimensional representations.                                 They noted rotors in 3.3% using 2D phase mapping, 9 to 14 patients demonstrated about 10 transient rotors, with a mean rotor duration of about 1.1 seconds. They noted none of the 10 rotors, however, were seen at the corresponding time segments and anatomical locations in 3D phase maps. When looking at 3D phases maps, 4 of the 10 corresponded with single wavefronts, 2 of 10 corresponded with simultaneous wavefronts, 1 of 10 corresponded with disorganized activity, and 3 of 10 had no coverage by the basket catheter at the corresponding 3D anatomical locations.                                 These data are important, in that they highlight the importance of when we consider reflecting 2-dimensional systems in a 3-dimensional world of atrial fibrillation. The role of ablating rotors is still in question. However, it is still an important question, and it requires continued study. The best way of identifying a rotor, knowing a rotor is a rotor, and understanding where the rotor is, are going to be critical to further evaluating whether actual ablation of these rotors has any relevance to long-term atrial fibrillation ablation.                                 The truth is, that we need to be sure that we are properly identifying all the rotors in order to help guide whether or not we are actually being successful in ablating atrial fibrillation. The importance of the study is in reflecting whether 2-dimensional representations of the 3-dimensional geometry is sufficient to reflect what is actually happening in that 3-dimensional geometry. These authors suggest that it is not.                                 One of the limitations, however, might be that when we wrap a 2-dimensional framework into 3 dimensions and perform additional post-processing, this might result in some degree of attenuation of the data. However, it does highlight the importance for continued rigorous evaluation of current approaches to phase mapping.                                 Several articles have been published in recent months as well, about different single processing techniques to evaluate whether or not a rotor is, in fact, a rotor and to help optimize identification of them.                                 The jury is still out on whether or not targeted ablation of rotors will, in fact, improve overall long-term atrial fibrillation ablation outcomes. The limitations might not necessarily be that rotors are not an appropriate target, but that we just don't understand entirely where rotors are, based on limited single processing options, or based on limitations of anatomical localization.                                 Next, delving into the realm of ablation at large, we review an article by Iwasawa et al., published in this past month's issue of Europace, entitled Trans Cranial Measurement of Cerebral Microembolic Signals During Left-Sided Catheter Ablation with the Use of Different Approaches - the Potential Microembolic Risk of a Transseptal Approach.                                 The authors note the importance of considering microemolization in subclinical brain damage during catheter ablation procedures. They evaluated microembolic signals detected by transcranial Doppler during ablation of supraventricular or ventricular arrhythmias with the use of either a transseptal or a retrograde approach.                                 The study set was small, only including 36 patients who underwent catheter ablation. They noted in about 11 patients left-sided ablation was done with transaortic approach, and in 9 patients a transseptal approach was used. The other 16 patients were not included, as they only had right-sided ablation.                                 The total amount of microembolic signature, based on transcranial Doppler were counted throughout the procedure and then analyzed offline. There is no significant difference in number of radio frequency applications, total energy delivery time, total application of energy, or total procedure time between the different groups. However, they did note that the mean total number of microembolic signals was highest in those undergoing transseptal approach to left-sided ablation. It was significantly lower in those having retrograde aortic approach, and lowest in those having right-sided only ablation.                                 Interestingly, many of the microembolic signals were detected during the transseptal puncture period, and then during the remainder of the procedure there was relatively even distribution of emboli formation. A frequency analysis suggested that the vast majority of microembolic signals are gaseous, in particularly Group 1 and Group 3, though only 91% in Group 2. No neurological impairment was observed in any of the patients after the procedure.                                 Recently, there's been a lot of focus on the potential long-term risk of cognitive impairments due to microembolic events in the setting of ablation. At least one recent paper in ventricular arrhythmias and several recent papers in atrial fibrillation ablation have suggested a fairly high risk of incidence cerebral emboli noted on MRI post ablation. While these results do not necessarily get at MRI lesions, they do suggest microembolic events. And what is most interesting, they look at microembolic events that occur throughout the entire ablation period with different approaches.                                 Interestingly, there is a massive spike in overall microembolic signals during the transseptal puncture period, and relatively even distribution throughout ablation, irrespective of application of radio frequency or not. Furthermore, while nearly all microembolic signals are gaseous, based on frequency analysis, with retroaortic approach or in those having right-sided only ablation, significantly less seem to be due to gaseous events in those having a transseptal approach.                                 It is known that there's possible damage to the internal dilation system when exposing it to transseptal needles or wires. Thus, one has to wonder whether some of the embolization could be from material associated with the actual transseptal puncture, either from portions of the punctured septum itself, or perhaps from the plastic material that which is being pushed transseptally.                                 These data still need to be considered and we have yet to see what the long-term applications of these kinds of findings are. It may be possible that while transseptal approach seems to offer more instant microembolic signals, if the long-term risk is no different, does it really matter?                                 However, these findings are provocative in the sense that they highlight potential significant differences and the risk of silent cerebral damage, based on the approach we use to ablation.                                 Changing gears, we next focus on the role of devices. And the first paper review is in the last month issue of JACC: Heart Failure, by Gierula et al., entitled Rate Response Programming Tailored to the Force Frequency Relationship Improves Exercise Tolerance in Chronic Heart Failure.                                 The authors sought to examine whether the heart rate at which the force frequency relationship slope peaks can be used to tailor heart rate response in chronic heart failure patients with cardiac pacemakers, and to see whether this favorably influences exercise capacity.                                 They performed an observational study in both congestive heart failure and healthy subjects with pacemaker devices. They then evaluated in a double-blind, randomized, controlled crossover study, the effects of tailored pacemaker rate response programming on the basis of a calculation of force frequency relationship based on critical heart rate, peak contractility, and the FFR slope.                                 They enrolled a total of 90 patients with congestive heart failure into the observational study cohorts, and 15 control subjects with normal LLV function. A total of 52 patients took part in the crossover study. They noted that those who had rate response settings limiting heart rate rise to below the critical heart rate were associated with greater exercise time and higher peak oxygen consumption, suggesting the tailored rate response program can offer significant benefit, particularly in congestive heart failure patients.                                 The importance of this trial is in that it highlights the importance of thoughtful decision-making in programming devices, and that group decision-making involving exercise physiologists, alongside pacemaker programming, and involving our congestive heart failure specialists might be the most critical in optimizing the approach to programming.                                 It might be that more aggressive measures are needed in congestive heart failure patients to decide on what optimal programming is, than it is in otherwise normal patients.                                 Staying within the realm of devices, we next focus on a publication by Sanders et al., published in this past month's issue of JACC: Clinical Electrophysiology, entitled Increased Hospitalizations and Overall Healthcare Utilization in Patients Receiving Implantable Cardioverter-Defibrillator Shocks Compared With Antitachycardia Pacing.                                 The authors sought to evaluate the effect of different therapies and healthcare utilization in a large patient cohorts. Specifically comparing antitachycardia pacing with high voltage shocks. They used the PROVIDE registry, which is a prospective study of patients receiving ICDs for primary prevention in 97 U.S. centers. They categorized these patients by type of therapy delivered, namely no therapy, ATP only, or at least one shock. They then adjudicated all ICD therapies, hospitalizations, and deaths.                                 Of the 1,670 patients included, there was a total follow-up of over 18 months. The vast majority, 1,316 received no therapy, 152 had ATP only, and 202 received at least one shock.                                 They noted that patients receiving no therapy and those receiving only ATP had a lower cumulative hospitalization rate and had a lower risk of death or hospitalization. The cost of hospitalization was known to be significantly higher for those receiving at least one shock than for those receiving only ATP therapy.                                 They noted no difference in outcomes or cost between patients receiving only ATP and those without therapy. Thus, the authors concluded that those receiving no therapy or those receiving only ATP therapy had similar outcomes, and had significantly reduced hospitalizations, mortality, and costs compared to those who received at least one high voltage shock.                                 The relevant findings from this study is similar to prior studies that suggest that any shock over follow-up is associated with potential increase in long-term mortality. The difficulty in assessing this, however, is the fact that it might be that those who have VT that can be appropriately ATP terminated, might be at a somewhat lower risk than those who need to be shocked to get out of their VT. Thus, the presumption of needing a shock to restore normal rhythm might suggest a higher risk cohort, it cannot be gleaned from traditional evaluation of morbid risk factors.                                 This is why the importance of considering how devices are programmed and whether or not a patient who has received shocks can be reprogrammed to offer ATP only therapy to terminate those same VTs, needs to be taken into consideration. How to best tailor this therapy, however, is still remaining to be determined, though more and more clinical trials are coming out to suggest in terms of optimal overall population-wide programming for devices.                                 Staying with the realm of devices, we next review an article by Koyak et al., in this past month's issue of Europace, entitled Cardiac Resynchronization Therapy in Adults with Congenital Heart Disease.                                 Heart failure is one of the leading causes of morbidity and mortality amongst patients with congenital heart disease. But there's limited experience in the role of cardiac resynchronization therapy amongst these patients. Thus, the authors sought to evaluate the efficacy of CRT in adults with congenital heart disease.                                 They performed a retrospective study on a limited number of 48 adults with congenital heart disease who received CRT, amongst four tertiary referral centers. They have defined responders as those who showed improvement in NYHA functional class or improvement in systemic ventricular ejection fraction. The median age at CRT implant was 47 years, with 77% being male. There was a variety of syndromes included.                                 They noted that the majority of patients, nearly 77%, responded to CRT, either by definition of improvement of NYHA functional class, or systemic ventricular function, with a total of 11 non-responders.                                 They noted that CRT was accomplished with a success rate comparable to those with acquired heart disease. However, the anatomy is much more complex and those technical challenges in achieving success o

Podcast summary of articles from the February 2018 edition of Journal of Emergency Medicine from the American Academy of Emergency Medicine.  Topics include chest pain stress tests, clinical scoring systems for chest pain, sterno-clavicular joint infections with board review on AV node reentry tachycardia and the mumps.  Guest speaker is Dr. Aurelia Cheng from the Metrohealth Emergency Medicine Residency.

Dr. Paul Wong:                  Welcome to the monthly podcast, On The Beat, for Circulation: Arrhythmia and Electrophysiology. I'm Dr. Paul Wong, editor in chief, with some of the key highlights from this month's issue. We'll also hear from Dr. Suraj Kapa, reporting on new research from the latest journal articles in the field. In our first article, Ratika Parkash and associates examined whether the outcomes following escalated antiarrhythmic drug therapy, or catheter ablation, depended on whether ventricular tachycardia with amiodarone refractory or sotalol refractory in patients with prior myocardial infarction in the VANISH study. At baseline, 169, or 65%, were amiodarone refractory, while the remaining were sotalol refractory. Amiodarone refractory patients had more renal insufficiency; 23.7% versus 10%. Worse, new ARC Heart Association class, 82.3% versus 65.5% class II or III; and lower ejection fraction, 29% versus 35%. Within the amiodarone refractory group, ablation resulted in a reduction of any ventricular arrhythmias compared to escalated drug therapy, with a hazard ratio of 0.53, P = 0.02. Sotalol refractory patients had trends towards higher mortality in VT storm with ablation, with no effect on ICD shocks. Within the escalated drug arm, amiodarone refractory patients had a higher rate of composite endpoint, with a hazard ratio of 1.94 and a P value of 0.01. In a trend toward higher mortality, hazard ratio 2.4, P = 0.07. While mortality was not different between amiodarone and sotalol refractory patients within the ablation treatment group. In our next study, Junaid Zaman and associates examined 57 cases in which local ablation of persistent atrial fibrillation terminated to sinus rhythm or organized tachycardia. The authors analyze unipolar electrograms collected during atrial fibrillation from multi-polar basket catheters to reconstruct isochronal activation maps for multiple cycles, and computational modeling and phase analysis were used to study mechanisms of map variability. At all signs of atrial fibrillation termination, localized, repetitive activation patterns were observed, 21% with complete rotational activity, 46% with partial rotational circuits, and 33% with focal patterns. In computer simulations incomplete segments of partial rotations coincided with areas of slow conduction, characterized by complex, multi-component electrograms. In our next article, Matthew Kalscheur and associates sought to use a novel machine-learning approach to predict outcomes following resynchronization therapy in the companion trial. The random forest algorithm resulted in the best performing model. In 595 CRTD patients in the companion trial, 105 deaths occurred, with a median follow-up of 15.7 months. The survival difference across subgroups differentiated by bundle branch block morphology and cure restoration did not reach significance, P = 0.08. The random forest model, however, produced quartiles of patients with an eight-fold difference in survival between those with the highest and lowest predictive probability for events, hazard ratio 7.96 with a P value of less than 0.0001. The model also discriminated the risk of composite endpoint of all cause mortality, or heart failure hospitalization, better than subgroups based on bundle branch block morphology and cure restoration. Future studies are needed to validate this model in other populations. In our next paper, Amr Barakat and associates examined the clinical outcomes of trans-venous lead extraction for CIED infection based on renal function. The authors examined 1,420 consecutive patients undergoing trans-venous lead extraction of infected CIEDs over a 14 year period. Groups with normal renal function, Group 1, consisting of 1,159 patients, Group 2, 163 patients with renal dysfunction not requiring dialysis, and Group 3, 98 patients on dialysis. Complete procedural success rates were comparable in the three groups: 94%, 96%, and 94% in Groups 1, 2 and 3, respectively. This was not statistically significant. The mortality rates were significantly higher in dialysis patients at one month. The procedure-related complication was 12.2% in dialysis patients versus 6.5% in Group 1 and 6.1% in Group 2. Other factors associated with mortality were lead material retention, functional New York Heart Association Class, and occurrence of procedural complications. In our next paper, Eric Johnson and associates studied the contribution of the current ITO, two left ventricular re-polarization in the human heart, since the current has been shown to have an important role in animal models. The authors found that using whole-cell voltage clamp recordings from myocytes, isolated from the left ventricle, non-failing human hearts, that there were two, distinct transient currents, ITO fast and ITO slow. The two currents have significantly different rates of recovery from inactivation and pharmacological sensitivities. ITO fast recovers in about 10 milliseconds, 100 times faster than ITO slow, and it's selectively blocked by KV4 channel toxin SNX 482. Using current clamp experiments, they found that regional differences in action potential wave forms, with a notch in phase one in the left ventricular subepicardial myocytes. In failing, left ventricular subepicardial myocytes, ITO fast was reduced, while ITO slow was increased. In addition, the notch and plateau potentials were depolarized, and action potential durations were prolonged, both statistically significantly. Slowing ITO fast inactivation results in a dramatic action potential shortening. The authors concluded that remodeling of ITO fast in failing, human left ventricular subepicardial myocytes, attenuates transmural differences in action potential wave forms. In our next paper, Ravi Vaidyanathan and associates examine the interaction between Caveolin 3 domain in the inward rectifier potassium channels. Although the IK1 current is mainly composed of Kir2.1, there are Kir2.2 and Kir2.3 heterotetromerisoforms that occur and modulate the IK1 current, but these have not been studied. Kir2.x isoforms have unique, subcellular co-localization in human cardiomyoctyes and co-immunoprecipitate with Cav3. Using induced pluripotential stem-cell-derived cardiomyocytes, the LQT9 Cav3 mutation, F97CCav3 resulted in actual potential prolongation. Based on the technique FRET, which is Fluorescent Resonance Energy Transfer, the authors calculated the distance between KR2.2 and cath ray proteins to be 6.61 nanometers. LQT9 is caused by Cav3 mutations. Prior work has shown that F97CCav3 mutation increases the late sodium current, and decreases KR2.1 current density by distinctive mechanisms. This study extends the authors' previous observations on the impact of LQT9 Cav3 mutation on Kir2.1 current, by demonstrating that mutation affects the Kir2.2 current. LQT9 causing Cav3 mutation differentially regulates current density and cell surface expression of Kir2.x homomeric and heteromeric channels. The authors show that the mutation does not affect Kir2.3 current, but the heterotetromer Kir2.2-2.3 demonstrated loss of function. Using the Li-Rudy [inaudible 00:09:45] model and myocyte mathematical model, the authors' data suggest that both loss of IK1 and increased sodium L are required for arrhythmia generation in LQT9. In our next study, Christophe Teuwen and associates use high resolution epicardial mapping electrodes, 128 or 192, with an inter-electrode distance of 2.0mm of the entire atrial surface in 164 patients. These patients were undergoing open-chest cardiac surgery. This study was designed to examine the conduction of atrial extrasystoles. The authors found that a higher degree of aberrancy was associated with a higher instance of conduction disorders. Most conduction disorders were provoked by atrial systoles emerging as epicardial breakthroughs. Atrial extrasystoles cause most conduction disorders in patients with left atrial dilatation or diabetes mellitus. In our next paper, Yuki Komatsu and associates examine 31 patients with idiopathic ventricular arryhthmias, using a two french microcatheter placed in a communicating vein between the great cardiac vein and small cardiac venous system, which passes between the aortic and pulmonary annulae, and is located in close associated with the left ventricular summit. They found that 14 patients had summit ventricular arryhthmias. The remaining 17 patients control group had ventricular arryhthmias originate from the right ventricular outflow track in the aortic cusps.  In patients with summit ventricular arryhthmias, the earliest activation during ventricular arryhthmias in the summit, preceded to cure as onset by 34 milliseconds. The summit ventricular arryhthmias exhibited inferior axes, negative polarity in lead one, deeper Q wave in AVL than AVR, nonspecific bundle branch morphology with an RS ratio in lead V1 of 0.67, distinguishing them from arryhthmias originating from the right ventricular outflow track or right ventricular cusp. Overall, ablation success was achieved in 10, or 71% of patients with summit ventricular arryhthmias, and 88% in the control group, P = 0.24. In our final paper, Deepak Padmanabhan and associates examine differences in mortality in patients with non-MRI conditional CID undergoing brain MRI compared to controls. Patients with CIDs undergoing brain MRI were compared with three control groups matched for age, sex, imaging year, and type of CID. These groups included 1) no CID and brain MRI, 2) CID in brain-computed CT, and 3) no CID in brain CT. They estimated all cause mortality at five years for CID MRI group, was not significantly different from patients who underwent CT, with or without a device. There was a significant increase in the mortality between CIED versus no CID MRI groups, hazard ratio 1.46 with a P value of 0.04. That's it for this month, but keep listening. Saraj Kapa will be surveying all journals for the latest topics of interest in our field. Remember to download the podcasts On the Beat. Take it away Saraj. Saraj Kapa:                          Thank you Paul, and welcome back to On the Beats where this month we'll be focusing on articles that are particularly hard-hitting, published across the literature in December of 2017. It's my pleasure to introduce 20 different articles that seem to have either particular interest or might change the field in the future. First, within the area of atrial fibrillation, we'll focus within the area of anticoagulation and stroke prevention. In the Journal of the American College of Cardiology, Vivek Reddy et al published on the five-year outcomes after left atrial appendage closure, from the Prevail and Protect AF trials. They included a total of 1,114 patients, with a total of 4,343 patient years of follow-up, randomized two to one to closure versus Warfarin. While ischemic stroke and systemic embolism of [inaudible 00:14:32] were numerically higher with closure, this did not reach statistical significance in terms of hemorrhagic stroke, unexplained death, and post-procedure bleeding favor left atrial appendage closure. These findings further support a role for left atrial appendage closure in the specific groups of patients enrolled in the Protect and Prevail Studies. Of course, we always need to understand, that extrapolation to patients who may not have met inclusion criteria will be difficult. In particular, given both trials had their own fundamental limitations in the Prevail study. There was a relatively low rate of [inaudible 00:15:09] in the Warfarin arm. And in turn, there was a relatively high complication rate in Protect AF with left atrial appendage closure. Part of the differences might be due to the fact that, with more experience, complication rates might decrease. Furthermore, a comparison with more novel agents, such as the new oral anticoagulants, remains to be seen. Next, within the realm of cardiac mapping and ablation for atrial fibrillation, we review an article by Vlachos et al published in the Journal of Cardiovascular Electrophysiology entitled Low-Voltage Areas Detected by High-Density Electroanatomical Mapping for Recurrence of Ablation after a Paroxysmal Atrial Fibrillation. They presented the results from a series of 80 patients undergoing ablation for paroxysmal atrial fibrillation, performing high-density voltage mapping to characterize the total area involved by low voltage. They demonstrated, when low voltage areas, defined as less than 0.4 millivolts, were seen in greater than 10% of the left atrial surface area, this served as an independent predictor of atrial fibrillation recurrence. These data support prior research, including that of MRIs, suggesting the characterization of the atrial substrate may correlate with likelihood of ablation success. Identifying methods however, to accurately and reproduce will identify these patients with more atrial substrate prior to ablation, remains to be seen. The importance of this, however, is our ability to better counsel patients on the likelihood of treatment success. Next within the realm of atrial fibrillation, we review elements of risk stratification managements. First, in the December issue of the Journal of American College of Cardiology, Takimoto et al published on how Eplerenone may reduce atrial fibrillation burden without preventing atrial electrical remodeling. In a randomized controlled ovine atrial tachy pacing model of atrial fibrillation. The authors provided daily, oral Eplerenone and compared this with a placebo. They showed that Eplerenone significantly reduced the rate of left atrial dilatation, with less smooth muscle actin protein, atrial fibril [inaudible 00:17:17]. Furthermore, Eplerenone further prolonged the time to persist in atrial fibrillation in 26% of animals. However, interestingly, Eplerenone did not prevent AF-induced electrical remodeling.  These data suggest that Eplerenone, or other medications that can be used to prevent or reverse structural remodeling, may offer an upstream therapy to reduce atrial fibrillation burden, and decrease likely the persistent atrial fibrillation. Giving the ever-growing population of patients suffering from atrial fibrillation, identifying upstream approaches to prevent it will be critical. Of course, these need to be taken with due consideration, however. Specifically, the model used here, namely that of an atrial tachy pacing model, might not be applicable to all human atrial fibrillation. Thus, whether or not such therapies actually offer benefit in clinical models, is as of yet unclear. Finally, from the realm of atrial fibrillation, we review the article by Rowin et al published in circulation entitled Clinical Profile of Consequences of Atrial Fibrillation Hypertrophic Cardiomyopathy. In patients presenting with hypertrophic cardiomyopathy, atrial fibrillation is known to be a significant co-morbidity. However, the implications of atrial fibrillation in terms of worsening of heart failure status, or long-term morbidity mortality are less clear. Rowin et al reviewed the natural history of atrial fibrillation amongst 1,558 patients, prospectively followed at a single center. Nearly 20% of the population developed atrial fibrillation with the majority having symptomatic paroxysmal atrial fibrillation. However, atrial fibrillation was not associated with any increase in cardiovascular mortality or worsening of heart failure status. Furthermore, mortality that was directly related to atrial fibrillation was nearly exclusively related to thrombolic stroke. Anticoagulation [inaudible 00:19:13] reduced this risk. The traditional scoring systems fared poorly in assessing the stroke risk of this population. About 121 patients underwent invasive rhythm control approaches, including 72 patients undergoing maze and 49 catheter ablation. The success rate of maze was significantly greater at around 75%. These data are important when counseling hypertrophic cardiomyopathy patients presenting with new-onset atrial fibrillation. While it is clear that paroxysmal atrial fibrillation has a significant impact on symptoms and quality of life, it does not cause worsened, overall, long-term outcomes. However, it does highlight the importance of anticoagulation in this population, nearly irrespective of the underlying risk score. In terms of rhythm control options, it appears that rhythm control options can be successful in these patients. Finding that catheter ablation is associated with a 40 to 50% success rate is in keeping with prior published data. Thus, consideration of when a patient needs to be referred to maze, needs to be considered in the clinical inpatient context. Changing gears, we will next review articles within the realm of ICDs, pacemakers, and CRT. In the New England Journal of Medicine this past month, Nazarian et al published on their experience regarding the safety of magnetic resonance imaging in patients with cardiac devices. They performed a prospective non-randomized study of the safety of, specifically, 1.5 tesla-strength MRI scans on legacy. In other words, not MRI conditionally-safe pacemakers and defibrillators. A total of 2,103 scans were done among 1,580 patients. They demonstrated no long term clinically significant adverse events. Nine patients did experience a reset to a backup mode, though eight of which were transients. The most common change seen acutely was a decrease in PVA amplitude in one percent of patients, and in a long term follow-up, 4% of patients experiencing a decrease in PVA amplitude, increase in atrial catheter sheer threshold, or increase in right or left ventricular capture threshold. However, none of these events were considered clinically significant. Furthermore, there was not a good [inaudible 00:21:23] group to know if this long term change in amplitudes or thresholds might have been seen in patients who had devices that were not exposed to MRI. These findings are complimentary to multiple, prior, published reports, indicating the safety of performing MRIs under clinical protocol in legacy pacemakers and defibrillators. It calls into question whether MRI conditional devices truly offer an additional safety factor furthermore, over legacy devices. Next we review an article by Lakkireddy et al published in Heart Rhythm entitled A Worldwide Experience, the Management of Battery Failures and Chronic Device Retrieval of the Nanostim Leadless Pacemaker. Lakkireddy et al reported their large multi-center experience on the overall risk of battery failure. Amongst 1,423 implanted devices there were 34 battery failures occurring, on the average, three years after implants. Furthermore, about 73 patients underwent attempted device retrieval, and this was successful in 90%, with the seven failures of retrieval being due to either inaccessibility of the docking button, or dislodgement of the docking button in one patient, in whom it embolized to the pulmonary artery. An additional 115 patients interestingly received an additional pacemaker after release of the device advisory. These data suggest that there may be as high as an overall 2% risk of battery failure with the Nanostim device, even late after implants. This highlights the need for close follow-up, even if the battery appears relatively stable up to two year after implants. Furthermore, almost 10% of devices cannot be successfully retrieved. However, in those patients, even with re-implantation of a separate device, there was no device-device interaction seen. Further innovation will be needed to optimize device longevity, and close follow-up of all patients undergoing implantation will be critical to understand the overall long term efficacy and safety when compared to other traditional devices. Finally, within the realm of device care, we focus on an article by Kiehl et al, again published in Heart Rhythm this past month entitled Incidence and Predictors of Late Atrial Ventricular Conduction Recovery Among Patients Requiring Permanent Pacemaker for complete heart block after cardiac surgery. They reviewed the likelihood of recovery of conduction in their retrospective cohort of 301 patients. Interestingly, 12% of patients had recovery of AV conduction on average six months after surgery. Those who did not recover tended to more likely have preoperative conduction abnormalities. Saraj Kapa:                          Findings that suggested a higher likelihood of long term conduction recovery included female sex and the existence of transient periods of AV conduction postoperatively. These data highlight that recovery of AV conduction is possible in a significant number of patients undergoing cardiac surgery. However, being able to predict long term recovery may assist in device selection, to avoid more costly device implantations that may not be needed over chronic follow-up. Prospective studies amongst larger numbers of patients are needed to better understand mechanisms of block, mechanisms of recovery, an optimal device in patient selection. Changing focus, we will next review two articles within the realm of supraventricular tachycardias. First we read an article by Han et al published in JACC Clinical Electrophysiology, entitled Clinical Features in Sites of Ablation for Patients With Incessant Supraventricular Tachycardia From Concealed Nodofascicular and Nodoventricular Tachycardias. Han and group describe three cases of concealed nodovascicular, nodoventricular re-entrant tachycardias, and focus on the different mechanisms of proving their participation in tachycardia. In all cases, atrial ventricular re-entering tachycardia was excluded. Successful ablation for these tachycardias occurred either at the slow pathway region, the right bundle branch, or the proximal coronary sinus. This is the first described case of incessant, concealed tachycardias related to these pathways. The importance of this article highlights an understanding the mechanisms proving the contribution to tachycardia, and the importance of recognition when performing electrophysiology studies, and being unable to reveal traditional mechanisms, which exist in most patients, such as atrial tachycardia, AVNRT or AVRT. Next we review an article by Guo et al published in Europace entitled Mapping and Ablation of Anteroseptal Atrial Tachycardia in Patients With Congenitally Corrected Transposition of the Great Arteries: Implications of Pulmonary Sinus Cusps. They reviewed three separate cases of anteroseptal atrial tachycardias in the setting of congenitally corrected transposition. They demonstrated that in these cases, there was successful ablation performed with the pulmonary sinus cusps. The result is successful and durable suppression. The reason this article is important lies in the fact that it's critical to understand both cardiac anatomy and cardiac nomenclature. The pulmonary valve in CCTJ is affectively the systemic ventricular arterial valve, given that the right ventricle is the systemic ventricle. Thus, mapping in this region of CCTJ abides the same principles as mapping the aortic valve in structurally normal hearts for similar tachycardias. However, understanding the nomenclature and that despite the variant anatomy, the utility of similar approaches to mapping of the systemic outflow are important when matching these complex, congenital anatomy or arrhythmia patients. Changing gears yet again, we review an article within the realm of sudden death and cardiac arrest. Baudhuin et al published in Circulation and Genetics entitled Technical Advances for the Clinical Genomic Evaluation of Sudden Cardiac Death. Baudhuin et al reviewed the utility of formal and fixed paraffin-embedded tissue, which is routinely obtained in an autopsy, to perform post-mortem, genetic testing. One of the main limitations to advising family members who have had prior family history of sudden death in closely related relatives, is that blood is often not available to perform DNA screening late after death. DNA however is often degraded in the tissues that are commonly available at autopsy, namely the formal and fixed paraffin-embedded tissues. The authors sought to evaluate if your next generation techniques could make these types of tissue adequate for diagnosis. They demonstrated amongst 19 samples, that performance characteristics were similar between whole blood and these tissue samples, which could be as old as 15 years. It can be critical to identify disease-causing mutations in family members, as individuals who might not yet be affected, but at risk, need to know about that overall risk. Given that decision to sequence might also not be universally applied at all centers, or in all situations, oftentimes these paraffin-embedded tissues might be the only available option, sometimes over a decade after death. This represents the first report of using next-generation sequencing approaches to successfully and accurately sequence for specific mutations using paraffin-embedded tissue. This may offer additional options to help family members achieve diagnoses for sudden death-inducing conditions. Within the realm of cellular electrophysiology, we review an article by Lang et al published in Circulation Research entitled Calcium-Dependent Arrhythmogenic Foci Created by Weakly Coupled Myocytes in the Failing Heart. Lang et al reviewed the effect of cell-cell coupling on the likelihood of triggered arryhthmias. In a [inaudible 00:28:45] model, they demonstrated the myocytes that are poorly synchronized with adjacent myocytes were more prone to triggered activity due to abnormal calcium handling when compared to myocytes with normal connection to adjacent cells. Thus, adequate coupling leads to voltage clamping during calcium waves, thus preventing triggering arrhythmias. While poorly coupled myocytes aren't able to to this due to a weakened currency, making them more prone arrhythmogenesis. These data highlight another critical cellular basis for arrhythmogenesis. In heart failure, while the focus for clinical management is typically areas of scar, there's clearly a role at the cellular level where cell-cell coupling abnormalities can lead to dynamic changes that can increase tendencies to arrhythmogenesis. The role in understanding the varying, arrhythmogenic risk based on varying factors, is important, and might have importance in the future advances in mapping technologies. Changing gears, we review an article published in the Journal of the American College of Cardiology by Mazzanti et al within the realm of genetic channelopathies entitled Hydroxyquinoline Prevents Life-Threatening Arrhythmic Events in Patients With Short QT Syndrome. They reviewed a cohort of 17 patients and demonstrated that hydroxyquinoline resulted in a reduction of arrhythmic events from 40% to 0% of patients. QTc prolongation was seen in all patients. These data clearly demonstrate that hydroxyquinoline plays a role in lowering the incidence of arrhythmic events in patients suffering from short QT syndrome. However, it's important to note that in many markets, quinoline has been difficult to access. In the specific case of QT syndrome thus, there's clearly a role for hydroxyquinoline. However, it also must be noted, the comparative efficacy with more commonly available drugs still needs to be evaluated. This past month has been of particular interest in the realm of ventricular arrhythmias, with multiple, potentially ground-breaking articles. One of the well-recited articles published this past month already is by Cuculich et al entitled Noninvasive Cardiac Radiation for Ablation of Ventricular Tachycardia published in the New England Journal of Medicine. Cuculich et al reported the first in-human data on the use of stereotactic body radiation therapy to perform noninvasive ablation of ventricular arryhthmias. Using a combination of noninvasive electrocardiographic imaging curing ventricular tachycardia, and stereotactic radiation, patients were treated with a single fraction of 25 [inaudible 00:31:15] while awake. A total of five patients were included with a mean ablation time of only 14 minutes. During the three months prior to treatment, there was a total of 6,577 VT episodes seen, and during a six week post-ablation period, considered a blanking period, there were 680 episodes. After this blanking episodes, there were only four episodes of VT seen over the ensuing 46 patient months. This study is important because it reflects the first in-human proof of concept that noninvasive ablation using radiation therapy traditionally as for treatment of solid tumors, may be affective in targeting cardiac tissue. Furthermore, modern techniques such as noninvasive electrocardiographic imaging might allow for a fully noninvasive experience for the patients. This is a vast advance seen within the realm of cardiac electrophysiology. In the early days, all we could do was map invasively and then have to go to much more invasive, open-heart surgery to treat arryhthmogenic substrates. Since the advent of catheter and radiofrequency ablation, surgical ablation is relatively fallen by the wayside, to a less invasive approaches. A completely noninvasive approach to successfully targeting tissue is potentially ground-breaking. However, there are several limitations in this study that can only be ascertained by reading the actual article. When we actually review the patients included, the long term follow-up was limited to only four patients, as one patient actually died within the blanking period, and in fact, this patient suffered from the largest burden overall of VT. Furthermore, amongst the remaining four patients, one required a redo ablation within the blanking period, and one had to be restarted on amioderone after the blanking period was over. Thus further data is really needed to clarify efficacy, given the overall success rate appears to be less than 50% on a per patient basis. Though on an overall episode basis, there was significant reduction. The exact type of radiation to be used also needs to be considered, within the realm of solid oncology. Stereotactic radiation is considered an older modality, with proton beam, and more recently, carbon beams offer more directed therapy. Thus, a lot more data is required to identify the promise of radiation therapy. Though again, this is a significant advance. Next, within the realm of invasive electrophysiology, we review an article by Turagam et al published in the JACC Clinical Electrophysiology entitled Hemodynamic Support in Ventricular Tachycardia Ablation: An International VT Ablation Center Collaborative Group Study. The utility of hemodynamic support during VT ablation is relatively unclear. Studies have been variable and limited. This group included 1,655 patients who underwent 105 VT ablations using hemodynamic support with a percutaneous ventricular assist device. Those undergoing support overall tend to be sicker, including lower ejection fractions and [inaudible 00:34:07] classes, and more VT events, including ICD shocks and VT storm. Hemodynamic support use interestingly, was an independent predictor of mortality with a hazard ratio of 5, though there was no significant difference in VT recurrence rates irrespective of the subgroup considered. These data indicate that, while patients are receiving hemodynamic support were overall sicker, there was no clear incremental benefit in use of hemodynamic support in terms of long term outcomes. In the area of substrate ablation, whether use of hemodynamic support to facilitate mapping during VT, actually alters outcomes remains to be seen. This study highlights the potential importance of randomized clinical approaches to better evaluate whether hemodynamic support truly alters the long term outcomes of the VT ablation. Next, we review an article by Munoz et al that focuses more on prediction of those patients who might be at risk for ventricular arrhythmias, again published in the last edition of JACC Clinical Electrophysiology and entitled Prolonged Ventricular Conduction and Repolarization During Right Ventricular Stimulation Predicts Ventricular Arrhythmias and Death in Patients With Cardiomyopathy. Munoz et al reviewed the relationship between paced QRS and pace Qtc and long term risk. A total of 501 patients with mean ejection fractions of 33% were included. Longer paced ventricular QRS and Qtc was associated with a higher risk of ventricular arrhythmia, and all caused death or arrhythmia, irrespective or ejection fraction. A paced QRS duration of 190 milliseconds was associated with 3.6 fault higher risk of arrhythmia, and a 2.1 fault higher risk of death or arrhythmia. These data suggest that findings during [inaudible 00:35:47] pacing and otherwise normal rhythm, including paced QRS and QTc may independently result in elevation of overall risk of ventricular arrhythmia and death. Physiologically these data make sense. In light of the fact that longer cure restorations are probably related to a greater degree of myopathy. While these data offer a prognostic indication, whether they alter outcomes or decision making regarding ICM implantation, remains to be seen. Next, also published in JACC Clinical Electrophysiology, Vandersickel et al reviewed a more cellular basis for toursades in an article entitled Short-Lasting Episodes of Toursades de Pointes in the Chronic Atrial Ventricular Model Have Focal Mechanism While Longer-Lasting Episodes are Maintained by Reentry. Vandersickel et al reviewed the mechanisms underlying toursades, and demonstrated that both focal and reentry mechanisms may exist. In five canines they used broadly distributed neuro electrodes to simultaneously map across the heart. They demonstrated that initiation and termination was always focal, but longer and non-terminal episodes always had reentry mechanisms. These data suggest that the mechanisms underlying toursades actually reflect a spectrum of potentially dynamic, electrophysiologic phenomenon the heart, including both focal and reentry activity. Understanding these mechanisms, and the fact that focal mechanisms almost universally underlie initiation may bring into consideration the optimal treatments whether in the form of pacing and defibrillation techniques or medication techniques for toursades. Finally, in the realm of ventricular arrhythmia, we review an article published in the last month's edition of Heart Rhythm by Penela et al entitled Clinical Recognition of Pure Premature Ventricular Complex-Induced Cardiomyopathy at Presentation. As we know, it's sometimes difficult to recognize patients when they present with frequent PVCs and a depressed injection fraction in terms of, whose injection fractions are purely caused by the presence of PVCs, and whose PVCs are only exacerbated by the presence of an underlying myopathy. The group included 155 patients and excluded all patients who did not normalize their elevated ejection fraction, or who had previously diagnosed structural heart disease, leaving a total cohort under consideration, of 81 patients. About 50% were diagnosed as having a PVC-induced cardiomyopathy on the basis of normalization of elevated function after PVC suppression. While the remainder was considered to have PVC exacerbated cardiomyopathy on the basis that things did not entirely resolve, and thus had an independent mechanism for nonischemic myopathy. Characteristics that suggested patients with a lower likelihood of EF normalization included those with longer intrinsic QRSs, above 130 milliseconds, a lower PVC burden of baseline, considered less than 17%, and larger [inaudible 00:38:33] greater than 6.3 cm. PVCs as a cause of [inaudible 00:38:35] are obviously a well-recognized treatable cause of myopathy, however again, it might be difficult to differentiate. Those patients whose PVCs are a result of the underlying myopathy versus those whose PVCs are the cause, and for whom ablation or suppression may reverse the myopathic process. The work of Penela et at offers an initial attempt at helping differentiate these processes, however validation of larger cohort is necessary. Next we review an article within the realm of syncopy entitled Prohormones in the Early Diagnosis of Cardiac Syncopy by Badertscher et al published in the Journal of the American Heart Association this month. They review the utility of circulating prohormones [inaudible 00:39:14] autonomic dysfunction or neurohormonal abnormalities, to differentiate cardiac from non-cardiac causes of syncopy in the emergency departments. They measured four novel prohormones in a multi-center study. In the emergency departments there is a specific protocol used to determine the perceived likelihood of the cause of syncopy to be cardiac versus non-cardiac. In addition to this, the prohormones are drawn. After this, everyone's final diagnosis was reached. Two independent cardiologists reviewed the cases to determine if it was a truly cardiac or non-cardiac cause of syncopy. Among 689 patients included, 125 overall were adjudicated as cardiac syncopy. Measure of the specific marker MR-proANP in combination with emergency department suspicion of syncopy, performed better than suspicion alone, to differentiate cardiac causes of syncopy. A combination of a circulating MR-proANP, less than 77, picomoles per liter, an [inaudible 00:40:17] probability of cardiac syncopy could be less than 20%, had a very high sensitivity negative predictive value of 99%. The significant resources are often used to manage patients with syncopy presenting to the emergency departments, and it's often extremely difficult at this stage to differentiate cardiac from non-cardiac causes of syncopy. And the amount of evaluation that can be done in the emergency department is often limited. Cardiac caused of syncopy are not good to miss, however, since these can include ventricular arrhythmias, and transient AV block, that might result in death as well. As is well-recognized, emergency department evaluation in clinical [inaudible 00:40:49] are limited in terms of their utility. This raises the utility of objective measures to help differentiates. These data suggest that circulating prohormones [inaudible 00:40:59] your hormonal function drawn during your emergency department evaluation, may be a useful adjunct to differentiate cardiac from non-cardiac syncopy. Whether they can be used to prospectively differentiate those patients requiring inpatient admission or now, however, remains to be seen. The last two articles we'll choose to focus on will fall under the realm of broader, other EP concepts. The first article we will review is by Varghese et al published in Cardiovascular Research entitled Low-Energy Defibrillation With Nanosecond Electric Shocks. Varghese et al reviewed the potential of low-energy nanosecond duration shocks for defibrillation in rapid hearts. In induced fibrillation examples, the repeated defibrillated nanosecond impulses as low as three kilovolts demonstrated effective defibrillation. The energy required is significantly lower than from monophasic shocks and longer pulse durations. Furthermore, there was no detectable evidence of electroporation, namely cardiac or so injury after defibrillation. Using nanosecond impulses, it may be feasible to defibrillate the heart with significantly lower energies. The implications for patients experiencing defibrillation, for example pain, is unclear without in-human studies. However, the ability to use lower energies could have implications in battery life. Further [inaudible 00:42:11] studies will be critical to study ambulatory efficacy as this research is performed in [inaudible 00:42:19] hearts. Finally, we review an article published in Circulation entitled Mortality in Supravascular Events After Heart Rhythm Disorder Management Procedures by Lee et al. Amongst three centers, a retrospective cohort study regarding the mortality and risk of supravascular events, was performed. They included a variety of heart rhythm [inaudible 00:42:40] procedures, including defibrillation threshold testing, lead extraction, device implant, and invasive electrophysiology studies and ablation procedures. Amongst 48,913 patients, 62,065 procedures were performed and an overall mortality of .36% was seen. Supravascular [inaudible 00:42:58] was lower at .12%. Interestingly, and expectedly, the highest risk was seen with lead extraction patients, with an overall mortality risk of 1.9%. Less than half of the deaths seen, however, were directly attributable to the procedure itself. The most common cause of procedural death was cardiac tamponade, largely seen amongst device implant patients. This is critical, as the number of ablation and other invasive electrophysiology procedures performed, is increasing. These data provide a large, contemporary experience regarding the overall risk attributable to a variety of heart rhythm disorder procedures. Interestingly, half of the procedure related deaths were associated with device implantation procedures. With the predominant cause being tamponade, highlighting the importance of early recognition of this treatable complication. Tamponade may not always be considered as a major issue after device implantation, however these data clearly suggest that it is. In addition, extraction, as expected, carried the highest incident of both supravascular events and mortality. Though, this is likely related to the higher rate of core morbidity in this population, including active infection. In summary, this month, we have reviewed 20 articles in various areas of electrophysiology published across the literature. Particularly high impact articles range from those reviewing experience regarding left atrial appendage closure and the efficacy of this, to the utility of using atrial fibrillation to predict risk and long term morbidity and mortality in hypertrophic cardiomyopathy, to further evidence regarding the safety of magnetic resonance imaging in legacy pacemakers and defibrillators, and novel considerations regarding supraventricular tachycardias and there diagnosis and management, especially invasively. Other potential groundbreaking articles included evidence that we can successfully use formal and fixed paraffin-embedded tissue that can be as old as 15 years, to successfully identify genetic mutations that might be responsible for sudden death. And evidence that using novel techniques, we might be able to perform completely noninvasive therapies for arrhythmias by using radiation therapies. However questions were also raised such as regarding the role of hemodynamic support for VT ablation. How to better differentiate those patients who will have recovery of AV conduction from those who won't, as they meet class I indications post cardiac surgery? And whether other factors such as right ventricular pacing during [inaudible 00:45:28] study might further differentiate patients at risk for ventricular arrhythmias in spite of a low ejection fractions. Many of the papers had to deal with tranlational work that still remains to be proven in terms of value at a clinical level, such as demonstrating mechanisms underlying trousades de pointes. Or the potential value of low-energy defibrillation with nanosecond electric shocks. Clinical protocols involving the use of prohormones in the early diagnosis of cardiac syncopy. How to differentiate PVC induced from other causes of myopathy, and how to manage, in the long term, these devices. Also, likely requires further study. Finally, covering all areas of electrophysiology, we reviewed one large article focusing on mortality in supravascular events after heart rhythm management disorder procedures at large. This article highlights the importance of considering institutional experience and reporting it to use as a benchmark to help better optimize our counseling of patients, as well as our procedures and protocols. I appreciate everyone's attention to these key and hard-hitting articles that we just focused on from this past month of cardiac electrophysiology across the literature. Thanks for listening. Now, back to Paul. Dr. Paul Wong:                  Thanks Seraj. You did a terrific job surveying all journals for the latest articles on topics of interest in our field. There's not an easier way to stay in touch with the latest advance. These summaries, and a list of all major articles in our field each month, can be downloaded from the Circulation Arrhythmia and Electrophysiology website. We hope you'll find the journal to be the go-to place for everyone interested in the field. See you next month.  

  Paul Wang:         Welcome to the monthly podcast On the Beat for Circulation, Arrhythmia, and Electrophysiology. I'm Dr. Paul Wang, Editor in Chief, with some of the key highlights from this month's issue. We'll also hear from Dr. Suraj Kapa, reporting on new research from the latest journal articles in the field.                                 In our first study, Boris Schmidt and associates studied 134 patients with persistent atrial fibrillation, randomized to laser balloon or wide area circumferential pulmonary vein isolation using irrigated radiofrequency current ablation and 3D mapping.                                 They found that 71% of patients in the laser balloon group had freedom from atrial fibrillation between 90 and 365 days after a single ablation, similar to 69% of patients in the radiofrequency group, p=0.40. In the laser balloon group, one patient developed stroke, one had false aneurysm and one had phrenic nerve palsy. In the radiofrequency group, two patients developed a false aneurysm and one patient needed surgical repair. Procedure and fluoroscopy times were similar between the two groups. The authors concluded that the two methods were associated with similar efficacy in patients with persistent atrial fibrillation.                                 In the next study, Kairav Vakil and associates examined the success of VT ablation in elderly patients who were part of the International VT Center Collaborative Study Group Registry. Of the 2,049 patients in the registry, 33% or 681 were greater than or equal to 70 years of age with a mean age of 75 years.                                 Compared to patients less than 70 years, patients 70 years or greater had higher in-hospital, 4.4% versus 2.3%, p=0.1 mortality, and also a higher one year mortality, 15% versus 11%, p=0.002. But they had a similar instance of VT recurrence, 26% versus 25% and a similar time to recurrence, 280 versus 289 days.                                 The authors concluded that VT ablation in elderly is feasible with reasonable safety and modestly higher in-hospital and one year mortality with similar rates of VT recurrence at a one year compared to younger patients.                                 In the next study, Angel Ferrero-de Loma-Osorio and associates studied the optimal dosage of cryotherapy using cryoballoon ablation of pulmonary veins. The study the prospective, randomized, multicenter, non-inferiority study including 140 patients with paroxysmal atrial fibrillation which was refractory to antirrhythmic drugs.                                 Patients were randomly assigned to a conventional strategy group of 180 seconds cryoablation applications per vein with a bonus freeze 70 patients or a shorter time application protocol with one application that lasted the time required for a electrical time to effect plus 60 seconds and a 120 second freeze bonus, 70 patients.                                 At one year followup there was no difference in freedom from atrial fibrillation 79.4% of the control group versus 78.3% in the study group, p=0.87. The time to effect was detected in 72% of the veins. The study and control group had similar mean number of applications per patient, 9.6 versus 9.9. compared to controls the study group had a significantly shorter cryotherapy time, 28.3 versus 19.4 minutes, p80 or >90, especially when one refers to the appropriate use criteria where appropriateness was reclassified based on what the age range was and what the indication was from a primary prevention defibrillator. Further study is need to understand whether we really should apply an age cutoff to the benefit of ICDs but it is an important thing to consider when counseling patients, especially in light of evolving evidence in this area.                                 Still staying in the realm of heart failure but now going to more basic electrophysiology, we review a paper published in Circulation this past month by Cho et al., entitled Delayed Repolarization Underlies Ventricular Arrhythmias in Rats With Heart Failure and Preserved Ejection Fraction.                                 Increasingly, heart failure with preserved ejection fraction is being diagnosed to the point where it is now approximately half of all diagnosed heart failure with incidences that continue to increase nevertheless. One of the leading causes of mortality in heart failure with preserved ejection fraction is sudden death but the underlying mechanisms for this is less clear.                                 Thus in a rat model, Cho et al., sought to evaluate why heart failure with preserved ejection fraction might result in an increase risk of sudden death. They exposed salt sensitive rats to a high salt diet and evaluated the effect on systolic and diastolic function. After verifying, some rats that suffered from HFpEF at this point versus control rats, they underwent programmed electrical stimulation and they measured corrected QT interval from surface ECG as well. Furthermore they did optical mapping, whole-cell patch clamping and quantitative polymerase chain reaction and Western blotting to evaluate ion channel expression.                                 They noted that 31 of 38 rats exposed to a high salt diet demonstrated diastolic dysfunction and preserved ejection fraction along with signs of heart failure. There was an increased susceptibility to ventricular arrhythmias amongst these particular rats when compared to controls. They also noted that the corrected QT interval was significantly longer. Interestingly optical mapping showed that these rats had prolonged action potentials and multiple reentry circuits during induced ventricular arrhythmias. Furthermore there was confirmed a delay of repolarization based on patch clamping with a downregulation of transient outward potassium currents or ITO. Finally they noted that there was a downregulation of IK1 as well as IKR.                                 Thus they felt that the susceptibility to ventricular arrhythmias was indeed markedly increased, at least in a rat model of HFpEF. These could be caused by QT prolongation, which is associated with delayed repolarization from downregulation of potassium currents and also associated multiple reentry circuits which can mediate ventricular arrhythmia. These findings are significant in that they highlight both potential targets for sudden death risk in the setting of HFpEF as well as potential targets for treatments that might prevent ventricular arrhythmias in the long term.                                 Staying within the realm of ventricular arrhythmias, we next review an article by Do et al., published in the Journal of the American Heart Association this past month, entitled Thoracic Epidural Anesthesia Can Be Effective for the Short‐Term Management of Ventricular Tachycardia Storm.                                 Similar to the earlier discussed article, of optogenetic stimulation of left stellate ganglion, even short term management options for VT storm are important. Some inject lidocaine or bupivacaine into the left stellate ganglion or into both stellate ganglia in order to get control. However, depending on comfort level, the utility of this may be variable at different institutions.                                 Thus, novel therapies aimed at modulating the autonomic nervous system that might be available at other institutions such as thoracic epidural anesthesia are important to consider. The group sought to evaluate via multicenter experience what the effect on VT storm was with thoracic epidural anesthesia.                                 They noted amongst 11 patients reviewed between July 2005 and March 2016 that the majority who underwent thoracic epidural anesthesia had incessant VT with a minority of them being polymorphic VT. Furthermore almost half of them had nonischemic cardiomyopathies. Almost half of the patients had a complete response to thoracic epidural anesthesia where the VT became quiescent. And one patient had a partial response.                                 Thus, they suggested that thoracic epidural anesthesia may be effective and should be considered as a therapeutic option in patients with VT storm, especially those with incessant VT, who are refractory to initial management. They also noted clinically that improvement in VT burden associated with deep sedation may suggest a higher likelihood of responding to thoracic epidural anesthesia. For a clinical electrophysiologist especially in community hospitals where rapid utilization of ablation may not be possible or other advanced methods of autonomic modulation might not be feasible, options such as thoracic epidural anesthesia are important to be considered. They exist in an armament that includes intravenous drugs, left stellate ganglion injections, general anesthesia and use of IV beta blockers. These findings are highly suggestive and the fact that certain clinical characteristics might suggest those that are more likely to benefit might just to clinicians exposed to a patient of VT storm what the next step should be.                                 Changing gears a little bit we will now review an article by Rafaat in the Journal of the American Heart Association entitled Swine Atrioventricular Node Ablation Using Stereotactic Radiosurgery: Methods and In Vivo Feasibility Investigation for Catheter‐Free Ablation of Cardiac Arrhythmias.                                 The group sought to demonstrate using a linear accelerator based stereotactic radiosurgery system whether or not atrioventricular node ablation could be safely performed with minimal damage to surrounding structures. They used the linear accelerator to apply energy in a pig model after implantation of a pacemaker using a CT scan to guide therapy. They also performed pathologic evaluation of the region of the AV node and the surrounding tissues. They found that all animals included had disturbances of AV conduction with progressive transition into complete heart block. There was no damage to the surrounding myocardium and all pigs had preserved systolic function echocardiography.                                 Thus they suggested that catheter free radioablation using this approach might be feasible in an intact swine. These findings are important because they build on other studies done by groups at other centers suggesting that noninvasive linear accelerator based therapies either using stereotactic radiosurgery with existing technologies, proton beams, carbon beams or other approaches, might offer feasible methodologies for noninvasive treatment for cardiac arrhythmias. Further study is indeed needed to validate what the effect on surrounding tissues actually is.                                 Next we will review an article published by Williamson et al., in JACC Clinical Electrophysiology this past month entitled Real-World Evaluation of Magnetic Resonance Imaging in Patients With a Magnetic Resonance Imaging Conditional Pacemaker System.                                 Results of four year prospective followup in over 2,600 patients, while MRI conditional pacemakers are more increasingly used, long term longevity as well as effects of multiple MRI scans in terms of MRI functioning the devices is unclear. Thus, the study was sought to be a large scale, real world evaluation of MRI in patients with MRI conditional pacemakers. They included over 2,600 patients in multiple centers and all these patients had a SureScan pacing system. They noted that there were no MRI related complications occurring during or after the MRI, meeting the primary objective. In fact, almost a third of the patients underwent two or more scans and even then there was no cumulative increase in problems in these patients. The pacing capture thresholds stayed stable throughout all patients.                                 Thus this report constituted the largest longitudinal MRI experience in patients implanted with an MRI conditional device. The importance of this is to be able to highlight to patients that in fact even multiple MRIs despite having a device in place is safe. There is an increasing body of data that suggests that however, MRIs might be safe in a controlled setting, even in patients with legacy pacemakers. Whether MR conditional pacemakers actually offer incremental safety over legacy pacemakers however, is less clear and will likely require randomized trials of a large scale given the low number of events to really come to a conclusion. However, in most centers where it's not possible to do MRIs in legacy pacemakers, this offers some level of certainty that patients will likely be safe even undergoing multiple MRIs in a setting of having chronic pacemakers that are MRI conditionally safe.                                 Staying within the realm of looking at large multicenter experiences, we review an article by Hosseini et al., entitled Catheter Ablation for Cardiac Arrhythmias, Utilization and In-Hospital Complications, 2000 to 2013, published in JACC Clinical Electrophysiology this past month.                                 In this study, Hosseini et al., sought to investigate the overall utilization and in-hospital complications associated with catheter ablation in of all types in the United States between 2000 and 2013 using the National Inpatient Sample and Nationwide Inpatient Samples. They included all patients 18 years of age and older who underwent inpatient catheter ablation over this time period.                                 They estimated total a total of almost 520,000 inpatient ablations performed in this time period with a median age of 62 years amongst patients. Interestingly the annual volume of ablations and the number of hospitals performing ablations increased year over year but the rate of complications and length of stay also increased. A large number, almost more than a quarter of inpatient ablation procedures were actually performed in low volume hospitals and in turn were associated with an increased risk for complications with an odds ratio 1.26. Independent predictors of in-hospital complications and in-hospital mortality included complex ablations for atrial fibrillation and ventricular tachycardia, older age and a greater number of comorbidities. In addition to this, lower hospital volumes was an independent predictor of complications.                                 Thus the authors note that there has been a steady progressive in the number of in-hospital catheter ablation procedures. However, despite the increasing number, the number of periprocedural complications is increasing which may be partly mediated by taking in sicker patients from a complex procedures but also to performing these at lower volume centers. These findings are critical when considering the future of ablation strategies and ablation performance when we consider multicenter experiences or when we consider where certain procedures might be performed based on the experience of the operator or the institution. Why exactly it is that lower volume centers of higher complication rates still needs to be evaluated. However, it should be understood that ablations are  complex procedures and thus require a certain amount of experience in order to allow for procedural efficacy and safety similar to any cardiac surgery or other procedure. It remains to be understood what the number of procedures to be able to be felt to be competent and safe should be. But, these findings should be considered by all providers based on their own personal experience and based their own personal numbers.                                 Staying with the realm of catheter ablation, we will next review an article by Haldar et al., published regarding Catheter ablation vs electrophysiologically guided thoracoscopic surgical ablation in longstanding persistent atrial fibrillation: The CASA-AF Study in last month's edition of Heart Rhythm.                                 In this article, they sought to evaluate catheter ablation outcomes for longstanding persistent atrial fibrillation as compared with those of thoracoscopic surgical ablation. There's a limited amount of data comparing these two methodologies for ablation. They included 51 patients with de novo symptomatic atrial fibrillation. 26 underwent thoracoscopic surgical ablation and the remainder underwent stepwise left atrial ablation with a primary end point being single-procedure freedom from atrial fibrillation and atrial tachycardia lasting >30 seconds without antiarrhythmic drugs at 12 months. They noted that single- and multi procedure freedom from atrial fibrillation was higher in the surgical ablation group than in the catheter ablation group. Namely the overall success rate from the surgical ablation group was 73% versus 32% in the catheter ablation group. It should be noted that there was testing of the surgical ablation lesion set by electrophysiologists that was felt increased success rate in achieving acute conduction block by 19%. It also should be noted that the complication rate in the surgical ablation group, was significantly higher than the catheter ablation group, namely 27% versus 8%. This did not reach statistical significance however, possibly due to the low numbers considered.                                 The conclusion from the authors was that meticulous electrophysiologically guided thoracoscopic surgical ablation as a first line strategy in long standing persistent atrial fibrillation, may provide excellent single procedure success rates as compared with traditional catheter ablation. However again, there is an increased upfront risk of nonfatal complications. These considerations are important when thinking about what strategy to use in specific patients. Whether at a large level, thoracoscopic surgical ablation should be routinely used is still unclear and larger studies are likely needed to compare different modalities of ablation to better evaluate which is the right one for which patients.                                 Again staying in Heart Rhythm in 2017, we next review an article by Sheldon et al., published regarding Catheter ablation in patients with pleomorphic, idiopathic, premature ventricular complexes.                                 When a patient presents with idiopathic PVCs that are a single monomorphic focus, it is often considered reasonable to ablate them. However when patients have pleomorphic PVCs or polymorphic PVCs, the role of ablation is less clear and often considered more complex. Thus in this study, Sheldon et al., sought to evaluate patients who underwent ablation with pleomorphic PVCs. They reviewed about 100 consecutive patients 31% of whom had pleomorphic versus 69% who had monomorphic PVCs, however all of who were considered idiopathic. They noted the overall success rate was lower in patients with pleomorphic PVCs, namely 71% versus 90%. In fact, the presence of pleomorphic PVCs was independently associated with unsuccessful ablation. Also, pleomorphic PVCs more often had an epicardial origin than did monomorphic PVCs. And repeat ablation procedures were required in almost 20% of the cohort. Interestingly, three of the patients who came back for another procedure, had an increase of a nonpredominant PVC and one patient had a newly emerged PVC focus.                                 The conclusion by Sheldon et al. Was the presence of pleomorphic PVCs can affect ablation outcomes but it's still possible to achieve successful elimination of the predominant PVC even if not all PVCs are targeted. Furthermore, they suggested that most recurrences are due to reemergence of the originally targeted predominant PVC morphology though sometimes other PVC morphologies may arise. Larger scale evaluation is still necessary to understand when a patient should be taken to ablation and when not. We recognize that sometimes the presumption of idiopathic might be due to a lack of consideration of other ideologies such as subclinical inflammation that can be related to myocarditis or sarcoidosis or other finding. Thus it should always be considered what the actual underlying substrate is with rigorous imaging such as MRI or PET scanning. However, the findings by Sheldon et al. suggest that just because there are multiple PVC morphologies present, does not necessarily mean that they cannot be ablated.                                 Switching gears away from PVCs, we next review an article by Romero et al. published in Heart Rhythm this past month entitled Emergence of atrioventricular nodal reentry tachycardia after surgical or catheter ablation for atrial fibrillation: Are we creating the arrhythmia substrate?                                 They reviewed patients who had AVNRT ablation performed and sought to evaluate how many of them had prior surgical or catheter ablation for atrial fibrillation. They reviewed cases of ablation for specifically persistent atrial fibrillation who eventually required a repeat ablation procedure and had a diagnosis of AVNRT at that time. A total of nine patients were identified meeting these characteristics. All of these patients were noted to have evidence of atrial fibrosis in the septum or proximal CS, and in fact six had undergone ablation either at the septum or the coronary sinus ostium or body and the other three had inferior mitral lines at a surgical MAZE approach. All had typical AVNRT inducible that was abolished with slow pathway ablation, though five required ablation in the roof of the coronary sinus or on the mitral valve annulus.                                 Thus Romero et al. concluded that ablation involving the septum or proximal CS may create a substrate that can induce AVNRT. These findings are important when we consider ablation. Oftentimes when we do ablation, we think of a targeting substrate without thinking about the substrate we might create. Thus, rigorous evaluation for other mechanisms of tachycardia that one might not think of because of the absence of it during the index ablation should always be considered such as the creation of substrate for AVNRT. While most of us will consider atrial flutters or focal atrial tachycardias or macro reentry atrial tachycardias as the principle mechanisms of tachycardia in patients returning after prior atrial fibrillation ablation should also be considered that we might be creating substrate for other types of arrhythmias such as AVNRT.                                 The next article we will review is published in the American Journal of Physiology, Heart and Circulatory Physiology by Yang et al., entitled Effect of ovariectomy on intracellular calcium regulation in guinea pig cardiomyocytes.                                 It is believed that long-term deficiency of ovarian hormones after ovariectomy can alter cellular calcium handling mechanisms in the heart that can in turn result in the formation of a proarrhythmic substrates. This is important when considering possible arrhythmogenic mechanisms in women who might be undergoing ovariectomy or who might be in a post menopausal state. Thus in a series of animals, they evaluated the effective of ovariectomy as well as estrogen supplementation to ovariectomized animals on calcium handling at the level of the heart. They demonstrated that the ovariectomized guinea pig cardiac myocytes had higher frequencies of calcium waves and isoprenaline challenged cells displayed more early after depolarizations after ovariectomy. In addition to this, they noted the observations of calcium regulation alternations were not observed in myocytes from ovariectomized guinea pigs who were supplemented with 17β-Estradiol suggesting that in fact, these changes in the arrhythmogenic substrate were due to ovarian hormone deficiency resulting in dysregulation of cardiac calcium.                                 While this was all performed at the level of guinea pigs, it is an important consideration again, as a potential mechanisms of cardiac arrhythmogenesis in women who might be undergoing ovariectomy or who might be post menopausal. In some cases ovarian hormones might be beneficial in regulating the arrhythmogenic substrate.                                 The next article we review is published in Heart this past month by Stewart et al., entitled Nitric oxide synthase inhibition restores orthostatic tolerance in young vasovagal syncope patients.                                 Syncope is probably one of the most difficult things that we treat in electrophysiology. In particular, vasovagal syncope. People have looked at different pacing maneuvers and specialized pacemakers for treatments. However, there's improving body of knowledge regarding other mechanisms, specific physiologic mechanisms that might underlie vasovagal syncope. This group in question had previously demonstrated that impaired post synaptic adrenergic responsiveness in those who have vasovagal syncope may be reversed by blocking nitric oxide synthase. Thus, they sought to evaluate volunteers who either had vasovagal syncope or were otherwise healthy, what the effect of a nitric oxide synthase inhibitor would be.                                 They demonstrated that arterial vasoconstriction is impaired in young vasovagal syncope patients but inhibiting nitric oxide synthase could correct this problem. Namely, that this might provide a potential mechanism of avoiding the changes in blood pressure associated with orthostatic intolerance resulting in vasovagal syncope. Whether or not this proves to be an ambulatory therapy still remains to be seen but at least in the acute study state within which these patients were evaluated, it suggests to be a potential promising target.                                 The next paper we review is also published in Heart this past month by Lazzerini et al., entitled Systemic inflammation as a novel QT-prolonging risk factor in patients with torsades de pointes.                                 There is increasing evidence of the role systemic inflammation can play in arrhythmogenesis and particularly in acquired long QT syndrome in patients with sarcoid or myocarditis and other disease states is well recognized that ventricular arrhythmias that are potentially life threatening can happen. What the role of correcting this inflammatory state is, is less clear. However, this group decided to evaluate whether systemic inflammation may represent a currently overlooked risk factor contributing to torsades de pointes in the general population. They looked at 40 consecutive patients who experienced torsades and enrolled them to evaluate circulating levels of different inflammatory biomarkers and compared them with patients with active rheumatoid arthritis, comorbidity or healthy controls. They demonstrated that in the torsades group, 80% of patients showed an elevated inflammatory markers and in fact a definite inflammatory disease was identifiable in 18 of the 40 patients with 12 having acute infections, five having immune mediated diseases and one described as other.                                 Thus they proposed that systemic inflammation via elevated IL-6 levels could represent a novel QT-prolonging risk factor that can contribute to torsades. In their group they showed that CRP reduction was associated with IL-6 level decrease and resulted in QTC shortening. It remains to be seen whether this increased inflammatory pathway might be due to the torsades event itself or the cause. However, it does bring up the interesting question of whether or not systemic inflammation may in fact be causing untoward effects on normal arrhythmic profiles resulting in a greater risk of ventricular arrhythmias.                                 The next article we review is published by Kottkamp et al., entitled Global multielectrode contact mapping plus ablation with a single catheter: Preclinical and preliminary experience in humans with atrial fibrillation in this past month's issue of the Journal of Cardiovascular Electrophysiology.                                 Within the realm of catheter ablation for atrial fibrillation, There's a constant search for new approaches to achieve either more durable or quicker or safer pulmonary vein isolation. It is well recognized that pulmonary vein isolation is the cornerstone of atrial fibrillation ablation. In this particular paper, they sought to evaluate the utility of a catheter, namely a basket catheter that could allow for both diagnostic mapping as well as targeted ablation. This novel catheter has a distal multielectrode array with 16 ribs with 122 gold-plated electrodes. With each electrode being able to ablate, pace and able to measure tissue contact, temperature, current, and intracardiac electrograms. They noted in three patients that complete pulmonary vein isolation was achieved in all 12 and in most veins, PVI was achieved with a single placement in front of that respective vein though in one case there was a single gap requiring reapplication.                                 This suggests a new technique for quote unquote, single shot pulmonary vein isolation. Furthermore, the fact that multiple electrodes could be used to map at the same time as performing ablation, suggest that there might be opportunities for mapping more than just the veins themselves. What the safety and utility of this approach would be over other quote unquote, single shot approaches, such as laser and cryo based balloon systems, is unclear. Furthermore, whether or not they actually reflect a paradigm that offer additional utility due to the ability for more mapping, also remains to be seen. However, the critical portion of understanding these different tools is being able to differentiate them in practice and understanding what their relative values and opportunities are will be critical as one makes selections of which technologies to use.                                 The next article we review is published in Europace this past month by Hellenthal et al., entitled Molecular autopsy of sudden unexplained deaths reveals genetic predispositions for cardiac diseases among young forensic cases.                                 While we recognize that coronary artery disease causes the majority of sudden cardiac deaths in the older population. When we have a young patient who experiences sudden cardiac death, we always have to be concerned about the role of a genetic component. This is not just important for the patient themselves but also for family members who might still be alive. In this study they sought to determine the portion of underlying genetic heart disease among unexplained putative sudden cardiac death cases from a large German forensic departments.                                 The number included were only 10 patients who had sudden unexplained death aged 19 to 40 years. DNA was analyzed for 174 candidate genes and also genetic testing was offered to affected families. Amongst 172 forensic cases again, 10 cases of sudden unexplained death were identified and a genetic disposition was found in eight of 10 cases, with pathogenic mutations in three and variants of uncertain significance in five. Furthermore, subsequent selective screening of the family members revealed two additional mutation carriers in family members who had not suffered from a sudden death event yet.                                 The role of molecular autopsy in patients is evolving. However, the amount of molecular autopsies that are sent are still too low. All patients who are young and die unexpectedly, might benefit from molecular autopsy beyond just traditional forensic pathology to understand whether or not there's a genetic predisposition that led to their event. This might help the family members of that affected individual, especially in understanding whether or not they may also be at risk.                                 The next article we review is by Constantino et al., entitled Neural networks as a tool to predict syncope risk in the Emergency Department in Europace this past month.                                 Many patients when they pass out immediately come into the emergency department. However, it can be very difficult to understand what the risk of that syncope patient is and thus many are automatically admitted to the hospital despite the fact that history might provide a lot of data. In this study, Constantino et al., sought to evaluate the utility for artificial neural networks in stratifying risk in patients presenting with syncope to the hospital. They analyzed individual level data from three prior prospective studies and included a a cumulative sample of 1,844 patients. They included ten variables from patient history, ECG, and the circumstances of syncope to train and test the neural network. They actually had two different approaches used for training and validating neural network given the exploratory nature of the study. They found that they could identify adverse events after syncope with a sensitivity if 95% if they used one approach versus 100% if they used an approach that considers more factors.                                 Thus the study suggested that artificial neural networks could effectively predict the short-term risk of patients with syncope after presenting to the emergency departments. They did not seek to address what the predictive capability of the artificial neural network would be when compared with traditional clinical judgment and existing rule sets that might exist in various emergency departments. The reason this study's important is that as artificial neural networks become more robust we might find that their role in complementing physician decision making might become more and more important. This is especially true on the front lines amongst emergency department physicians or in other groups and consideration of employment of novel technologies or rule sets or methodologies to augment decision making on risk of patients who are being evaluated might need to be considered. It also might help individual stratify patients into those that require sooner evaluation.                                 The final article we review is published in the Journal of Interventional Cardiac Electrophysiology this past month by Schmier et al., entitled Effect of battery longevity on costs and health outcomes associated with cardiac implantable electronic devices: a Markov model-based Monte Carlo simulation.                                 Economic effects of increasing utilization of cardiac implantable electronic devices is of increasing concern. We also note that a lot of focus goes on what the battery life of a device is. However, how that battery longevity might affect overall cost and health outcomes is less clear. Thus in this study, Schmier et al., sought to develop a Monte Carlo Markov model simulation model to evaluate what happens to patients based on the battery longevity. They sought evaluations such as infection and non-infectious complication rates as well as overall costs over the lifetime of that individual patient. These outcomes were largely derived from Medicare data. They noted that an increase in battery longevity was an associated reduction in the number of revisions needed by 23%, the number of battery changes needed by 44%, the number of infections by 23%, the number of non-infectious complications by 10% and total costs per patient by 9%.                                 Thus, they demonstrated that using batteries that have longer longevity could be associated with fewer adverse outcomes and reduced healthcare costs. The understanding of the magnitude of the cost benefits of extended battery life is critical and how to optimize the battery life is also critical. It might be that as we move forward, when encountering a situation or a patient in which the battery life is far less than expected, consideration of the reasons why that battery life was limited will be critical in order to optimize the ongoing chronic care of that patient. Both to reduce the burden on the healthcare system and to improve that individual patient's long term outcomes in terms of infectious risk or other issues.                                 This is primarily simulation model and was not necessarily tested in a prospective fashion though this would be quite difficult given the long duration over which would be required to see a lot of these beneficial costs and complication rate effects. However, it is provocative in the fact that it allows us to understand that there might be benefits from taking further care in selecting not just the right device based on indication but the right device based on patient age, the number of general changes one expects a patient to have and what the longevity of that patient is expected to be.                                 I appreciate everyone's attention in these key and hard hitting articles that we have just focused on from this past months of cardiac electrophysiology across the literature. Thanks for listening. Now back to Paul. Paul Wang:         Thanks Suraj. You did a terrific job surveying all journals for the latest articles on topics of interest in our field. There's not an easier way to stay in touch with the latest advances. These summaries and a list of all major articles in our field each month can be downloaded from the Circulation, Arrhythmia and Electrophysiology website. We hope you'll find the journal to be the go to place for everyone interested in the field. See you next month.    

This week we welcome Andy Little onto the show to discuss the modified Valsalva maneuver for breaking SVT. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_102_0-AVNRT_Final_Cut.m4a Download Leave a Comment Tags: Adenosine, AVNRT, Cardiology, SVT, Tachydysrhythmia Show Notes Read More Rebel EM: The REVERT Trial – A Modified Valsalva Maneuver to Convert SVT SGEM: This is a SVT and I'm Gonna Revert It Using a Modified Valsalva Manoeuvre Appelboam A et al. Postural Modification to the Standard Valsalva Manoeuvre for Emergency Treatment of Supraventricular Tachycardias (REVERT): A Randomised Controlled Trial. Lancet 2015. PMID: 26314489 Read More

This week we welcome Andy Little onto the show to discuss the modified Valsalva maneuver for breaking SVT. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_102_0-AVNRT_Final_Cut.m4a Download Leave a Comment Tags: Adenosine, AVNRT, Cardiology, SVT, Tachydysrhythmia Show Notes Read More Rebel EM: The REVERT Trial – A Modified Valsalva Maneuver to Convert SVT SGEM: This is a SVT and I’m Gonna Revert It Using a Modified Valsalva Manoeuvre Appelboam A et al. Postural Modification to the Standard Valsalva Manoeuvre for Emergency Treatment of Supraventricular Tachycardias (REVERT): A Randomised Controlled Trial. Lancet 2015. PMID: 26314489 Read More

This week, we review a simplified approach to determining the rhythm on an EKG with a tachydysrhythmia. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_88_0_Final_Cut.m4a Download One Comment Tags: Atrial Fibrillation, AVNRT, SVT, Tachycardias, Tachydysrhythias, Ventricular Tachycardia Show Notes Take Home Points When looking at a tachy rhythm that isn't sinus tach, quickly differentiate by determining if the QRS complexes is narrow or wide and then determine if the rhythm is regular or irregular. This approach quickly drops the rhythm into 1 of 4 boxes and makes rhythm determination much easier Each of those 4 categories has a small set of rhythms included. Narrow and irregular – AF, Aflutter with variable block or MFAT. Narrow and regular – SVT or Aflutter. Wide and irregular – Torsades, VF, AF with aberrancy or a BBB. Wide and regular – VTach, SVT with aberrancy or SVT with a BBB. If you see wide and regular, the top 3 diagnoses are VT, VT and VT. Assuming VT and treating for that will almost never send you astray Read More EM: RAP: Episode 84 – Tachycardia Core EM:

This week, we review a simplified approach to determining the rhythm on an EKG with a tachydysrhythmia. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_88_0_Final_Cut.m4a Download One Comment Tags: Atrial Fibrillation, AVNRT, SVT, Tachycardias, Tachydysrhythias, Ventricular Tachycardia Show Notes Take Home Points When looking at a tachy rhythm that isn’t sinus tach, quickly differentiate by determining if the QRS complexes is narrow or wide and then determine if the rhythm is regular or irregular. This approach quickly drops the rhythm into 1 of 4 boxes and makes rhythm determination much easier Each of those 4 categories has a small set of rhythms included. Narrow and irregular – AF, Aflutter with variable block or MFAT. Narrow and regular – SVT or Aflutter. Wide and irregular – Torsades, VF, AF with aberrancy or a BBB. Wide and regular – VTach, SVT with aberrancy or SVT with a BBB. If you see wide and regular, the top 3 diagnoses are VT, VT and VT. Assuming VT and treating for that will almost never send you astray Read More EM: RAP: Episode 84 – Tachycardia Core EM: A Si...

Carolyn: Welcome to circulation on the run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. [Carolyn Nam 00:00:08], associate editor from the national heart center and Duke National University of Singapore ...     In just a moment we will be discussing the exciting new results of the [Prague 00:00:21] 18 study of prasugrel versus ticagrelor in patients with acute myocardial infarction treated with primary or cutaneous coronary intervention. But first, here's your summary of this week's issue ...     The first study represents the largest published study on the association between PR interval and cardiac resynchronization therapy with defibrillator versus implantable cardioverter defibrillator and real world outcomes. Dr. Friedman and colleagues from Duke Clinical Research Institute studied 26,451 CRT eligible patients from the National Cardiovascular Data Registry ICD Registry. They found that a PR interval at or above 230 milliseconds was associated with increased rates of heart failure, hospitalizations, or death among CRTD but not ICD patients. The real world comparative effectiveness of CRTD versus ICD was significantly less among patients with a PR interval above 230 milliseconds compared to patients with a shorter PR interval.     The authors discuss that these findings may be due to the association between a prolonged PR interval and factors associated with lower rates of CRT response such as non-left bundle branch block morphology, ischemic heart disease, or atrial arrhythmias. It could also be due to the association between delayed AV conduction, disordered diastolic filling, and contemporary CRT reprogramming strategies. The take home message is: in CRT patients with a prolonged PR interval, recognize that they are at high risk for poor outcomes and merit close follow up and consideration of AV optimization ...     The next study is the first adolescent study of serum lipidomics that identifies a new panel of serum glycerophosphocholines that are associated with cardiovascular risk. First author Dr. [Sine 00:02:29], corresponding author Dr. [Palsova 00:02:31], and colleagues from Hospital for Sick Children in University of Toronto recognize that atherogenic dislipidemia is traditionally assessed with high abundance lipids, such as cholesterol and triacylglycerols, which accumulate at millimolar levels in blood. Current advancements in mass spectrometry now allow the discovery and study of new low abundance lipids, which circulate at micro- or nanomolar blood levels. And one such example are the glycerophosphocholine metabolites.     They studied a population based sample of 990 adolescents with age range 12-18 years using liquid chromatography electrospray ionization mass spectrometry. They identify several novel glycerophosphocholines that were associated with multiple cardiovascular disease risk factors. Mediation analysis revealed that these novel glycerophosphocholines mediated their respective relationships between visceral fat and cardiovascular disease risk factors. Furthermore, a particular glycerophosphocholine shown recently to predict incident coronary heart disease in older adults was already associated with several cardiovascular disease risk factors in these adolescents.     The clinical implication is that the development of a lipidomics signature that could facilitate early intervention or treatment of those at high risk of cardiovascular disease or monitor response interventions could help triage limited healthcare resources. Furthermore, future research on glycerophosphocholines might improve biological understanding of disease and identify potential drug targets to impede cardiovascular disease development ...     The next study also describes plasma lipidomic profiles but this time in patients with type 2 diabetes. This study is from first author Dr. [Elchuri 00:04:35], corresponding author Dr. [Meekly 00:04:37], and colleagues from the Baker IDI Heart and Diabetes Institute in Melbourne, Australia. These authors performed a targeted lipidomic analysis using liquid chromatography electrospray ionization tandem mass spectrometry in a case cohort of 3,779 patients with type 2 diabetes and one or more additional cardiovascular risk factors from the advance trial.     They found that sphingolipids, phospholipids, cholesterol esters, and glycerol lipids were associated with future cardiovascular events and cardiovascular death. The addition of 7 lipid species to a base model of 14 traditional risk factors and medications improved the prediction of cardiovascular events. The prediction of cardiovascular death was also improved with the incorporation of 4 lipid species to the base model. These results were further validated in a subcohort of type 2 diabetes from the lipid trial. In summary, this important study demonstrates the potential of plasma lipid species as biomarkers for cardiovascular risk stratification in diabetes ...     The last study sheds new light on the optimal ablation method for atypical atrioventricular nodal reentrant tachycardia or atypical ARNVT. Dr. [Catrisis 00:06:10] and colleagues from Beth Israel Deaconess Medical Center, Harvard Medical School in Boston, Massachusetts study 2,079 patients with AVNRT subjected to slow pathway ablation. In 113 patients, atypical AVNRT or coexistent atypical and typical AVNRT without other concomitant arrhythmias was diagnosed. Ablation data and outcomes were compared to a group of age and sex matched control patients with typical AVNRT. The authors found that in the atypical group slow pathway ablation was accomplished from the right septum in 110 patients and from the left septum in 3 patients. There was no need for additional ablation lesions at other anatomical sites and no cases of AV block were encountered.     In summary AVNRT, regardless of the type, appears to be successfully ablated by targeting the anatomic area of the slow pathway. When a right septal approach is not successful, the anatopic area of the slow pathway can be ablated from the left septum and so it seems the slow pathway participates in both typical and atypical AVNRT. The take home messages are that catheter ablation at the anatomical area of the slow pathway from the right or left septum may be the treatment of choice for atypical AVNRT. The approach is not associated with an increased risk of inadvertent AV block. The recurrence rate following ablation of atypical AVNRT may not be significantly higher than that seen following the ablation of typical AVNRT.     Those were the highlights from this week's issues. And now for our feature paper ...     We're so pleased to have with us today for our podcast interview first and corresponding author of the Prague 18 study, Dr. [Zuzana Motovska 00:08:12] from Charles University in Prague. Welcome Zuzana.   Zuzana: Thank you for having me.   Carolyn: We're also so lucky to have Dr. [Gabriel Stig 00:08:21], associate editor from Paris, and I understand you're even traveling at the moment. Thank you, Gabriel for making the time.   Gabriel: Yes, hello Carolyn, hello Zuzana.   Carolyn: So let me start by congratulating you Zuzana on this first head-to-head comparison study of prasugrel versus ticagrelor in patients with acute myocardial infarction treated with primary or cutaneous coronary intervention. And what a lovely study acronym of course, Prague 18. Could you maybe start by describing, in the Czech Republic before your study, how were clinical decisions being made between prasugrel and ticagrelor in these patients?   Zuzana: The current guidelines prefer newer P2Y12 inhibitors over clopidogrel for patients with acute coronary syndromes. Prasugrel and ticagrelor are being increasingly used in patients [with just 00:09:15] primary PCI in Czech Republic. Analysis of our registry documented that doctors did not view these two drugs as interchangeable and prasugrel is a drug associated with a high risk of bleeding. Our data show that safety in terms of bleeding risk was the most important aspect under consideration when choosing one of new agents for an individual patient. The same observation has been reported from other contemporaries from other countries and according to the published subgroup analysis of [stratum 00:09:54] and other studies we have also perceived prasugrel to be a more effective agent for primary PCI. We prefer this drug in patients with a high thrombotic risk.   Carolyn: Could you, maybe now, clearly describe what you did in this study and what were your findings?   Zuzana: The Prague 18 study truly [inaudible 00:10:19] was designed to test the hypothesis on whether one of the newer drugs, prasugrel or ticagrelor, is more effective and safer than the other one in acute myocardial infarctions, which is the primary [treatment 00:10:36] strategy. We randomized the total 1,230 in 14 participating sites. I highlighted hemodynamic instabilities, was not an [excluding 00:10:52] criterion for study participation. The patients were randomized for prasugrel or ticagrelor immediately on hospital arrival and the recommended dosing regiments were used for both drugs. The prasugrel dose was reduced during the maintenance phase in patients over 75 and [reduced vein 00:11:12] was the [sixth 00:11:14] feature around presence of both these parameters was an exclusion criterion.     So, what we find. Fewer [unsourced 00:11:23] primary endpoint composed of all cause of death or reinfarction show serious bleeding or urgent vessel revascularization within 7 days after randomization or discharge if prior to the seventh day. They did not differ between groups, either for in 4 person prasugrel group and in 4.1 person in ticagrelor group. The appearance of key secondary end point composed of cardiovascular death, nonfatal MI, or nonfatal stroke. Within 30 days did not show any significant difference between prasugrel and ticagrelor, furthermore no significant difference was found in any of the components of the primary and secondary endpoints and also no significant difference was observed in the appearance of definite vein thrombosis [inaudible 00:12:17] days after randomization.     So the study did not show any difference between ticagrelor and prasugrel in the early phase of a mild [treatable 00:12:26] primary PCI. Because of small sample size the confidence for the estimation of the [interval 00:12:35] of either were quite high, however we identify differences, which are very low in absolute numbers and [inaudible 00:12:45]   Carolyn: That was very nicely explained Zuzana, thank you. Now could you share a little bit more about, were you powered for this analysis and the decision to stop early.   Zuzana: Oh yes, the power analysis was computed for primary endpoint difference of 2.5 person and the needed sample size was estimated at 2,500 patients. The interim analysis led to a decision to terminate the study prematurely because of futility. No significant difference in primary endpoint was found between the two study drugs in the course of the entire randomization process, moreover the difference in appearance of the primary endpoint between the compare groups was declining with a growing number of randomized patients and analyzed on the different 0.1% and this was the decision why we stopped the trial prematurely.   Carolyn: Right. Gabriel could you comment a little bit as the associate editor managing this paper, how do you think it's going to impact practice?   Gabriel: First of all, let me start by congratulating Zuzana and the team of the Prague 18 trial for this academic trial. I think it's really important that we have a clinically led effort to investigate optimal treatments in modern cardiology in general and specifically in acute coronary syndromes. We've known for several years now, through large randomized trials, that the novel P2Y12 agents, ticagrelor and prasugrel, are clearly superior to clopidogrel but we don't know which of the two agents to choose and we know that comparison across trials are fraught with major methodological problems. So with evidence that prasugrel is superior to clopidogrel for PCI treated ACS patients, there was evidence that ticagrelor was superior to clopidogrel for ACS patients in general but we didn't have any rational data on which to base a rational selection process between the two agents.     Really, I think it's an important issue and often people state that these are delicate differences between agents, and we shouldn't expect that this is going to impact clinical outcomes. Actually it does impact clinical outcomes because we know that those novel agents have had a roughly 20% reduction in major heart outcomes compared to clopidogrel so this is not a moot point. It's not a minute difference, it's a huge difference and it's an important clinical issue. That's my first point, I think it's an important question and I really want to commend the investigators for launching this trial despite not having the support of industry.     The second point I want to make is I think that the results from the trial are not yet complete because we don't have the one year follow-up and I know that this is planned and the investigators are continuing follow-up of their patient cohort, which I think is going to be important because it's conceivable that differences may emerge over time as was, in fact, the case in some of the previous trials. In [plato 00:15:49] there was a modest difference early on but the curves diverged over time between clopidogrel and ticagrelor so it's conceivable that differences that are absent at 30 days might emerge over time.     In fact, I have a question for Zuzana. One of the interesting features and important issues that needs to be addressed is ... I know that in some sites in the Czech Republic, because of the out of pocket expenses related to the cost of the novel agents, it was allowed for patients to be switched back to clopidogrel after hospital discharge. Do you have any sense of what is the proportion of patients who are scaled back to clopidogrel instead of prasugrel or ticagrelor after initial index submission?   Zuzana: Thank you Gabriel, it's true the study ... a lot of patients who are unable to bear the cost associated with long term treatment with the study medications and switch to clopidogrel. Therefore, a second goal of the study was to assess the rate, the reason, and also the consequences of switching from a study drug to clopidogrel after the acute phase in the course of 12 months follow-up. We are not focusing on the study completion and analysis that are related to the second study. There are, of course, patients who switch from prasugrel or ticagrelor to clopidogrel also in first 30 days and this proportion was about one third of patients.   Gabriel: The other point I want to make really relates to the power issues and Zuzana already pointed out herself this important issue. The paper is actually accompanied by an excellent and very cogent editorial by Steve [Webiok 00:17:31], who discusses explicitly and in great detail the issue of sample size. We know that the relative difference between the novel agents and clopidogrel is in the range of 20% so we might expect that the difference between the two novel agents themselves, when we compare prasugrel and ticagrelor, might be less. Yet the study was powered for actually a greater relative risk reduction than what was seen in the pivotal trials of prasugrel and ticagrelor compared to clopidogrel. So the study is really on the low end of the power spectrum and I think, as you pointed out Zuzana, it's important to keep in mind that the confidence interval for the relative risk between ticagrelor and clopidogrel both act together on prasugrel, both for the primary endpoint, which is a combination of efficacy and safety, as well as for the key secondary endpoint of efficacy.     It's really very wide and we can't rule out a major benefit or a major detrimental effect of one agent versus the other. I think this is important to keep in mind because many people equate a neutral result of a trial, a non-significant result, particularly in the [secondary 00:18:36] trial, with lack of difference or clinical equivalence or non-inferiority and I think it's important to remember the readers that this is not a non-inferiority trial, it's not a clinical equivalence trial, it's superiority trial that is actually with a neutral result. It's really and important issue.     Yet, because it's the first head-to-head comparison, because it's an academic effort independent, and because it's going to report one year outcomes, I think this is a critical effort and the investigators need to be lauded for that. Even if this study isn't powered, it will be able to be pulled in further meta-analysis with other upcoming studies that are similar that also may be underpowered and provide us with a hint of evidence of what might be the best agent to use, which is an every day clinical question. This is a very, very common condition and any unbiased evidence we can get from randomized trials is very valuable ...   Carolyn: Thank you, everyone, for listening to this episode of circulation on the run. Tune in next week ...  

Commentary by Dr. David Wilber

On this podcast we review some background on AVNRT and focus on Emergency Department management. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_20_0_Final.m4a Download 2 Comments Tags: AVNRT, PSVT, REVERT Trial, Tachydysrhythmias Show Notes AVNRT with Aberrancy vs. VT REBEL EM: SVT with Aberrancy Versus VT Amal Mattu's ECG Case of the Week: August 26th, 2013 Valsalva Maneuver ALiEM: Tricks of the Trade: Valsalva Maneuver By Using a 10cc Syringe St. Emlyn's: JC The REVERT Trial Adenosine in AVNRT Larry Mellick: Treating SVT with Adensoine ALiEM: Trick of the Trade: Combining Adenosine with the Flush Verapamil in AVNRT RAGE Podcast:

On this podcast we review some background on AVNRT and focus on Emergency Department management. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_20_0_Final.m4a Download 2 Comments Tags: AVNRT, PSVT, REVERT Trial, Tachydysrhythmias Show Notes AVNRT with Aberrancy vs. VT REBEL EM: SVT with Aberrancy Versus VT Amal Mattu's ECG Case of the Week: August 26th, 2013 Valsalva Maneuver ALiEM: Tricks of the Trade: Valsalva Maneuver By Using a 10cc Syringe St. Emlyn's: JC The REVERT Trial Adenosine in AVNRT Larry Mellick: Treating SVT with Adensoine ALiEM: Trick of the Trade: Combining Adenosine with the Flush Verapamil in AVNRT RAGE Podcast:

On this podcast we review some background on AVNRT and focus on Emergency Department management. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_20_0_Final.m4a Download 2 Comments Tags: AVNRT, PSVT, REVERT Trial, Tachydysrhythmias Show Notes AVNRT with Aberrancy vs. VT REBEL EM: SVT with Aberrancy Versus VT Amal Mattu’s ECG Case of the Week: August 26th, 2013 Valsalva Maneuver ALiEM: Tricks of the Trade: Valsalva Maneuver By Using a 10cc Syringe St. Emlyn’s: JC The REVERT Trial Adenosine in AVNRT Larry Mellick: Treating SVT with Adensoine ALiEM: Trick of the Trade: Combining Adenosine with the Flush Verapamil in AVNRT RAGE Podcast: