Podcasts about ventricular tachycardia

Send us a textThis week, Dr. Mike Fralick and special guest, Dr. Laiya Carayannopoulos from the Intern at Work Podcast and our Medicine Pods collaboration, discuss two recent papers exploring oxygenation in acute respiratory failure and the use of ablation versus anti-arrhythmic medication for ventricular tachycardia. Two papers, here we go!High-Flow Nasal Oxygen vs Noninvasive Ventilation in Patients with Acute Respiratory Failure: The RENOVATE Randomized Clinical Trial (0:00 – 14:45).Catheter Ablation or Antiarrhythmic Drugs for Ventricular Tachycardia (14:45 – 22:55).And for the Good Stuff:Medicine Pods! (22:55 – 23:51).Sign-up to our mailing list to receive link to attend the Royal College Epidemiology Crash Course hosted by Dr. Mike FralickSupport the show

Welcome back Rounds Table Listeners!We are back today with our Classic Rapid Fire Podcast!This week, Dr. Mike Fralick and special guest, Dr. Laiya Carayannopoulos from the Intern at Work Podcast and our Medicine Pods collaboration, discuss two recent papers exploring oxygenation in acute respiratory failure and the use of ablation versus anti-arrhythmic medication for ventricular tachycardia. Two papers, here we go!High-Flow Nasal Oxygen vs Noninvasive Ventilation in Patients with Acute Respiratory Failure: The RENOVATE Randomized Clinical Trial (0:00 – 14:45).Catheter Ablation or Antiarrhythmic Drugs for Ventricular Tachycardia (14:45 – 22:55).And for the Good Stuff:Medicine Pods! (22:55 – 23:51).Sign-up to our mailing list to receive link to attend the Royal College Epidemiology Crash Course hosted by Dr. Mike FralickQuestions? Comments? Feedback? We'd love to hear from you! @roundstable @InternAtWork @MedicinePods

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances discusses a recently published original research paper on technique and outcomes of intracardiac echocardiography to assist anatomical isthmus ablation in repaired Tetralogy of Fallot patients with ventricular tachycardia.

Commentary by Dr.  Jian'an Wang.

Did you miss AHA 2024? Listen here to brief discussions of the latest research. Eric Rubin is the Editor-in-Chief of the Journal. Jane Leopold is a Deputy Editor of the Journal. Stephen Morrissey, the interviewer, is the Executive Managing Editor of the Journal. E.J. Rubin, J. Leopold, and S. Morrissey. NEJM at AHA — Catheter Ablation or Antiarrhythmic Drugs for Ventricular Tachycardia. N Engl J Med. DOI: 10.1056/NEJMe2414471.

Being A Vet Saved Her Life When Veterinarian Dr. Sarah Boston noticed a lump on her body, she insisted that it was cancerous, even though other doctors said no. She did an ultrasound at her office and validated her worst fear. The lump was removed, and she is now cancer-free. Listen Now What Would You Do For Your Dog? When this week's Hero Person found out his pup had Ventricular Tachycardia, a rare condition where a dog has a rapidly fast and sometimes irregular heartbeat, Scott Clare drove almost 5,000 miles and spent over $10,000 to treat Buck-O. Listen Now Bit 100,000 Times Brian Barczyk had 30,000 snakes at home. Yes, he was bitten 100,000 times. And yes, the ladies dig it! While Brian told people he breeds snakes, he actually said he cleaned snake poop for a living! He ran one of the world's largest snake breeding facilities and hatched over 30,000 baby snakes a year! They sold to beginner hobbyists and advanced collectors. They had snakes as cheap as $25 all the way up to $125,000 a piece. Listen Now Removing Sap Animal Radio Dogfather Joey Villani has several foolproof ways to get tree sap out of your dog's hair and that hard-to-get-to spot between their pads. No need to cut out the hair if you use the right stuff. Listen Now Read more about this week's show.

Ventricular Tachycardia Stable by Albuquerque Fire Rescue

Supra Ventricular Tachycardia Made Easy by Albuquerque Fire Rescue

With Pranav Bhagirath, Amsterdam University Medical Centre, Amsterdam - Netherlands & Helmut Puererfellner, Ordensklinikum Linz Elisabethinen, Linz - Austria. Link to editorial Link to paper  

Commentary by Dr. Edward Gerstenfeld

We look at the most common ECG rhythms and patterns seen in Medicine, including main identifying features of each. Consider subscribing on YouTube (if you found any of the info useful!): https://www.youtube.com/channel/UCRks8wB6vgz0E7buP0L_5RQ?sub_confirmation=1Patreon: https://www.patreon.com/rhesusmedicineBuy Us A Coffee!: https://www.buymeacoffee.com/rhesusmedicineRecommended sources for further reading:https://litfl.com/ecg-library/https://ecgwaves.com/Timestamps:0:00 Sinus Rhythm (Sinus Tachycardia & Sinus Bradycardia1:06 Atrial Fibrillation 2:35 – AF video link2:38 Atrial Flutter4:26 Premature Ventricular Contraction (PVCs) & Premature Atrial Contractions (PACs)5:40 Bundle Branch Block (LBBB & RBBB) 6:41 1st Degree AV Block7:03 2nd Degree AV Block - Mobitz 1 (Wenckebach) & Mobitz 2 (Hay)7:39 3rd Degree Heart Block (Complete Heart Block) 8:15 Heart Block Video Link8:19 Ventricular Tachycardia & Ventricular Fibrillation10:20 ST ElevationReferences:Nickson, C - Life in the Fast Lane (2023) Atrial Fibrillation. Available at https://litfl.com/atrial-fibrillation/Buttner, R. Burns, E - Life in the Fast Lane (2022) Atrial Flutter. Available at https://litfl.com/atrial-flutter-ecg-library/Larkin, J. Burns, E - Life in the Fast Lane (2021) AV Block: 1st Degree. Available at https://litfl.com/first-degree-heart-block-ecg-library/Burns, E. Buttner, R - Life in the Fast Lane (2021) AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon). Available at https://litfl.com/av-block-2nd-degree-mobitz-i-wenckebach-phenomenon/Burns, E. Buttner, R - Life in the Fast Lane (2022) AV Block: 2nd degree, Mobitz II (Hay block). Available at https://litfl.com/av-block-2nd-degree-mobitz-ii-hay-block/Larkin, J. Buttner, R. - Life in the Fast Lane (2023) AV Block: 3rd Degree. Available at https://litfl.com/av-block-3rd-degree-complete-heart-block/Buttner, R. Burns, E - Life in the Fast Lane (2023) Ventricular Tachycardia – Monomorphic VT. Available at https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/Burns, E. Buttner, R - Life in the Fast Lane (2022) The ST Segment. Available at https://litfl.com/st-segment-ecg-library/British Heart Foundation Atrial Flutter and Atrial Fibrillation. Available at https://www.bhf.org.uk/informationsupport/heart-matters-magazine/medical/ask-the-experts/atrial-flutterECG Waves The ECG Book. Available at https://ecgwaves.com/course/the-ecg-book/Please remember this podcast and all content from Rhesus Medicine is meant for educational purposes only and should not be used as a guide to diagnose or to treat. Please consult a healthcare professional for medical advice. 

In this episode, I'll give you the inside scoop on amiodarone so you can truly grasp why it is *the* most prescribed antiarrhythmic medication. We'll unpack its unique mechanism of action that makes it so effective, share a real-world case that shows amiodarone in action, as well as have a candid talk about its adverse effects. Join me to find out why after 40 years, this versatile antiarrhythmic still has a prime place in the hospital. The story of amiodarone is a fascinating one - and as nurses, we owe it to our patients to know it!Check out Nicole Kupchik's exam reviews and practice questions at nicolekupchikconsulting.com. Use the promo code UPMYGAME20 to get 20% off all products.Do you need help with your resume, interviewing, or need career coaching? Check out Sarah at New Thing Nurse:Get 15% off of her resume and cover letter templates using the promo code UPMYGAMENursing students and new grad career services Experienced RN career servicesNP career servicesUp My Nursing Game is partnering with VCU Health Continuing Education to offer FREE continuing education credits for registered nurses. Click here to obtain nursing credit.See the show notes at upmynursinggame.com.The key moments in this episode are:00:03:22 - Ventricular Tachycardia 00:05:00 - How Amiodarone Works 00:09:06 - Indications and Dosages 00:11:47 - Adverse Effects 

Welcome to Episode 30 of “The 2 View,” the podcast for EM and urgent care nurse practitioners and physician assistants! Show Notes for Episode 30 of “The 2 View” – oral phenylephrine, visual diagnosis plans, and NSVT. Oral Phenylephrine Myers Z. FDA panel: Many oral allergy meds don't work. WTTV CBS4Indy. Published October 15, 2023. Accessed October 17, 2023. https://cbs4indy.com/news/fda-panel-many-oral-allergy-meds-dont-work/ Neurosyphilis Review Hamill MM, Ghanem KG, Tuddenham S. State of the art review: neurosyphilis. Clin Infect Dis. Published August 18, 2023. Accessed November 1, 2023. doi: 10.1093/cid/ciad437 Visual Diagnosis - Behcet's Disease Behcet's Disease. Vasculitis Foundation. Published July 18, 2012. Accessed October 17, 2023. https://www.vasculitisfoundation.org/education/behcets-disease/ ACEP Clinical Policy on Ischemic Stroke Clinical Policies – Acute Ischemic Stroke. ACEP. Published May 2023. Accessed November 2, 2023. https://www.acep.org/patient-care/clinical-policies/acute-ischemic-stroke The VAN Assessment to Identify Large Vessel Occlusion Strokes. Core EM. Published May 17, 2018. Accessed November 2, 2023. https://coreem.net/journal-reviews/the-van-assessment/ Los Angeles Motor Scale (LAMS). MDCalc. Accessed November 2, 2023. https://www.mdcalc.com/calc/3959/los-angeles-motor-scale-lams Rapid Arterial oCclusion Evaluation (RACE) Scale for Stroke. MDCalc. Accessed November 2, 2023. https://www.mdcalc.com/calc/3941/rapid-arterial-occlusion-evaluation-race-scale-stroke NSVT: Non-Sustained Ventricular Tachycardia Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. Published August 1, 2018. Accessed October 17, 2023. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000549 Farzam K, Tivakaran VS. QT Prolonging Drugs. StatPearls Publishing; 2023. Accessed October 17, 2023. https://www.ncbi.nlm.nih.gov/books/NBK534864/ Foth C, Gangwani MK, Ahmed I, Alvey H. Ventricular Tachycardia. StatPearls Publishing; 2023. Accessed October 17, 2023. https://www.ncbi.nlm.nih.gov/books/NBK532954/ Ep 1 Lady G and Courage Under Fire. Burnt. Published January 27, 2021. Accessed November 2, 2023. https://podcasts.apple.com/us/podcast/ep-1-lady-g-and-courage-under-fire/id1551194920?i=1000506903956 Glaucomflecken. Will and Kristin's Cardiac Arrest Story with Paramedic Lieutenant Aaron Gregg. Published August 22, 2023. Accessed October 17, 2023. https://www.youtube.com/watch?v=CQtYoKPNsrM Laslett DB, Cooper JM, Greenberg RM, et al. Electrolyte Abnormalities in Patients Presenting With Ventricular Arrhythmia (from the LYTE-VT Study). Am J Cardiol. PubMed. NIH: National Library of Medicine: National Center for Biotechnology Information. Published August 15, 2020. Accessed October 17, 2023. https://pubmed.ncbi.nlm.nih.gov/32565090/ Nonsustained ventricular tachycardias. Bmj.com. BMJ Best Practice. Accessed October 25, 2023. https://bestpractice.bmj.com/topics/en-us/831 PVCs and Nonsustained VT: When to Worry? How to Treat? - Penn Physician VideoLink.; 2015. Published January 7, 2015. Accessed October 17, 2023. https://videolink.pennmedicine.org/videos/pvcs-and-nonsustained-vt-when-to-worry-how-to-treat TualatinValleyFire. Dr. Will Flanary - Cardiac Arrest Survivor. Published February 16, 2021. Accessed October 17, 2023. https://www.youtube.com/watch?v=wu9uAwnSrJU Recurring Sources Center for Medical Education. Ccme.org. http://ccme.org The Proceduralist. Theproceduralist.org. http://www.theproceduralist.org The Procedural Pause. Emergency Medicine News. Lww.com. https://journals.lww.com/em-news/blog/theproceduralpause/pages/default.aspx The Skeptics Guide to Emergency Medicine. Thesgem.com. http://www.thesgem.com Trivia Question: Send answers to 2viewcast@gmail.com Be sure to keep tuning in for more great prizes and fun trivia questions! Once you hear the question, please email us your guesses at 2viewcast@gmail.com and tell us who you want to give a shout-out to. Be sure to listen in and see what we have to share!

About this interview: I've let Adam introduce himself - "I was a high profile, Senior Sports Physiotherapist and Head of Medical for professional sports clubs including regional and national Rugby League and at the PGA Golf Tour, Professional Ballet and MOD. I was extremely physically fit and in very good health. Unfortunately, after having the AstraZeneca, Covid vaccine, I became severely unwell and have experienced Pulmonary Embolisms, Ventricular Tachycardia, Severe demyelination of nerves, Myopathy, Dysautonomia, Chronic chest pain to name only a few of my main health problems sustained. My life has been completely destroyed. I can no longer work and have had to move in with my mum. I'm housebound without help and find it extremely difficult to manage on a day to day basis both physically and mentally and have needed a carer. I am speaking out about my experience to raise awareness and hopefully stop this happening to anybody else. I hope people can learn from my experience. I hope one day all the vaccine injured get justice for themselves and their families." Links - Twitter Adam Rowland Twitter GoFundMe Adam Rowland GoFundMe If you value my podcasts, please support the show so that I can continue to speak up by choosing one or both of the following options - ⁠Buy me a coffee⁠ If you want to make a one off donation. Join my Substack To access additional content, you can upgrade to paid from just £3.50 a month To sponsor the Doc Malik Podcast contact us at ⁠hello@docmalik.com⁠  About Doc Malik: Orthopaedic surgeon Ahmad Malik is on a journey of discovery when it comes to health and wellness. Through honest conversations with captivating individuals, Ahmad explores an array of topics that profoundly impact our well-being and health. You can follow us on social media, we are on the following platforms: ⁠Twitter Ahmad⁠ | ⁠Twitter Podcast⁠ | ⁠Instagram Ahmad⁠ | ⁠Instagram Podcast

Commentary by Dr. Edward Gerstenfeld

Commentary by Dr. Valentin Fuster

Commentary by Dr. Usha Tedrow and Dr. Timothy Maher

CardioNerds Co-Founder, Dr. Amit Goyal, along with Series Co-Chairs, Dr. Yoav Karpenshif and Dr. Eunice Dugan, and episode Lead, Dr. Sean Dikdan, had the opportunity to expand their knowledge on the topic of ventricular tachycardia and electrical storm from esteemed faculty expert, Dr. Janice Chyou. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Electrical storm (ES) is a life-threatening arrhythmia syndrome. It is characterized by frequently occurring bouts of unstable cardiac arrythmias. It typically occurs in patients with susceptible substrate, either myocardial scar or a genetic predisposition. The adrenergic input of the sympathetic nervous system can perpetuate arrythmia. In the acute setting, identifying reversible triggers, such as ischemia, electrolyte imbalances, and heart failure, is important. Treatment is complex and varies based on previous treatments received and the presence of intra-cardiac devices. Many options are available to treat ES, including medications, intubation and sedation, procedures and surgeries targeting the autonomic nervous system, and catheter ablation to modulate the myocardial substrate. A multidisciplinary team of cardiologists, intensivists, electrophysiologists, surgeons, and more are necessary to manage this complex disease. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Management of Ventricular Tachycardia and Electrical Storm Electrical storm is defined as 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. It occurs more commonly in ischemic compared to non-ischemic cardiomyopathy, and it is associated with a poor prognosis and high cardiovascular mortality. The classic triad of electrical storm is a trigger, a myocardial susceptible substrate, and autonomic input perpetuating the storm. Triggers for electrical storm include ischemia, heart failure, electrolyte abnormalities, hypoxia, drug-related arrhythmogenicity, and thyrotoxicosis. A thorough evaluation of possible triggers is necessary for each patient, but it is uncommonly found. The evaluation may include laboratory studies, genetic testing, advanced imaging, or invasive testing. Acute treatment options involve acute resuscitation, pharmacotherapy with antiarrhythmics and beta-blockers, device interrogation and possible reprogramming, and sedation. Subacute treatment involves autonomic modulation and catheter ablation. Surgical treatments include sympathectomies and, ultimately, heart transplant. Catheter ablation is safe and effective for the treatment of electrical storm. In select patients, hemodynamic peri-procedural hemodynamic support should be considered. Show notes - Management of Ventricular Tachycardia and Electrical Storm Simple diagram of the classic “triad” of ES (see reference 10). Treatment algorithm provided by the 2017 AHA/ACC/HRS guidelines (see reference 1). 1. Define electrical storm. Electrical storm (ES), also called “arrhythmic storm” or “VT storm” refers to a state of cardiac instability associated with 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. Sustained VT refers to 30 seconds of VT or hemodynamically unstable VT requiring termination in < 30 seconds. Incessant VT refers to continued, sustained hemodynamically stable VT that lasts longer than one hour. VT is incessant or recurrent when it recurs promptly despi...

Holy Defibrillations! Ventricular Tachycardia in AmericaWebsite: http://www.battle4freedom.comNetwork: https://www.mojo50.comStreaming: https://www.rumble.com/c/Battle4FreedomStreaming Live on RUMBLE @ https://rumble.com/v28vn24-holy-defibrillations-ventricular-tachycardia-in-america.htmlhttps://www.dailymail.co.uk/news/article-11730275/John-Fetterman-rushed-hospital-doctors-check-hes-suffered-stroke.htmlhttps://www.dailymail.co.uk/health/article-11727673/Have-caught-stomach-flu-recently-Cases-rising-US.htmlhttps://www.dailymail.co.uk/health/article-11719067/NYC-mayor-Eric-Adams-FINALLY-scraps-Covid-vaccine-mandates-city-workers.htmlhttps://www.dailymail.co.uk/news/article-11729393/Bill-Gates-defends-use-private-jets-claims-not-problem.htmlhttps://www.dailymail.co.uk/news/article-11729383/Connecticut-socialite-walks-free-serving-half-sentence-filming-children-nude.htmlhttps://www.dailymail.co.uk/news/article-11728257/Elderly-rancher-charged-murder-migrant-shooting-spent-two-weeks-bars.htmlhttps://www.dailymail.co.uk/news/article-11730181/College-student-22-thanks-God-chosen-join-Boston-reparations-task-force.htmlhttps://www.dailymail.co.uk/news/article-11719045/New-cartoon-features-black-kids-singing-song-reparations-owes-black-Americans.htmlhttps://www.hopkinsmedicine.org/health/conditions-and-diseases/ventricular-tachycardia#:~:text=Ventricular%20tachycardia%20most%20often%20occurs,Cardiomyopathy%20or%20heart%20failureVentricular tachycardia most often occurs when the heart muscle has been damaged and scar tissue creates abnormal electrical pathways in the ventricles. Causes include:• Heart attack• Cardiomyopathy or heart failure• Myocarditis• Heart valve diseaseWhat are the symptoms of ventricular tachycardia?When ventricular tachycardia lasts a short time, there may be no symptoms except palpitations — a fluttering in the chest. But ventricular tachycardia lasting more than 30 seconds may cause more severe symptoms:• Chest pain• Dizziness• Fainting• Shortness of breath• Cardiac arresthttps://www.dailymail.co.uk/news/article-11728355/Roar-order-Leopard-mauls-five-people-straying-Indian-courthouse.htmlhttps://www.dailymail.co.uk/news/article-11728625/Larry-Elder-says-likely-hes-going-run-President-2024.html

Dr. Ed Group joined us from Global Healing Center to talk about colon health, healing the body through detoxification and much more! Dr. Group is the author of such books as Health Begins in the Colon, The Green Body Cleanse: How to Live Green & Live Well! as well as his ever popular book entitled Complete Colon Cleanse: The At-Home Detox Program to Restore Good Health, Boost Vitality, and Ensure Longevity. We were honored to have him back on the show today. We did a show with Dr. Group about four years ago which you can listen to by clicking here. We have to have Dr. Group on more often, not only does he have amazing products but he's a wealth of information. In today's show with Dr. Ed Group we talked about colon health and how gut health really is the first place to clean up if you want to make big progress in your health. The gut controls everything. The old saying is true..."All disease begins in the gut" LISTENER QUESTIONS ------------------------ (LIPOMAS) Hi Justin, Can you please ask Dr. Group his opinion on the cause and then the treatment (if any) for multiple lipomas in men? I had my first lipoma when I was in my early teens and then developed more in my late 20s and now I have even more in my late 30s. I would love to know his thoughts. Most doctors just say these are hereditary and happen for an unknown reason. Some research has implicated a genetic defect in cell multiplication. But why does this defect happen later in life and what could be the trigger? Some other doctors think they have to do with toxins. That the body is sequestering toxins in the fat cells and the cells are multiplying to hold ever more toxins. I believe that many more people develop Lipomas than is acknowledged. They just have smaller and fewer ones and so don't have an issue with them. Thanks for asking! Lawrence Baltimore, MD ------------------------ (HEART PALPITATIONS) I am 65 years old with Diabetes, which I take insulin for. That is the only medication I take, but I do take multiple supplements in Dr. Group's Iodine. I was diagnosed several years ago with Ventricular Tachycardia and my heart kicks in to over 200 beats per minute heart rate and all different times of the day about every 6 weeks. The only options given were drugs, which I will not do or an ablation, which seems counter intuitive as I have researched, and found it only works a certain percentage of the time. That said, these episodes last anywhere from 1-10 hours and the only way I get them to stop is through vomiting and sometimes it has to be multiple times before my heart settles back in to normal rhythms. I believe I am missing something in my diet, have tried numerous things, but so far, no success. These episodes are getting increasingly hard to endure and I am concerned that this is putting enormous stress on my heart and blood vessels. I realize this is probably more of a complex situation than can be handled in a forum such as this, but I would be grateful for any help or direction you can give me. Sincerely, Tom P -------------------------- (NO THYROID) I do have a question for Dr. Group (who I love by the way!) I would like to know how iodine works and plays a part with someone who no longs has a thyroid. I also would like to know a good dose since I don't have a thyroid. Thank you so much! I have wanted to ask him that for over a year!! #happyhealing Lisa W. -------------------------- (COLON HEALTH) Dr. Ed Group: Is the oxy powder good for a peristalsis problem? Half the time I eliminate only after two days which I know isn't normal. I consume several cups of organic vegies/juices/day and stay off sugar and most grains. Thanks. Katie ------------------------ (BONE LOSS) My main health concerns right now are bone loss Especially Jaw Bones how to cure or increase bone mass. Frank ----------------- (PSORIASIS) Hi guys,

The most concerning type of syncope!  When a patient suddenly passes out from either an arrhythmia or a structural abnormality of the heart... this needs to be investigated and treated... next time they might not wake up from it!If you love learning from other people's mistakes, you will love this episode of when I didn't realize my patient was in V-tach and walked him back to his room!We discuss all of the reasons the heart might cause you to pass out and a little about the challenges of being an ER Triage Nurse in this final episode of the year and the last episode in a 4 part series on syncope.  So make sure you also check out episode #32, #33, and #34 to learn seizure vs syncope, reflex syncope, and orthostatic syncope. If you would like to check out the 1hr, 1 CE course, go to:www.rapidresponseandrescue.comyou can use coupon code: PODCAST22To get $22 off the cost of the course now until the end of 2022

This week we enter the world of cardiogenetics and electrophysiology when we review the topic of catecholaminergic polymorphic ventricular tachycardia (CPVT). Is there a 'best' beta blocker for the treatment of this condition? Why is one better than others? How should one manage the patient who is intolerant of beta blockade but needs it for prevention of arrhythmia? What is the role of flecainide, sympathectomy or even ICD's for these patients? PhD candidate and physician Dr. Puck Peltenburg and CPVT world authority, Dr. Christian van der Werf (both of University of Amsterdam) share their deep insights this week. doi: 10.1161/CIRCULATIONAHA.121.056018. Epub 2021 Dec 7

Ventricular Tachycardia Database Development and Detection Guest: Michele Pelter, R.N., Ph.D. Hosts: Anthony H. Kashou, M.D. (@anthonykashoumd) Joining us today to discuss Ventricular Tachycardia Database Development and Detection designed to improve hospital-based ECG monitoring is Michele Pelter, R.N., Ph.D., associate professor in the School of Nursing at the University of California San Francisco. Her current work has focused on improving the detection of transient myocardial ischemia and most recently understanding false ECG alarms that might contribute to alarm fatigue in nurses. Specific topics discussed: Why is identifying ventricular tachycardia during hospital-based ECG monitoring a problem? Why is ventricular tachycardia the focus? What are some algorithm deficiencies? How might the annotated ventricular tachycardia database help improve the problem of false ventricular tachycardia alarms? Other projects that Dr. Pelter is working on related to hospital-based ECG monitoring. Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. Facebook: MayoCVservices LinkedIn: Mayo Clinic Cardiovascular Services NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.

Commentary by Dr. Valentin Fuster

The post Episode 78. Management of Ventricular Tachycardia in the ED by LANCE RAY, PHARMD, BCPS appeared first on The Pharm So Hard Podcast.

Case report of a life-threatening cardiac arrhythmia following the use of hemp oil and the addition of the supplement berberine. Herbal supplements can have serious adverse side effects on their own or if combined with other supplements or medications.

My guest for this episode is Dr. Ashkan Ehdaie, an Electrophysiologist at Cedars-Sinai Medical Center in Los Angeles. Dr. Ehdaie is currently an Assistant Professor of Cardiology and Associate Director of the Clinical Cardiac Electrophysiology Fellowship Training Program.I interview Dr. Ehdaie about the different types of Vtach, the risks and outcomes associated with treating each type, and we dig into some of the protocols used for various scenarios where Vtach requires treatment, both medically and surgically. All Things Afib is hosted by me, Dr. Armin Kiankhooy. As a board-certified cardiothoracic surgeon, my focus is on advanced treatments for heart and lung failure and minimally-invasive surgical treatments for atrial fibrillation such as the Hybrid Maze procedure. You can find me on staff at Adventist Health Heart and Vascular Institute in St. Helena California. Discussion points:How is Vtach different from supraventricular tachycardia?What are the different types of Vtach?What is the conversation when a patient is diagnosed with Idiopathic Vtach?Where is the threshold between treating with meds or ablation?Why does malignant Vtach occur?Monomorphic vs. polymorphicThe medications that can cause polymorphic VtachPatient follow up procedures and the LifeVestWe do imaging for Afib at a certain time post-procedure, when do you do it for Vtach?What is the success rate when treating with ablation?How much Vtach is too much?A study focusing on reviving tissue, instead of destroying it with ablationWhat else should our listeners know? “That Vtach is not one-dimensional, it has many presentations and complications.” Resources:Dr. Ashkan Ehdaie Cedars-SinaiDr. Ashkan Ehdaie LinkedInDr. Kiankhooy LinkedInAll Things AFib Website All Things AFib TwitterAll Things AFib YouTube Channel

Commentary by Drs. Kalyanam Shivkumar and Sumeet S. Chugh

Commentary by Dr. Valentin Fuster

When was the last time you had your blood pressure checked? Do you know what your resting heart rate is? If you're exercising to lose weight or change the way you look, there are some important health markers you can use to track your progress instead. On this episode, Dr Sarah explains why you should keep an eye on your blood pressure and your heart rate. The information in this podcast is for general use, always consult your doctor or physiotherapist before undertaking a new exercise program. Contact us:womenlikeyoupodcast@gmail.com   WLY resources and recommendations: Australian guidelines to reduce health risks from drinking alcohol https://www.nhmrc.gov.au/health-advice/alcohol  CVD checkhttp://www.cvdcheck.org.au/calculator Influence of Physical Activity on Hypertension and Cardiac Structure and Function https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4624627/#R6 Physical Activity and the Prevention of Hypertensionhttps://pubmed.ncbi.nlm.nih.gov/24052212/ Target Heart Rate and Estimated Maximum Heart Ratehttps://www.cdc.gov/physicalactivity/basics/measuring/heartrate.htm WLY newsletter subscription  The Women Like You podcast is recorded on the lands of the Gadigal people of the Eora nation. We pay our respects to elders past, present and emerging. We acknowledge Aboriginal and Torres Strait Islander peoples as the First Australians and Traditional Custodians of the land where we live, work, and exercise. See omnystudio.com/listener for privacy information.

Jimmy and Charles met when they were 18 and 19 years old, just a few years after Charles had been diagnosed with idiopathic ventricular tachycardia (IVT). At 13 he underwent surgery to implant a pacemaker, which regulates his heart rate during IVT episodes when his heart beats chaotically. Charles was […]

With Christian van der Werf, Amsterdam University Medical Center - Netherlands & Pier Lambiase, University College London, London - United Kingdom. Link to paper Link to editorial

The most common wide-complex tachycardia, VTach is a must-know for the IM Shelf Exam and wards. Come learn how to pick up this diagnosis on an EKG, and learn how the management of VTach changes based on patient presentation...oh, and some of the many side effects of amiodarone. 

Welcome back to our weekend Cabral HouseCall shows! This is where we answer our community's wellness, weight loss, and anti-aging questions to help people get back on track! Check out today's questions:  Julie: Hi Dr Cabral, my daughter (18) was diagnosed with Mono just before basketball playoffs in 2020. To help her with her energy levels during that time she was given a b12 injection before each game. Within a month or so she developed severe acne after never having skin issues of any kind so we feel certain it is injection related. Do you have any suggestions for clearing this type of acne. It is severe and beginning to scar her face. Thank you for your help! Julie Thomas: Hi Dr. Cabral, I recently completed the 21 day detox, and I am also in the process of achieving level one and level two IHP certification. I truly enjoy your passion and ability to teach all the material in an effective, engaging, and enjoyable way!  I wear an Oura ring to track sleep and other variables such as HRV. On day two of the 21 day detox, I noticed an obvious and significant increase in my HRV that lasted for the entirety of the 21 day period. Following the completion of the detox, I noticed my HRV settled back into my normal/pre-detox levels. The magnitude of the HRV change was roughly 20ms. My question is - To which component of the detox would you attribute the favorable increase in heart rate variability? I assume it's one or more of the ingredients in either the FM or AYU detox, but I would really appreciate any insight you can offer. Would it be recommended to use a supplement to increase HRV on a regular basis, or is it just better to focus on a holistic approach to maximize PNS activation? Thank you! Tom Savita: Hi Dr. Cabral, I'm very grateful for you and your podcast! I was wondering, what are your thoughts on the COVID-19 Vaccine. Thank you. Savita Victoria: Hi Cabral! I just learned that my 5 year old niece has a heart murmur. Do you have any recommendations she should follow for this? Currently and also growing up in effort to eventually grow out of it ? Thank you! Bethany: Hi Dr. Cabral - love your podcast and appreciate what you do for all of us. I have a question regarding my 17 year old daughter. She has recently been diagnosed with Aortic Ventricular Tachycardia and arrhythmia. My question is... can this be caused by Hashimoto's, which she has also recently been diagnosed with - her thyroid antibodies are off the chart. Additionally, any words or advice you can give regarding treatment for this to help ease our anxiety would be appreciated. It's obviously scary for us parents when anything health related is happening with our children. Thank you! Aaron: Hi Dr. Cabral! Thanks for sharing your knowledge with these podcasts. Would you discuss the difference between Vitamin D3 absorption and utilization? I have listened to a TON of your podcasts, and relistened to all the Vit D topics. You mention needing cofactors like Vit K, Mg, etc. I use 2 scoops of DNS in almond milk each morning with my 6 drops Vit D3, take Histpro, B-complex, and 1Mg at lunch, and balanced zinc with Mg at dinner. My Vit D levels with PCP won't go much above 33. (I had gone from 5 drops to 7 with no change, so settled in on roughly 35units/lbs.) I have heard others say oil based capsules are better than drops for accurate dosing. Do you recommend drops because there is some level of sublingual capillary absorption? If so, do I need to take the DNS a couple hours before Vit D so the cofactors are already in my system, ready to work? Are the cofactors primarily for absorption of Vit D into the body, or primarily for conversion of Vit D for use in the body? This question is getting long, and I hope you understand what I'm asking. Thanks again for getting deep on bio-regulatory medicine! Thank you for tuning into today's Cabral HouseCall and be sure to check back tomorrow where we answer more of our community's questions!  - - - Show Notes & Resources: http://StephenCabral.com/1989 - - - Get Your Question Answered: http://StephenCabral.com/askcabral   - - - Dr. Cabral's New Book, The Rain Barrel Effect https://amzn.to/2H0W7Ge - - - Join the Community & Get Your Questions Answered: http://CabralSupportGroup.com - - -  Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Stress, Sleep & Hormones Test (Run your adrenal & hormone levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - > View all Functional Medicine lab tests (View all Functional Medicine lab tests you can do right at home for you and your

From #CodaZero Live, David Carr chats with Sara Gray about treating recurrent ventricular tachycardia. A 50-year-old male arrives in the emergency room with chest pain. Upon examination, it is clear that he is experiencing recurrent episodes of V-tach. Defibrillation isn't working, so what happens next? Treating recurrent ventricular tachycardia with Dr Sara Gray. For more head to: codachange.org/podcasts

In this episode, Dr Saad Fyyaz discusses key points from a recent case report published in EHJ – Case Reports.

Commentary by Dr. Valentin Fuster

Heart disease comes in many variants...My name is DeeDee Blue and in my case I have been diagnosed with Cardiomyapothy, Congestive Heart Failure, Ventricular Tachycardia and because of these diagnoses I also have an implantable device attached to my heart called a Defibrillator (an apparatus used to control heart fibrillation by application of an electric current to the chest wall or heart). I decided to share part of my story of livng with heart disease and how it has affected my life! My prayers through this video is to inspire others who may feel discouraged about being diagnosed with any form of the disease and to induce thoughts of implementing preventative measures in order to maintain a healthy heart function for those not diagnosed! Please like share and comment! *DISCLAIMER* I am not a medical professional and in no way am I experienced to diagnose or offer suggestion on medical direction..Please consult a physician! #respectyourhealth​ #GODBLESS

mayoclinic.org

In this episode I visit with Dr. Melissa Robinson from the University of Washington to discuss the management of ventricular tachycardia. Our discussion focuses on decisions regarding ICD implantation, anti-arrhythmic drugs and catheter ablation. Through 3 cases that highlight the heterogeneity of VT, we talk about the nuances of these decisions. Links to articles referenced: … Continue reading Ventricular Tachycardia – Dr. Melissa Robinson →

Commentary by Dr. Valentin Fuster

Ventricular tachycardia, particularly in the setting of heart failure, can be frightening. Recent research has provided better mapping techniques and tools to improve the treatment of ventricular tachycardia. Dr. Anter describes the multidisciplinary approach to treatment of ventricular tachycardia at Cleveland Clinic.

Dr. Anter talks about his experience working with Dr. Mark Josephson, a pioneer in the field of electrophysiology. He describes the challenges of ventricular tachycardia ablation, particularly in the setting of heart failure, current research addressing these challenges, and his vision for ventricular tachycardia care in the future.

Join cardiology fellow Dr. Amar Parikh and faculty discussant Dr. Jay Montgomery as they review the approach to the management of ventricular tachycardia!

Humble Howard and his Ventricular Tachycardia, plus the US hospital experience / The miracle of travel insurance and The Chambers Plan / Fred calls in from Mexico / Amanda is Guest Fred / Dan Duran weather live / The Emergency Zamboni Goalie haunting Leafs fans forever.

Commentary by Dr. Valentin Fuster

With Pier Lambiase & Sherry Honarbakhsh, Barts Health NHS Trust, London - UK Paper link Editorial link

This week we review pearls from the EEMCrit conference back in January 2018. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_138_0_Final_Cut.m4a Download Leave a Comment Tags: BRASH, Hyperkalemia, TTP, Ventricular Tachycardia, VTach Show Notes Show Notes Core EM: Procainamide vs Amiodarone in Stable Wide QRS Tachydysrhythmias (PROCAMIO) PulmCrit: Myth-Buesting: Lactated Ringers is Safe in Hyperkalemia, and Is Superior to NS PulmCrit: BRASH Syndrome Read More

This week we review pearls from the EEMCrit conference back in January 2018. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_138_0_Final_Cut.m4a Download Leave a Comment Tags: BRASH, Hyperkalemia, TTP, Ventricular Tachycardia, VTach Show Notes Show Notes Core EM: Procainamide vs Amiodarone in Stable Wide QRS Tachydysrhythmias (PROCAMIO) PulmCrit: Myth-Buesting: Lactated Ringers is Safe in Hyperkalemia, and Is Superior to NS PulmCrit: BRASH Syndrome Read More

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.  

Dr. 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 for the latest journal articles in the field.                                                 The first article in this month's issue is by Yoav Michowitz and Associates who examine the morphological ECG characteristics of left posterior fascicular ventricular tachycardia and differentiated from right bundle branch block and left anterior hemiblock aberrancy. 183 ECGs with left posterior fascicular ventricular tachycardia in patients who underwent ablation were identified using a systematic Medline search were examined and compared to 61 ECGs with right bundle branch block in left anterior hemiblock aberrancy with no obvious cardiac pathology by echocardiography.                                                 Using four variables including atypical right bundle branch block like V1 morphology, positive QRS in aVR, V6R greater than S ratio of less than one and QRS less than or equal to 140 ms, a prediction model was developed that predicted posterior fascicular ventricular tachycardia with a sensitivity of 82% and a specificity of 78%. Patients with three out of four positive variables had a high probability of having left posterior fascicular ventricular tachycardia whereas patients with less than or equal to one positive variable always had right bundle branch block plus left anterior hemiblock.                                                 In the next article, Anna Thøgersen and associates describe a case series of 10 patients in whom implantable cardioverter defibrillators failed to treat ventricular tachyarrhythmias. The authors examine whether consensus derive generic rate threshold cutoffs between 185 and 200 beats per minute were employed in this case series. In nine patients, ventricular fibrillation did not satisfy program detection criteria. Five patients died with untreated ventricular fibrillation, four had cardiac arrest requiring external shocks and one was rescued by a delayed ICD shock. Seven of these patients had slowest detection rates that were consistent with generic recommendations but not tested in a peer review trial for their manufacturer’s ICDs.                                                 In the reported cases, manufacturer specific factors interacted with fast detection rates to withhold therapy including strict ventricular fibrillation episode termination rules, enhancements to minimize T-wave over sensing and features that restrict therapy to regularly rhythms in VT zones. Untreated ventricular fibrillation despite recommended programming accounted for 56% of the deaths and 11% of all of deaths. The authors concluded that complex and unanticipated interactions between manufacturer specific features and generic programming can prevent therapy for ventricular fibrillation.                                                 In the next article, Miguel Rodrigo and associates describe from 17 simulations of atrial fibrillation, atrial flutter and focal atrial tachycardia the ability to understand signal processing that can affect identification of reentrant activity using electrograms, body surface potential mapping and electrocardiographic imaging ECGI phase maps. Reentrant activity was identified by singularity point recognition and raw signals and in signals after narrow band pass filtering at the highest dominant frequency.                                                 Reentrant activity was identified without filtering in 60% of unipolar records but filtering was required to increase reentrant activity detection from 1% to 62% in bipolar recordings. The filtering resulted in residual false reentrant activity in about 30% of bipolar recordings. The authors concluded that rotor identification is accurate and sensitive and does not require additional signal processing in measured or noninvasively computed unipolar electrograms while bipolar electrograms and body surface potential mapping do require highest dominant frequency filtering in order to detect rotors at the expense of a decrease specificity.                                                 In the next article, Raymond Yee and associates examine the ability of a new automated antitachycardia pacing algorithm to reduce ICD shocks. The new automated ATP algorithm was based on electrophysiologic first principles and prescribed the ATP sequences in real time using the same settings for all patients. In 144 patients who had dual chamber or CRT ICDs as well as a history of one or more ICD treated VT or VF episodes or a recorded sustained monomorphic ventricular tachycardia episode. Detection was sent to ventricular fibrillation interval detection of 24 out of 32 ventricular tachycardia interval detection of 16 or greater in a fast VT zone of 242 to 320 ms.                                                 There were 1,626 treated episodes in 49 patients over 14.5 month’s follow up. Data logs permitted adjudication of 702 episodes including 669 sustained monomorphic ventricular tachycardia episodes, 20 polymorphic ventricular tachycardia episodes, 10 SVT episodes and three mal sensing episodes. The novel automated antitachycardia pacing algorithm terminated 39 out of 69 episodes or adjusted 59% of the sustained monomorphic ventricular tachycardia events in the fast VT zone, but 509 out of 590 or 85% adjusted in the VT zone and 6 out of 10 in the VF zone. No SVTs were converted to VT or VF and no anomalous ATP behavior was observed. The authors concluded that this new automated ATP algorithm could be used safely in all zones without need for individualized programming.                                                 In the next study Pablo Ávila and associates studied the incidence and clinical predictors of atrial tachycardias in adults in a cohort of 3,311 patients with congenital heart disease. Prospectively followed in a tertiary center for 37,607 person years. The study patients were divided into three categories; 49% simple, 39% moderate and 12% complex congenital heart disease. In this cohort, 153 or 4.6% of patients presented with atrial tachycardia. The atrial tachycardia burden was highest in complex congenital heart disease such as single ventricle 22.8% or D-TGA 22.1%.                                                 The authors found that univentricular physiology, previous intracardiac repair, systemic right ventricle, pulmonary hypertension, pulmonary regurgitation, pulmonary AV valve regurgitation and pulmonary and systemic ventricular dysfunction were independent risk factors for developing atrial tachycardia. At the age of 40 years, atrial tachycardia free survival in patients with zero risk factors was 100%. With one risk factor, it was 94%. With two risk factors was 76% and three or more risk factors was 50%. These authors confirm these findings in a validation cohort.                                                 In the next article, Khidir Dalouk and associates compare clinical outcomes between ICD patients followed up in a telemedicine videoconferencing clinic and a conventional in person clinic. In this retrospective study, the authors compared time to first appropriate ICD therapy, time to first inappropriate ICD therapy, time to first shock and overall survival. The authors studied 287 patients in the telemedicine videoconferencing clinic group and 236 patients in the conventional in person clinic over mean follow-up duration of 4.8 years. The authors found that telemedicine videoconferencing clinic was not inferior to in person follow-up for the pre-specified outcomes.                                                 In the next article, Elisabeth Mouws and associates studied the epicardial breakthrough waves in sinus rhythm possibly giving insight to the arrhythmogenic substrate in atrial fibrillation. In 381 patients with ischemic or valvular heart disease, intraoperative epicardial mapping with intro electro distance of 2 mm was performed of the right atrium, Bachmann’s bundle, the left atrioventricular groove and the pulmonary vein area. Epicardial breakthrough waves were referred to as sinus node breakthrough waves if they were the earliest right atrial activated site. A total of 218 epicardial breakthrough waves and 57 sinus node breakthrough waves were observed in 168 patients or 44%.                                                 Epicardial breakthrough waves mostly occurred at the right atrium and 48% at the left atrioventricular groove and 31% followed by Bachmann’s bundle and 12% and the pulmonary vein area and 9%. Epicardial breakthrough waves occurred most often in ischemic heart disease patients 49% to valvular patient's 17%. Epicardial breakthrough wave electrograms most often consisted of double or fractionated electrograms seen in 63%. Fractionated epicardial breakthrough wave potentials were more often observed at the right atrium or Bachmann's bundle. The authors concluded that epicardial breakthrough waves are present in over a third of patients possibly indicating muscular connections between the endocardium and epicardium that may enhance the occurrence of epicardial breakthrough waves during atrial fibrillation promoting AF persistence.                                                 In the next article, Shouvik Haldar and associates compare horizontal and vertical orientation bipolar electrograms with novel omnipolar peak to peak voltages in sinus rhythm and atrial fibrillation using a high density fixed multi-electrode plaque placed on the epicardial surface of the left atrium in dogs. Bipolar orientation had significant impact on bipolar electrogram voltages obtained either in sinus rhythm or atrial fibrillation. Omnipole Vmax values were 99.9% larger than both horizontal or vertical electrograms in sinus rhythm in larger than horizontal or vertical electrograms in atrial fibrillation.                                                 Further vector analysis of omnipole electrograms showed that omnipolar electrograms can record electronic voltage unaffected by collision and fractionation. The authors concluded that omnipolar electrograms can attract maximal voltages from AF signals which are not influenced by directional factors, collision or fractionation compared to contemporary bipolar techniques.                                                 In our final article for the month, Pauline Quenin and associates examine the efficacy of screening in relatives of subjects who died suddenly. The authors provided clinical screening to 64 families who experienced unexplained sudden cardiac death before age 45 in a prospective multicenter registry. The diagnosis was established in 16 families, 25% including Brugada syndrome, long QT syndromes, dilated cardiomyopathy and hypertrophic cardiomyopathy. The diagnostic yield was mainly dependent on a number of screen relatives with 3.8 screen relatives in the diagnosed family versus 2.0 in the non-diagnosed families rising to 40% with at least three relatives.                                                 It additionally increased from 9% to 41% when both parents were screened. Diagnostic performance was also dependent on the exhaustiveness of the screening. 70% of complete screening versus 25% with incomplete screening with 17 Brugada syndrome and 15 long QT syndrome diagnoses based on pharmacologic tests. The authors concluded that even without autopsy, familial screening after sudden death in young patients is effective greatly increasing the likelihood of diagnosis in families.                                                 That's it for this month but keep listening. Suraj Kapa will be surveying all journals for the latest articles on topics of interest in our field. Remember to download the podcast On the Beat. Take it away Suraj. Suraj Kapa:                          Thank you Paul. It is my pleasure to welcome everybody back to our continued series of On the Beat articles from across the electrophysiology literature especially selected to highlight their potential importance in terms of either current or future practice within the realm of cardiac electrophysiology. Again, my name is Suraj Kapa and it is my pleasure to walk us through a variety of hard-hitting articles.                                                 Today we’ll be starting within the realm of atrial fibrillation specifically as it relates to cardiac mapping and ablation. The first article was by Iwasawa et al entitled Temperature Controlled Radiofrequency Ablation for Pulmonary Vein Isolation in Patients with Atrial Fibrillation published in volume 70 of the Journal of the American College of Cardiology. In this article, Iwasawa and colleagues discuss the role of novel temperature controlled irrigated ablation catheter to attempt to obtain deeper transmural lesions in cardiac tissue, specifically they tested the utility of a diamond embedded tip for rapid cooling accompanying six surface thermocouples to better reflect tissue temperature.                                                 They demonstrated in this first in human series that a temperature controlled irrigated ablation could produce rapid, efficient and durable PV isolation. The importance of this particular article lies in the continued development of novel tools that can achieve pulmonary vein isolation either more safely or more quickly. This was highlighted in the article by Iwasawa et al when they demonstrated that the mean radiofrequency application duration was significantly less by almost a factor of three and those using the novel radiofrequency ablation catheter versus those with older models.                                                 They also noted that there was lower acute dormant pulmonary vein re-conduction rates and patients tend to have more frequent durable isolation when remapped after ablation. While the study group only consisted of 35 patients within the treatment group and 35 patients within the control group, the potential of these novel catheters to achieve aims of both shortening procedure duration as well as improving procedure and success need to be taken in consideration.                                                 The next article is by Dr. Gopinathannair entitled Atrial Tachycardia after Surgical Atrial Fibrillation Ablation Clinical Characteristics, Electrophysiological Mechanisms and Ablation Outcomes from a large multicenter study published in the August 2017 issue of JACC Clinical Electrophysiology. In this article, Dr. Gopinathannair reviews the outcomes of cardiac mapping and ablation targeted atrial tachycardias occurring after surgical atrial fibrillation ablation. They reviewed a large number of patients nearly 137 undergoing catheter ablation for symptomatic postsurgical atrial fibrillation ablation atrial tachyarrhythmias across three high volume institutions in the United States.                                                 They demonstrated that the vast majority had a left atrial origin though up to a third also had a right atrial origin further atrial tachyarrhythmias. The predominant circuits noted were cavotricuspid isthmus but also frequently perimitral roof and left or right pulmonary veins. In addition, most of the patients namely 93% had at least one pulmonary vein reconnection requiring re-isolation. The key point with the article however were the outcomes. They demonstrated that acute termination inducibility could be achieved in as many as 97% of right atrial and 93% of left atrial tachyarrhythmias in the setting of prior surgical ablation.                                                 Furthermore, 12 month followup demonstrated an 80% success rate. Traditionally, surgical atrial fibrillation ablation is seen as a complex procedure with the remapping of arrhythmias requiring a lot more complexity. However, these findings cross a large group of patients suggesting that we can have a high rate of success should propose to individuals that perhaps targeted ablation at these postsurgical atrial tachyarrhythmias should be amenable towards ablation especially at high volume complex ablation centers.                                                 Next will discuss the article by Pathik et al entitled Epicardial-Endocardial Breakthroughs through Stable Macroreentry: Evidence from ultra-high-resolution three-dimensional mapping published in Heart Rhythm in August 2017. In this article, the group of Pathik et al decided to review whether epicardial-endocardial breakthrough could be discerned during stable right atrial macroreentry using high density and high spatial resolution three-dimensional mapping. Twenty-six patients were studied and they noted that up to 14 patients had evidence of epicardial-endocardial breakthrough. Using systematic entrainment confirmation, stable atrial macroreentry with epicardial-endocardial breakthrough was consistently demonstrated.                                                 The principle of epicardial-endocardial breakthrough or dissociation is critically important during cardiac mapping. While widely accepted for ventricular mapping, the tradition because of lack of available tools and atrial mapping has suggested that endocardial only mapping should reveal the entire cardiac circuits. Advances in signal processing as well as cardiac mapping techniques and technologies has allowed for better discernment of potentially deeper manifestations of cardiac tissue involvement in cardiac arrhythmias. As been well recognized that there can be significant epicardial and endocardial dissociation in cases of persistent atrial fibrillation.                                                 The article by Pathik et al is important in that it highlights that such events can manifest themselves even in the setting of relatively organized or stable atrial macroreentry. Part of the reason this becomes so critical is that when we consider endocardial only remapping and rely on these signals alone, we may run into situations where we miss a significant chamber of atrial tissue namely the epicardium, thus the focus of this article and the consideration of it in the clinician's repertoire of cardiac mapping and ablation should lie in an understanding of the fact that the entire story of an electrical circuits may not be told by traditional endocardial mapping alone without consideration for epicardial-endocardial breakthrough.                                                 The next article we will focus on is by Dr. Chun et al regarding the impact of cryoballoon versus radiofrequency ablation for paroxysmal atrial fibrillation on healthcare utilization and costs and economic analysis. This was from the FIRE and ICE Trial published in the Journal of the American Heart Association this past month. In this study they sought to assess payer cost following cryoballoon or radiofrequency catheter ablation for paroxysmal atrial fibrillation. They demonstrated that there are cost savings of as much as $355,000 related to the use of cryoballoon over traditional radiofrequency catheter ablation. This reduction in resource use and payer costs was consistent across three different national healthcare systems.                                                 Furthermore, the reason for the reduced cost was primarily attributable to fewer repeat ablations and a reduction in cardiovascular rehospitalizations with cryoballoon ablation. In this era of cost reduction, it is important to consider the potential implications of use of novel technologies in terms of procedural costs. The ability to identify novel techniques that can actually both reduce costs and either achieve equal or improved outcomes needs to be strongly considered. While the three national healthcare systems reviewed here might not reflect all healthcare systems or all insurance needs, it still brings up an important economic consideration that all novel technology may not necessarily result in increased costs, and utilization must be considered both in the context of the particular system as well as the particular provider.                                                 Changing pace, we’ll move on with an atrial fibrillation to the role of anticoagulation. The first major article recently published is by Pollack et al regarding the use of Idarucizumab for dabigatran Reversal, the full cohort analysis published the New England Journal of Medicine. Idarucizumab is a monoclonal antibody fragments developed to reverse the anticoagulant effect with dabigatran and represents the first reversal agent available for reversal of any of the novel oral anticoagulant drugs. In this study which is both multicenter, prospective and open label, patients were enrolled to undergo treatment with this reversal agents.                                                 A total 503 patients were included and the median maximum percentage reversal dabigatran was 100% which was measured using the diluted thrombin time or the ecarin clotting time. In those with active bleeding, the median time to cessation of bleeding was around 2.5 hours. Furthermore, in a surgical cohorts who underwent reversal in order to accommodate them going to surgery, the time to initiation of an intended procedures was 1.6 hours with periprocedural hemostasis assessed as normal in 93%, mildly abnormal in 5% and moderately abnormal in 1.5%. Thrombotic events occurred in about 6.3% of patients undergoing reversal because of active bleeding and then 7.4% undergoing reversal for surgical accommodation.                                                 Mortality rates were around 18% to 19%. Thus it was demonstrated that in emergency situations Idarucizumab can rapidly, durably and safely reverse the anticoagulant effect of dabigatran. However, it is important to note that there was a signal for thrombotic events and consideration of the risk of rapid reversal of anticoagulation regardless of the type of anticoagulation in combination with the actual need for reversal should be considered in the patient context.                                                 The next article we will review is by Jackevicius et al entitled Early Non-persistence with Dabigatran and Rivaroxaban in Patients with Atrial Fibrillation, published in Heart this past month. In this article, the group reviewed how patients manage being on their novel oral anticoagulants over the course of time after initial diagnosis and prescription. One of the concerns regarding novel oral anticoagulants is given the fact that there is no actual tracking or no actual measurements needed to ensure continued adherence to the drug, whether or not there will be higher rates of nonpersistence with use of these novel oral anticoagulants.                                                 Amongst 15,857 dabigatran users and 10,119 rivaroxaban users, they noted that at six months about a third of patients were nonpersistent with either drug. In those patients who were nonpersistent with use of the drug, the combined endpoint of stroke, TIA and death was significantly higher with hazard ratios of 1.76 in the dabigatran cohort and 1.89 in the rivaroxaban cohort. Furthermore, the risk of stroke or TIA was markedly higher in nonpersistent patients with about a hazard ratio of 3.75 in dabigatran nonpersistence and 6.25 in rivaroxaban nonpersistence.                                                 Given these relatively high rates of nonpersistence in clinical practice and the negative outcomes associated with nonpersistence, this highlights the importance of continued validation of the need for persistence with use of oral anticoagulation in patients prescribed these perceived to be at high risk of stroke associate with atrial fibrillation. In an era of improving drug use or improving drugs that can be used without the need for blood testing, it must also be considered that these drugs may be more easily stopped on the patient's own discretion without any knowledge from a provider as there is no active blood test associated. Thus this further highlights the importance of continued discussion between patients and physicians over the course of therapy and care regarding the need for continuation.                                                 Changing paces. We review the article by Godier et al entitled Predictors of Pre-procedural Concentrations of Direct Oral Anticoagulants a prospective multicenter study published at the European Heart Journal. We all know that one of the major issue with a direct oral anticoagulants is that these patients frequently undergo elective invasive procedures and in this setting the management can be very challenging specifically as it relates to when the direct oral anticoagulants should and can be safely stopped.                                                 In clinical practice, there is wide variability in the timing by which providers inform patients to stop these new oral anticoagulants prior to invasive procedure. In this prospective multicenter study, 422 patients were evaluated with preprocedural DOAC concentrations and routine hemostasis assays performed to determine those patients who achieved a minimal preprocedural concentration based on the timing of their discontinuation of the drug. They ranged the duration of discontinuation of the oral anticoagulant from 1 to 218 hours. They noted after a 49 to 72 hour discontinuation period, 95% of the concentration of the direct oral anticoagulants in patients had levels that were significantly low suggesting safety and proceeding with any sort of invasive procedure.                                                 Thus a 72 hour discontinuation period predicted sufficiently low concentrations of DOACs with 91% specificity. In multivariable analyses, duration of the DOAC discontinuation with creatinine clearances and antiarrhythmics were independent predictors of a minimal preprocedural DOAC concentration, namely better renal function, longer duration of DOAC discontinuation and interestingly the use of antiarrhythmic drugs were all associated with lower DOAC concentrations. The conclusion from this article was a last DOAC intake of three days before a procedure resulted in a minimal preprocedural anticoagulant effect for almost all patients considered.                                                 The exception would be in moderate renal impairment especially in dabigatran treated patients and antiarrhythmics in anti-Xa-treated patients could result in the need for longer DOAC interruption. Thus, the key things here to note are that antiarrhythmics can result in the need for longer DOAC interruption to achieve minimal blood concentrations and that similarly moderate renal impairment especially in dabigatran treated patients may result in the same. Another outcome other studies suggested a lack of association between routine assays such as routine hemostasis assays and DOAC concentrations suggesting that in situations where testing is believed to be needed routine assays should not replace DOAC concentration measurement in decision-making regarding whether or not the DOAC has sufficiently gone down in concentration to safely proceed.                                                 Along these lines, the final article we will review within the realm of anticoagulation is by Brendel et al entitled the Anticoagulant Effect of Heparin during Radiofrequency Ablation in Patients Taking Apixaban or Rivaroxaban published in the Journal of Interventional Cardiac Electrophysiology this past month. One concern regarding the use of the direct oral anticoagulants is the fact that during procedures where heparin is needed, knowledge of how much heparin to give is unclear. This is both in the setting of understanding what the synergistic effect of the simultaneous and continued use of apixaban or rivaroxaban or other direct oral anticoagulants in combination with heparin might be and also what the effect on actual activated coagulation time might be.                                                 As it is felt that be ACT may not necessarily reflect the true anticoagulant activity of drugs. Thus in a prospective study, Brendel et al studied about 90 patients with atrial fibrillation undergoing radiofrequency ablation procedures. During radiofrequency ablation, unfractionated heparin was given to maintain ACT of 250 to 300 ms with blood samples taken before and up 360 minutes after heparin administration. They demonstrated that heparin displayed a lower anti-Xa activity in rivaroxaban treated patients compared to apixaban treated patients.                                                 In contrast, D-dimer and prothrombin fragment F1+2 plasma levels indicated a higher activation of the coagulation cascade in apixaban/heparin combinations than in rivaroxaban/heparin combinations. While there was clear differences in the level of anticoagulant effect, depending on which DOAC was combined with heparin, they had no clinical impact in terms of bleeding or thromboembolic complications from the procedure. This article is significant in that it highlights that there are clear and different biochemical responses based on which DOAC is used in combination with heparin during radiofrequency ablation.                                                 While in the small study, there was no clear effect on clinical impact, precautions should still be considered when monitoring periprocedural hemostasis in DOAC patients to avoid mismanagement especially considering the variability that might occur between DOACs themselves and not just between DOACs and warfarin.                                                 Changing paces to risk stratification and management within atrial fibrillation. We’ll review the article by Labombarda et al entitled Increasing Prevalence of Atrial Fibrillation and Permanent Atrial Arrhythmias in Congenital Heart Disease published in this past month's issue of the Journal the American College of Cardiology. In this article, they sought to assess the types and patterns of atrial arrhythmias, associate factors and age-related trends in a multicenter cohort of patients with adult congenital heart disease. What they demonstrated is that by far the most common presenting arrhythmia was intraatrial reentrant tachycardia in almost two-thirds of patients with the remaining including atrial fibrillation in up to 30% of patients and focal atrial tachycardias in up to 10% of patients.                                                 The association of intraatrial reentrant tachycardia with congenital heart disease was stronger with higher complexities of congenital heart disease. With those with more complex defects having a higher frequency of IART than those with simple effects. Furthermore, as is commonly seen in the general population, the frequency of atrial fibrillation increased with age to eventually suppress IART as the most common arrhythmia in those greater than equal to 50 years of age. The predominant arrhythmia pattern was paroxysmal in almost two-thirds of patients though almost 30% were persistent.                                                 Furthermore, the frequency of permanent atrial arrhythmias increased with age. While it is commonly seen that patients with congenital heart disease were living longer and as a result it is expected that the frequency of arrhythmias in this population will likely increase. The interesting outcome from the study is the high frequency of intraatrial reentrant tachycardia as the presenting atrial arrhythmia in patients with congenital heart disease and also with the predominantly paroxysmal pattern. The finding also that atrial fibrillation increases in prevalence highlights the importance of closely monitoring these patients in order to assess for anticoagulation needs and options for treatment.                                                 Changing gears to cellular electrophysiology. We focus on an article by Qiao et al entitled transient Notch activation induces long-term gene expression changes leading to sick sinus syndrome in mice published in this past month's issue of Circulation Research. Notch signaling programs cardiac conduction during development and in the adult ventricle. It is noted that injury can induce notch reactivation resulting in global transcriptional and epigenetic changes. Thus, the group sought to determine whether notch reactivation may alter atrial ion channel gene expression arrhythmia inducibility.                                                 They demonstrated that notch signaling regulates transcription factor in ion channel gene expression in adult atrial myocardium. With reactivation inducing electrical changes resulting in sinus bradycardia, sinus pauses and a susceptibility atrial arrhythmias, altogether contributing to a phenotype resembling sick sinus syndrome. The importance of these findings lies in the mechanism underlying sick sinus syndrome.                                                 While we search for genetic clues for why patients might develop atrial fibrillation or sick sinus syndrome or sinus bradycardia as they age, the importance of activation of typically quiet signaling patterns in the adult myocardium and their role in arrhythmogenesis is important because it might highlight novel targets for treatment. Understanding how the arrhythmogenic substrate develops and the mechanisms underlying it, may allow for a better understanding of why in certain patients certain drugs may be effective or not or certain invasive therapies may be effective or not.                                                 Next with the realm of electrocardiography, we’ll review the article by Christophersen et al entitled 15 Genetic Loci Associated with Electrocardiographic P-wave published in Circulation Genetics this past month. Similar to the previous article by Dr. Qiao et al, the importance of the article by Christophersen et al lies in the identification of a number of genetic underpinnings for what forms the final electrocardiographic P-wave that is seen.                                                 Six novel genetic loci associated with P-wave duration and six novel loci associated with P-wave terminal force were identified by the group. Both in the case of the transient Notch activation findings as well as in the findings related to a specific genetic loci associated with electrocardiographic P-wave abnormalities might highlight potential genetic targets either with existing drugs not traditionally used for atrial electrophysiology or potentially future drug targets.                                                 Changing gears yet again, we’ll move on to their own sudden death cardiac arrest and specifically to an article published by Fallavollita et al entitled the denervated myocardium is preferentially associate with sudden cardiac arrest in ischemic cardiomyopathy a pilot competing risks analysis of cost specific mortality. Previous studies identify multiple factors associated with total cardiac mortality but we all recognize the ejection fraction has limited value. Thus within this article published in Circulation: Cardiovascular Imaging, the group decided to do a competing risks analysis the National Institutes of Health sponsored prediction of arrhythmic events with positron emission tomography trial.                                                 They demonstrated that sudden cardiac arrest was correlated with greater volumes of denervate myocardium based on defects on positron emission tomography using a norepinephrine analog carbon 11 hydroxy ephedrine. However, they also demonstrated that other factors such as lack of angiotensin inhibition therapy, elevated BNP and large left particular end-diastolic volume were further associated with sudden cardiac arrest.                                                 The importance of potential modifying factors to better attribute cardiac arrest risk and thus the need for defibrillator or other therapies in patients with myopathy needs to continue to be highlighted especially in light of recently published Danish and other studies suggesting that the mortality benefit conferred by ICD is an ischemic and nonischemic populations may not be equivalent in newer studies. The fact that further risk stratification opportunities can exist underlying the pathophysiologic basis for why these patients develop ventricular arrhythmias is critical. While recognized for a few decades now that myocardial denervation may be associated with sudden cardiac arrest risk, this study highlights the continued need for further study to help further clarify these populations.                                                 Moving onto the realm of genetic channelopathies, we review the article by Anderson et al entitled Lidocaine Attenuation Testing: An in vivo Investigation of Putative LQT3-Associated Variants in the SCN5A-encoded sodium channel published in this past month's issue of Heart Rhythm. Long QT syndrome type 3 represents one of the more difficult types of long QT syndrome to adequately diagnose both by genetic testing as well as through traditional means. Approximate 2% of healthy individuals can have rare variance of uncertain significance in the SCN5A channel and thus distinguishing true LQT3 causative mutations for background genetic noise can be quite difficult in this population.                                                 Anderson et al decided to assess the utility of lidocaine attenuation testing in evaluating patients with possible LQT3. They gave a loading dose of 1 mg per kg of intravenous lidocaine followed by continuous infusions of 50 micrograms for 20 minutes. If the corrected QT interval shortened by at least 30 ms, the LAT was defined as positive. They demonstrated that use of this test can help distinguish true LQT3 causative mutations from otherwise noncontributory variance of uncertain significance. Thus in this era of increasing genetic testing where one might identify a variant of uncertain significance in either a family member affected with sudden cardiac arrest or in a patient being evaluated for any sort of uncertain significant variant, the use of lidocaine testing in those variance as they apply to LQT type 3 may offer significant clinical use.                                                 Next we will review the article by Ishibashi et al published in this past month's edition of Heart entitled Arrhythmia Risk and Beta Blocker Therapy in Pregnant Woman with Long QT Syndrome. One of the biggest concerns of patients with long QT syndrome especially woman is pregnancy. The fact is because of the different hormonal states, it is possible that pregnancy may alter arrhythmic risk and the safety of beta blocker therapy given both the potential fetal effects as well as the continued efficacy at the level those seen previously.                                                 Thus Ishibashi et al reviewed 136 pregnancies across 76 long QT pregnant patients. They retrospectively analyzed clinical and electrophysiological characteristics in pregnancy outcomes in both the presence and absence of beta blocker therapy. All of the beta blocker group had prior events while the majority of the nonbeta blocker group had not been diagnosed with pregnancy. Pregnancy was noted to increase heart rate in those not treated with beta blockers, but interestingly, between the two groups there was no significant difference over the course of pregnancy in QT intervals.                                                 In the beta blocker group, only two events occurred and these were relegated to the postpartum period. However, 12 events occurred in the nonbeta blocker group either during pregnancy and half or in the postpartum period and the remaining half. There was no difference in this frequency of spontaneous abortion between the two groups, and furthermore, fetal growth rates and proportion of infants with congenital malformation were similar between the two groups. However, premature delivery and low birth weight infants were more common in those taking beta blockers.                                                 Given the high risk of events and the relative safety of beta blocker therapy in this population of patients with long QT who become pregnant, it was felt that the use of early diagnosis and beta blocker therapy could be critical both the during pregnancy and during the postpartum period. It was also felt the beta blocker therapy may be tolerated for babies in long QT pregnant patients. This highlights that the continued use of beta blockers throughout the pregnancy and consideration of the introduction of beta blockers in those not already on them during pregnancy may be an important consideration.                                                 Finally within the realm of genetic channelopathies, we focus on the article by Roberts et al entitled Loss of Function in KCNE2 Variants: True Monogenic Culprits of Long QT Syndrome or Proarrhythmic Variants Requiring Secondary Provocation published in this past month's issue of Circulation: Arrhythmia Electrophysiology. As we identify more and more genes the baby is associated with long QT syndrome, the understanding of the clinical phenotype associated with that syndrome requires better study. In this particular study, Roberts et al reviewed the role of long QT syndrome type 6 stemming from mutations in the KCNE2 encoded voltage gated channel beta subunits.                                                 They reviewed mutations identified during arrhythmia evaluation from either inherited arrhythmia clinics or the Rochester long QT syndrome registry. They demonstrated that the high allelic frequencies of LQT6 mutations in the Exome aggregation consortium database and the absence of previous documentation of genotype phenotype segregation suggest many KCNE2 variants and potentially all were actually erroneously designated as LQT as causative mutations. Instead, it was felt the KCNE2 variants may actually confer proarrhythmic susceptibility when provoked by additional environmental and/or acquired or genetic factors.                                                 What they are saying is that identifying the KCNE2 variants as the principal culprits may be over calling the role of the KCNE2 variants and instead it might be a combination of effects such as two hit affect the requires further provocation by either outside or additional genetic factors. Furthermore, complex genetic studies were likely needed to better understand how variants and genes that may not have been previously designated as disease causing play a role in the actual disease process, whether as potentiating other factors that might exist that might also otherwise be relatively benign or as unique singular hits that might by themselves result in the clinical phenotype.                                                 Next moving onto the realm of ventricular arrhythmias, we first focus on an article published in this past month's issue of the American Journal of Physiology, Heart and Circulatory Physiology by Howard Quijano et al entitled Spinal Cord Stimulation Reduces Ventricular Arrhythmias during Acute Ischemia by Attenuation of Regional Myocardial Excitability. In this article, they demonstrated in a porcine model ventricular ischemia that spinal cord stimulation decrease sympathetic nerve activation regionally in ischemic myocardium while having no effect on normal myocardium. They demonstrated that the antiarrhythmic effects conferred by spinal cord stimulation were likely secondary to attenuation of some sympathoexcitation locally in ischemic myocardium rather than changes in the global myocardial electrophysiology.                                                 This is important because it highlights the mechanisms by which spinal cord stimulation may confer in antiarrhythmic benefits in both animal and human models. As we search for novel interventions that can be used for the treatment of ventricular arrhythmias, understanding the underlying pathophysiologic mechanisms by which they work is critical. The understanding that the use of spinal cord stimulation is primarily conferred in a regional way primarily in terms of its effect on an ischemic myocardium, further study is also needed in terms of how the effect is seen in nonischemic myopathies where there may be more patchy scar in the same role of denervation, nerve sprouting and hyper innervation may play different roles.                                                 In the next article we choose to focus on is by Berte et al entitled a New Cryo-energy for Ventricular Tachycardia Ablation a Proof of Concept Study published in this past month's edition of Europace. One of the key problems in ventricular tachycardia ablation is the lack of transmural lesion formation. This is an important determinant of arrhythmia recurrence. Thus the group decided to do a proof of concept study to evaluate the safety and efficacy of a new and more powerful cryoablation system for ventricular ablation. They demonstrated that a novel cryoablation system to create large transmural ventricular lesions, whether it delivered by endocardial or epicardial approach. It was felt that this technology can hold potential for both surgical and catheter-based VT ablation in humans.                                                 While primarily studied in sheep models, it nevertheless highlights the importance of novel therapies that might better achieve through and through lesions. There are many different novel products being developed for the hope of achieving transmural lesions partly to target the myocardial circuits and partly to ensure achievement of through and through lesions without leaving residual potential substrate, because of only partial thickness lesions. These include things like needle ablation catheters, the safety of which still has to be fully evaluated, bipolar ablation or the use of technology such as novel cryo-energy approaches. Comparative efficacy of these different approaches however will be critical to determining which one is safest and best in any given clinical situation.                                                 Next we’ll review the article by Venlet et al published this past month's issue of Circulation Arrhythmia and Electrophysiology entitled Unipolar Endocardial Voltage Mapping in the Right Ventricle: Optimal Cutoff Values Correcting for Computed Tomography-derived Epicardial Fat Thickness and their clinical value for substrate delineation. The work by [inaudible 00:53:37] and others highlighted the importance of using unipolar and bipolar voltage cutoffs and helping delineate areas of both endocardial as well as potentially more distal such as epicardial scar during endocardial mapping. It is felt the low endocardial unipolar voltage during bipolar voltage mapping endocardially may indicate epicardial scar.                                                 However, the primary issues, the additional presence of epicardial fat both in the right ventricle and left ventricle and how this epicardial fat may effect normal unipolar voltage cutoffs. Thus, Venlet et al decided to review using computed tomography data the effective epicardial fat on unipolar voltage cutoffs. They demonstrated that endocardial unipolar voltage cutoff of 3.9 millivolts was more accurate than previously reported cutoff values for right ventricular epicardial scar during endocardial mapping.                                                 It was further demonstrated that while epicardial abnormal electrograms may be associated with transmural scar when associated with low endocardial bipolar voltage, the additional use of endocardial unipolar voltage and normal bipolar voltage sites can improve the diagnostic accuracy resulting in identification of all epicardial abnormal electrograms at sites with less than 1 mm of fat. Thus, the unipolar voltage not only assisted in evaluating whether epicardial scar was present, but also in further clarifying epicardial abnormal electrograms in terms of whether or not they truly represented potential transmural scar.                                                 Finally, within the realm of electrogram mapping of ventricular arrhythmias, we focus on the article by Magtibay et al entitled Physiological Assessment of Ventricular Myocardial Voltage using Omnipolar Electrograms published in the Journal of the American Heart Association this past month. Bipolar electrograms are traditionally used to characterize myocardial health. However, dependence on these electrograms may reduce the reliability of voltage assessment along different planes of arrhythmic myocardial substrates.                                                 Thus, newer catheters rely on evolving tools that might allow for different approaches to bipolar mapping. Using omnipolar electrograms, Magtibay et al studied in healthy rabbits, pigs and diseased humans under paced conditions the role of two bipolar electrode orientations both horizontal and vertical. Voltage maps were created for both bipoles and omnipoles, and they noted that electric orientation affected the bipolar voltage map with an average absolute difference between horizontal and vertical of up to 0.25 millivolts in humans. Thus, they demonstrated omnipoles can provide physiologically relevant and consistent voltages along the maximal bipolar direction and provide an advantage over traditionally obtained bipolar electrograms.                                                 When we consider the use of evolving techniques to get an understanding of myocardial health whether for the purpose of cardiac mapping and ablation or even for the purpose of other intervention such as cardiac biopsy, understanding what the voltage abnormalities perceived actually are is critical to understanding what substrate is actually being targeted. However, given directionality issues in terms of assessment of voltage as well as relative orientation of the catheter in understanding the relevance of received voltage, use of novel signal processing and electro designs are important to consider in the light of their effects on substrate mapping compared to traditional techniques.                                                 Changing gears yet again, but nevertheless related to cardiac mapping and ventricular arrhythmias, we focus on article by Yalagudri et al published in this past month's issue of the Journal of Cardiovascular Electrophysiology entitled A Tailored Approach for Management of Ventricular Tachycardia in Cardiac Sarcoidosis. While in a small number of patients, nearly 14 patients, they attempt to develop a methodology for approaching patients with cardiac sarcoidosis for management of their ventricular arrhythmias. Patients with either cardiac myocarditis or cardiac sarcoidosis represent a particularly difficult cohort to treat.                                                 Prior work by Dr. Roderick Tung and others has demonstrated the high-frequency of perceived inflammatory abnormalities based on cardiac FDG PET scanning amongst patients with ventricular arrhythmias. Whether this reflects cardiac sarcoidosis or other hypermetabolic activity is unclear. However, how to take into account the FDG PET abnormalities when deciding whether or not to take a patient for ablation or how to best treat them in light of their primary disease process is critical.                                                 In this study, the group tried to tailor therapy for ventricular tachycardia and cardiac sarcoidosis according to the phase of disease results. Namely based on the degree of inflammation noted on the FDG PET scan. They noted that via their named clinical protocol, that this tailored therapy could result in good clinical outcome and avoid unnecessary immunosuppression in some patients. Whether or not the use of this tailored therapy approach may apply in larger populations remains to be seen.                                                 Finally within the realm of other EP concepts that might apply broadly across the electrophysiology landscape, we focus on two articles. The first is by Kudryashova et al entitled Virtual Cardiac Monolayers for Electrical Wave Propagation in Nature Scientific Reports this past month. It is the complex structure of cardiac tissue that is considered to be one the main determinants of whether a substrate becomes arrhythmogenic or not. Multiple mathematical and computational models have been developed in order to recapitulate this complex cardiac structure. However, there been varying degrees of limitations in these approaches.                                                 Using a joint in silico-in vitro approach, the group carefully characterized the morphology of cardiac tissue and cultures of neonatal rat ventricular cells and then proposed mathematical models to result in tissue morphology that could be recapitulated for virtual studies of cardiac electrophysiology mainly in order to study wave propagation. They demonstrated in their virtual cardiac monolayers, that the simulated waves had the same anisotropy ratios and wave form complexity as those in in vitro experimental models.                                                 Thus, they demonstrated that they could reproduce both the morphological and physiological properties of cardiac tissue in a virtual landscape. These findings are critical to improving the ability to better study the effects of different antiarrhythmic drugs or interventional techniques on overall cardiac electrophysiology. The difficulty in existing techniques using traditional in vitro cultures is the fact that they’re costly and requires sacrifice of animals that adds to the additional cost of routine studies. The ability to recapitulate actual hearts within a virtual landscape to mimic the cardiac electrophysiology and then study it in a more controlled setting that can be reproducible based on the availability of appropriate computing power is important in terms of future studies within the realm of our field.                                                 The final article we will review is by Das and Dutta published in Physical Review E this past month entitled Controlling Three-Dimensional Vortices using Multiple and Moving External Fields. One of the key studies over the course of the last several years has been that of the role of the spiral and scroll waves in not just atrial fibrillation but ventricular fibrillation and other arrhythmias. It is well recognized that the spiral or scroll waves depending on whether one thinks in a two dimensional or three dimensional substrate may have significant contribution to arrhythmogenesis. Whether targeting the spiral or scroll waves actually eliminates arrhythmias remains to be fully elucidated. However, it also remains to be elucidated exactly how one should control the spiral or scroll waves.                                                 The review by Das and Dutta demonstrated that in fact the spiral or scroll waves could actually be physically moved around and controlled using moving external electric fields and thermal gradients. They show that the scroll rings can be made to trace cyclic trajectories on a rotating electric field or that application of thermal gradients in addition to electric field could deflect the motion and change the nature of a trajectory of a spiral or scroll wave. These findings are important in that they might represent non-ablative techniques that can eventually be used to control spiral or scroll waves in cardiac media, and thus result in either their alteration or termination without the need for additional cardiac injury.                                                 One the biggest problems with additional cardiac ablation in cases such as atrial fibrillation is the fact that they often lead to additional regions of scarring that might lead towards further organized atrial arrhythmias. However, the ability to potentially terminate critical sites responsible for arrhythmogenesis in real time without the need for ablation may represent novel interventions or devices in the future.                                                 I appreciate everyone's attention to these key and hard-hitting articles that we have just focus on from this past month of cardiac electrophysiology across the literature. Thanks for listening. Now back to Paul. Dr. Paul Wang :                 Thanks Suraj. You did a terrific job surveying all journals for the latest articles on topics of interest in our field. There is 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 could be downloaded from the Circulation: Arrhythmia and Electrophysiology website. We hope that you’ll find the journal to be the go to place for everyone interested in the field. See you next month.

Today, we're going to show you how this presents and how to manage your patient when it does. You better know this life threatening arrhythmia! Subscribe to our YouTube here: http://www.youtube.com/subscription_center?add_user=paboards - Follow us on Instagram here: https://www.instagram.com/paboards/ and https://www.instagram.com/pance_panre_usmle_review/ - Ace your exams: https://learn.physicianassistantboards.com/collections - Have questions about this video? Email gray@physicianassistantboards.com

Commentary by Dr. Valentin Fuster

In this episode, Andy discusses ventricular tachycardia, a topic that can be difficult to understand but very important in critical care settings.

Want more of this show? Subscribe in iTunes: HERE Subscribe in Google Play: HERE Read our massive post on EKG Interpretation for Nurses here: https://www.nrsng.com/interpret-ekgs-heart-rhythms/ The post EKG08: VTach and VFib (Ventricular Tachycardia and Fibrillation) appeared first on NURSING.com.

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...

This week we discuss the ED management of cardiac arrest with VFib and pulseless VTach. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_62_0_Final_Cut.m4a Download One Comment Tags: Cardiac Arrest, Dual Defibrillation, OHCA, Ventricular Dysrhythmias, Ventricular Fibrillation, Ventricular Tachycardia Show Notes Take Home Points In cardiac arrest, the most important interventions are to deliver electricity quickly when it's indicated and to administer good high-quality compressions with minimal interruptions to maximize your compression fraction. Medications like epinephrine and amiodarone have never been shown to improve good neurologic outcomes in the ACLS recommended doses. Don't focus on them. Consider pre-charging your defibrillator to minimize pauses in CPR and maximize your chance for ROSC Finally, remember that as Emergency Physicians, we are specialists in the resuscitation of cardiac arrests. ACLS is just a starting point. Push your understanding of taking care of these patients so you can deliver the best care possible Additional Reading Core EM:

This week we discuss the ED management of cardiac arrest with VFib and pulseless VTach. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_62_0_Final_Cut.m4a Download One Comment Tags: Cardiac Arrest, Dual Defibrillation, OHCA, Ventricular Dysrhythmias, Ventricular Fibrillation, Ventricular Tachycardia Show Notes Take Home Points In cardiac arrest, the most important interventions are to deliver electricity quickly when it's indicated and to administer good high-quality compressions with minimal interruptions to maximize your compression fraction. Medications like epinephrine and amiodarone have never been shown to improve good neurologic outcomes in the ACLS recommended doses. Don't focus on them. Consider pre-charging your defibrillator to minimize pauses in CPR and maximize your chance for ROSC Finally, remember that as Emergency Physicians, we are specialists in the resuscitation of cardiac arrests. ACLS is just a starting point. Push your understanding of taking care of these patients so you can deliver the best care possible Additional Reading Core EM:

This week we discuss the ED management of cardiac arrest with VFib and pulseless VTach. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_62_0_Final_Cut.m4a Download One Comment Tags: Cardiac Arrest, Dual Defibrillation, OHCA, Ventricular Dysrhythmias, Ventricular Fibrillation, Ventricular Tachycardia Show Notes Take Home Points In cardiac arrest, the most important interventions are to deliver electricity quickly when it’s indicated and to administer good high-quality compressions with minimal interruptions to maximize your compression fraction. Medications like epinephrine and amiodarone have never been shown to improve good neurologic outcomes in the ACLS recommended doses. Don’t focus on them. Consider pre-charging your defibrillator to minimize pauses in CPR and maximize your chance for ROSC Finally, remember that as Emergency Physicians, we are specialists in the resuscitation of cardiac arrests. ACLS is just a starting point. Push your understanding of taking care of these patients so you can deliver the best care possible Additional Reading Core EM:

Recognition and treatment methods for an abnormally fast heart rate.

Host: Jennifer Caudle, DO Guest: Francis Marchlinski, MD Host Dr. Jennifer Caudle welcomes Dr. Francis E. Marchlinski, Richard T. and Angela Clark President's Distinguished Professor and Director of the Electrophysiology Laboratory at the University of Pennsylvania. Dr. Marchlinski will review the epidemiology of PVCs, the kinds of problems that PVCs can cause, and how these problems manifest as symptoms in patients. He will also review the effectiveness of catheter ablation as a current treatment option for ventricular tachycardia (VT), a potenially serious complication of PVC's.

Host: Jennifer Caudle, DO Guest: Francis Marchlinski, MD Host Dr. Jennifer Caudle welcomes Dr. Francis E. Marchlinski, Richard T. and Angela Clark President's Distinguished Professor and Director of the Electrophysiology Laboratory at the University of Pennsylvania. Dr. Marchlinski will review the epidemiology of PVCs, the kinds of problems that PVCs can cause, and how these problems manifest as symptoms in patients. He will also review the effectiveness of catheter ablation as a current treatment option for ventricular tachycardia (VT), a potenially serious complication of PVC's.

Host: Jennifer Caudle, DO Guest: Francis Marchlinski, MD Host Dr. Jennifer Caudle welcomes Dr. Francis E. Marchlinski, Richard T. and Angela Clark President's Distinguished Professor and Director of the Electrophysiology Laboratory at the University of Pennsylvania. Dr. Marchlinski will review the epidemiology of PVCs, the kinds of problems that PVCs can cause, and how these problems manifest as symptoms in patients. He will also review the effectiveness of catheter ablation as a current treatment option for ventricular tachycardia (VT), a potenially serious complication of PVC's.

Host: Jennifer Caudle, DO Guest: Francis Marchlinski, MD Host Dr. Jennifer Caudle welcomes Dr. Francis E. Marchlinski, Richard T. and Angela Clark President's Distinguished Professor and Director of the Electrophysiology Laboratory at the University of Pennsylvania. Dr. Marchlinski will review the epidemiology of PVCs, the kinds of problems that PVCs can cause, and how these problems manifest as symptoms in patients. He will also review the effectiveness of catheter ablation as a current treatment option for ventricular tachycardia (VT), a potenially serious complication of PVC's.

Commentary by Dr. Valentin Fuster

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Dr. Michael Hoskins. Catheter Ablation of Ventricular Tachycardia. Recorded 2012-03-05. Recorded 2012-09-24.