Podcasts about pericardial

CardioNerds cofounders, Dan Ambinder joins Drs. Aishwarya Pastapur, Oyinkansola Osobamiro, and Rafik Issa from the University of Michigan for drinks in Ann Arbor. They discuss the following case of pericardial decompression syndrome. Expert commentary is provided by Dr. Brett Wanamaker. Notes were drafted by Dr. Aishwarya Pastapur and Dr. Rafik Issa. The episode audio was engineered by CardioNerds Intern student Dr. Atefeh Ghorbanzadeh. A woman in her 50s with a past medical history of stage IV lung cancer (with metastatic involvement of the liver, bone, and brain), previous saddle pulmonary emboli, pericardial effusion, and malignant pleural effusions presents with dyspnea. She was found to have a pericardial effusion with tamponade physiology relieved by pericardiocentesis. We discuss the management of cardiac tamponade, indications for pericardiocentesis, how to monitor for post-pericardiocentesis complications, and what to keep on your differential diagnosis for decompensation after pericardiocentesis. We discuss the epidemiology, pathophysiology, diagnosis, and management of pericardial decompression syndrome. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Pericardial Decompression Syndrome Pearls - Pericardial Decompression Syndrome Diminished heart sounds, a low-voltage EKG with electrical alternans, elevated jugular venous pressure/pulsations (JVP), and the presence of pulses paradoxes are important findings that could suggest tamponade. McConnell sign is strongly concerning for right ventricular failure and pulmonary hypertension, potentially due to acute pulmonary embolism. Mechanical thrombectomy for pulmonary embolism is not feasible if the emboli are diffusely scattered without a central lesion to target. For patients who experience decompensation following pericardiocentesis, consider perforation, tamponade re-accumulation, or pericardial decompression syndrome (PDS). When possible, avoid draining more than 1L of pericardial fluid at once to minimize the risk of PDS. Notes - Pericardial Decompression Syndrome What is Pericardial Decompression Syndrome (PDS), and how does it present? Pericardial decompression syndrome is a rare, life-threatening syndrome occurring in about 5-10% of cases with paradoxical worsening of hemodynamics after pericardial drainage. The clinical presentation ranges from pulmonary edema to cardiogenic shock to death, occurring a few hours to days after a successful pericardiocentesis. What is the underlying mechanism for PDS? The pathophysiology behind PDS is debated, but there are three proposed mechanisms: Paradoxical Hemodynamic Derangement: After pericardiocentesis, venous return to the RV rapidly increases, resulting in RV expansion and potentially septal deviation towards the LV. Subsequently, the LV experiences decreased preload while still facing increased afterload as a compensatory response to obstructive shock, leading to decompensation.Myocardial Ischemia: Increased intrapericardial pressure may impair coronary perfusion, leading to myocardial ischemia. Upon pericardiocentesis, there is myocardial stunning with increased demand due to increased venous return and cardiac output Sympathetic Withdrawal: Withdrawal of sympathetic activation after drainage of pericardial fluid can trigger cardiovascular collapse What are the risk factors for developing PDS, and how can we mitigate those risks for prevention? Generally, patients with long-standing pericardial effusion with chronic compression of the heart, such as those with malignant pericardial effusions, are more vulnerable to developing PDS after pericardioc...

In today's VETgirl online veterinary CE podcast, we're going to talk about pericardial effusion -; from how to diagnose it, what the clinical signs are, and how to treat it! Most importantly, tune in to learn how to perform a successful pericardiocentesis.

In this episode of the Better Edge podcast, Mohamed M. Al-Kazaz, MD, assistant professor of Cardiology at Northwestern Medicine, discusses the prevalence of pericardial disease, the different ways that it presents itself and diagnostic criteria. Dr. Kazaz also talks about the variety of treatment options and multidisciplinary approach that Northwestern Medicine provides as well as the advancements that are on the horizon in treating pericardial disease.

Dr Marilena Giannoudi discusses pericardial disease with Professor Abdallah Al-Mohammad. In this episode of Clinical Conversations, Dr Marilena Giannoudi discusses pericardial disease with Professor Abdallah Al-Mohammad. Professor Al-Mohammad provides a detailed overview of pericardial disease and offers helpful insights, especially highlighting the importance of gaining detailed histories and requesting targeted investigations when receiving these patients at the front door. Professor Al-Mohammad is a Consultant Cardiologist and Professor of Cardiology for Sheffield Teaching Hospital. Their interests are in heart failure, infective endocarditis and cardiac imaging. -- Follow us -- https://www.instagram.com/rcpedintrainees https://twitter.com/RCPEdinTrainees -- Upcoming RCPE Events -- https://events.rcpe.ac.uk/ Feedback: cme@rcpe.ac.uk

CardioNerds Cofounder Dr. Amit Goyal is joined by an esteemed group of UCLA cardiology fellows – Dr. Patrick Zakka (CardioNerds Academy Chief), Dr. Negeen Shehandeh (Chief Fellow), and Dr. Adrian Castillo – to discuss a case of primary cardiac angiosarcoma. An expert commentary is provided by Dr. Eric Yang, beloved educator, associate clinical professor of medicine, assistant fellowship program director, and founder of the Cardio-Oncology program at UCLA.   Case synopsis: A female in her 40s presents to the ED for fatigue that had been ongoing for approximately 1 month. She also developed night sweats and diffuse joint pains, for which she has been taking NSAIDs. She was seen by her PCP and after bloodwork was done, was told she had iron deficiency so was on iron replacement therapy. Vital signs were within normal limits. She was in no acute distress. Her pulmonary and cardiac exams were unremarkable. Her lab studies showed a Hb of 6.6 (MCV 59) and platelet count of 686k. CXR was without significant abnormality, and EKG showed normal sinus rhythm. She was admitted to medicine and received IV iron (had not consented to receiving RBC transfusion). GI was consulted for anemia work-up. Meanwhile, she developed a new-onset atrial fibrillation with rapid ventricular response seen on telemetry, for which Cardiology was consulted. A TTE was ordered in part of her evaluation, and surprisingly noted a moderate pericardial effusion circumferential to the heart. Within the pericardial space, posterior to the heart and abutting the RA/RV was a large mass measuring approximately 5.5x5.9 cm. After further imaging work-up with CMR and PET-CT, the mass was surgically resected, and patient established care with outpatient oncology for chemotherapy.  CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - primary cardiac angiosarcoma Episode Schematics & Teaching Pearls – primary cardiac angiosarcoma The pericardium is composed of an outer fibrous sac, and an inner serous sac with visceral and parietal layers.   Pericardial masses can be primary (benign or malignant) or metastatic. There are other miscellaneous pericardial masses.  Imaging modalities for the pericardium include echocardiography, cardiac CT and cardiac MRI. There is also role for PET-CT in pericardial imaging for further characterization of pericardial masses.   Cardiac angiosarcomas are extremely rare but are the most common cardiac primary malignant tumors.  Evidence-based management if lacking because of paucity of clinical data given the rarity of cardiac angiosarcomas. Surgery is the mainstay of therapy. Radiotherapy and chemotherapy are often used as well.  Notes – primary cardiac angiosarcoma Pericardial Anatomy  The pericardium is a fibroelastic sac composed of two layers.   Outer layer: fibrous pericardium (

Studies in Androgenetic Alopecia and Alopecia Areata   STUDIES REFERENCED   MINOXIDIL CONCENTRATIONS   Singh et al (starts at 10:10). Does topical minoxidil at concentrations higher than 5% provide additional clinical benefit? Clin Exp Dermatol. 2022 Nov;47(11):1951-1955   Olsen EA, Dunlap FE, Funicella T et al (starts at 13:22). A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and placebo in the treatment of androgenetic alopecia in men. J Am Acad Dermatol 2002; 47: 377–85   McCoy J, Goren A, Kovacevic M, Shapiro J (starts at 16:02). Minoxidil dose response study in female pattern hair loss patients determined to be non-responders to 5% topical minoxidil. J Biol Regul Homeost Agents 2016;30: 1153–5   Goldust M (starts at 17:25). Minoxidil 15% solution versus minoxidil 5%solution in the treatment of androgenetic alopecia. Br JDermatol 2020;183(Suppl): 91 (abstract BH107)   Ghonemy S, Alarawi A, Bessar H (starts at 18:11). Efficacy and safety of a new 10% topical minoxidil versus 5% topical minoxidil and placebo in the treatment of male androgeneticalopecia: a trichoscopic evaluation. J Dermatolog Treat 2021;32: 236–41     JAK INHBITORS FOR ANDROGENETIC ALOPECIA   Casale F et al (starts at 22:19). Are Janus kinase (JAK) inhibitors beneficial in the treatment of androgenic alopecia? Int J Dermatol. 2022 Nov;61(11):e457-e458.   BOTOX FOR ANDROGENETIC ALOPECIA   English RS Jr and Ruiz S (starts at 29:30). Use of Botulinum Toxin for Androgenic Alopecia: A Systematic Review. Skin Appendage Disord. 2022 Mar;8(2):93-100   Shon U, Kim MH, Lee DY, Kim SH, Park BC (starts at 33:48). The effect of intradermal botulinum toxin on androgenetic alopecia and its possible mechanism. J Am Acad Dermatol. 2020 Dec;83(6):1838–9.     PLATELET RICH PLASMA TREATMENTS FOR ANDROGENETIC ALOPECIA Gupta AK and Bamimore M (starts at 39:09). Platelet-Rich Plasma Monotherapies for Androgenetic Alopecia: A Network Meta-Analysis and Meta-Regression Study. J Drugs Dermatol. 2022 Sep 1;21(9):943-952.   de Oliveira AFQ et al (starts at 42:25). Use of autologous platelet-rich plasma in androgenetic alopecia in women: a systematic review and meta-analysis. J Dermatolog Treat. 2022 Oct 31:1-11.   LOW DOSE ORAL MINOXIDIL SIDE EFFECTS   Dlova et al (starts 45:41). Pericardial, pleural effusion and anasarca: A rare complication of low-dose oral minoxidil for hair loss. JAAD Case Rep. 2022 Aug 11;28:94-96.   Randolph M, Tosti A (starts at 53:22). Oral minoxidil treatment for hair loss: a review of efficacy and safety. J Am Acad Dermatol. 2021;84(3): 737-746.     LOW DOSE ORAL MINOXIDIL EFFICACY AND SAFETY     Gupta AK et al (starts at 57:33). There Is a Positive Dose-Dependent Association between Low-Dose Oral Minoxidil and Its Efficacy for Androgenetic Alopecia: Findings from a Systematic Review with Meta-Regression Analyses. Skin Appendage Disord. 2022 Sep; 8(5): 355–36     JAK INHIBITORS AND VENOUS THROMBOEMBOLISM Chen T-L et al (starts at 1:02:14). Association of Risk of Incident Venous Thromboembolism With Atopic Dermatitis and Treatment With Janus Kinase Inhibitors: A Systematic Review and Meta-analysis. JAMA Dermatol. 2022 Aug 24;e223516.   King B et al (1:05:33). Two Phase 3 Trials of Baricitinib for Alopecia Areata. N Engl J Med. 2022 Mar 26.   Misra D et al (starts at 1:11:19). Cardiovascular risks associated with Janus kinase inhibitors: peering outside the black box. Clin Rheumatol. 2022 Oct 20.     RISING PREVALENCE OF ALOPECIA AREATA IN JAPAN   Campos-Alberto E et al (starts at 1:13:00). Prevalence, comorbidities, and treatment patterns of Japanese patients with alopecia areata: A descriptive study using Japan medical data center claims database. J Dermatol. 2022 Nov 2.   COVID VACCINATION AND ALOPECIA AREATA RISK   Tassone F et al (starts at 1:15:21). Alopecia Areata Occurring after COVID-19 Vaccination: A Single-Center, Cross-Sectional Study. Vaccines (Basel). 2022 Sep 5;10(9):1467.   Nguyen B and Tosti A (starts at 1:21:22). Alopecia areata after COVID-19. J Eur Acad Dermatol Venereol. 2022 Aug 11;10.1111/jdv.18491.   Babadjouni  A et al (starts at 1:30:21). COVID-19 vaccination related exacerbations of hair loss in patients with moderate-to-severe alopecia areata on systemic therapy. JAAD Case Rep . 2022 Nov;29:181-185.   Chen C-H et al (starts at 1:36:55). Intractable alopecia areata following the second dose of COVID-19 vaccination: Report of two cases. Dermatol Ther. 2022 Sep;35(9):e15689.  

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In today's VETgirl online veterinary CE podcast, we will be evaluating two methods of pericardiocentesis based off a study by Cook et al entitled Prospective evaluation of pericardial catheter placement versus needle pericardiocentesis in the management of canine pericardial effusion. Pericardial effusion in dogs is a condition we see with some degree of frequency in the ER. The urgency of this condition arises from the buildup of trapped fluid in the small sac surrounding the heart, located between the pericardial lining and the myocardium. Normally this space is so small that you can't really see it on an emergency ultrasound scan without a cardiologist and a diagnostic ultrasound. When enough fluid builds up in the pericardial sac, this space becomes easier to see on emergency ultrasounds. But more importantly, as the fluid accumulates, the pressure in this trapped space compresses the heart chambers, preventing adequate filling of the heart, and results in less blood exiting the heart, and so less blood and oxygen is supplied to our vital organs. This condition is called cardiac tamponade and represents one of the causes of “obstructive shock.” Clinical signs that may clue us in to the presence of cardiac tamponade include Beck's triad of: 1) low blood pressure 2) muffled heart sounds 3) and jugular venous distention, and often the patient is also tachycardic which is the body's compensatory response to the lower cardiac filling volumes.

In this month's EM Quick Hits podcast Justin Morgenstern & Eddy Lang discuss the problem of overdiagnosis in EM, Anand Swaminathan's approach to indications and dosing of thrombolytics for submassive (intermediate risk) pulmonary embolism, Tahara Bhate's QI Corner on a patient with unexplained shortness of breath, Brit Long on emergency treatment of the bleeding hemophilia patient... The post EM Quick Hits 39 Overdiagnosis, Lytics for Submassive PE, Pericardial Effusion, Hemophilia Treatment appeared first on Emergency Medicine Cases.

Commentary by Dr. Valentin Fuster

Welcome to the 14th episode of 5 Minute Medicine! In this episode, we will be exploring Pericardial Effusion and Cardiac Tamponade. We will discuss a clinical case, definitions, pathophysiology, symptoms, clinical features, diagnosis, supportive tests and treatment! All of the highest yield information is covered, with many easy ways to remember the important features of this pathology such as analysing “Beck's Triad”! We will also delve into understanding why some of the classic features of this condition occur, such as “pulsus paroxidus.” Follow us on Spotify to be notified of our releases. We would really appreciate if you rate us 5 stars and give us a review on Apple Podcasts if you have the time too, as this really helps our discoverability follow our Ig @5.min.medicine for quizzes and notes on the topics!

Pericardial tamponade is one of the Ts in our H&T reversible causes of cardiac arrest. Review of physiology/mechanism of tamponade. Some common causes of tamponade and the signs a patient will exhibit prior to arresting. Differentiating Tamponade for Tension pneumothorax. The treatment of cardiac tamponade with pericardiocentesis. Connect with me: Website:  https://passacls.com (https://passacls.com) https://twitter.com/PassACLS (@PassACLS) on Twitter https://www.linkedin.com/company/pass-acls-podcast/ (@Pass-ACLS-Podcast) on LinkedIn Good luck with your ACLS class! Check out the pod resources page at passacls.com for a link to a Ninja Nerd's episode on pericardial tamponade.

This week we delve into cardiac surgery and review a recent paper from Rady Children's Hospital about patch material and outcomes in the CHD surgical patient. What are the reasons that glutaraldehyde is used to treat patches used for surgery and what are the potential benefits and disadvantages? What sorts of patches are best for what indications? Are there data to suggest superiority of one patch material versus another? We speak with the senior author of this week's work, Assistant Professor of Surgery at Mount Sinai, Dr. Raghav Murthy about this interesting topic. DOI: 10.1016/j.athoracsur.2020.11.014

This week we review a recent work from Utrecht University in The Netherlands on the topic of postoperative pericardial effusion following congenital heart surgery. Some use steroids, some NSAIDs and some colchicine. Are there any data supporting one agent versus the other? We speak with the first author of this work, Poznan University of Medical Sciences student, Nirmiti Somani about this practical and important issue in congenital heart surgery. DOI: 10.1007/s00246-022-02820-4

Looking for more information on this topic? Check out the Congenital Adrenal Hyperplasia brick. If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/ from our Musculoskeletal, Skin, and Connective Tissue collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology.

Ambreen Fatima Ali, MD, Cardiovascular Medicine Fellow, presents a rare care of constrictive pericarditis. Diagnostic testing including various imaging techniques and CT guided biopsy leads to the diagnosis of pericardial mesothelioma. An expert panel led by Dr. Allan Klein, Director of the Pericardial Center discuss this case and issues surrounding the topic.

Welcome to episode 15 on cardiomyopathies and pericardial diseases! Join us as we delve into the highest yield etiologies of pericardial diseases and cardiomyopathies, including presentation, distinguishing factors, and management. Enjoy!

The diagnosis and management of pericardial disease has evolved. There are new technologies to help better care for these patients. Dr. Allan Klein, Director of the Center for the Diagnosis and Treatment of Pericardial Diseases, discusses new advancements and studies regarding pericarditis.

Pericarditis is a word that has been used a lot lately. There have been many changes in the world of pericarditis. Dr. Allan Klein, Director of the Center for the Diagnosis and Treatment of Pericardial Diseases, talks about the diagnosis, causes and treatment of pericarditis.

This episode covers pericardial effusions.Written notes can be found at https://zerotofinals.com/surgery/cardiothoracic/pericardialeffusion/ or in the cardiothoracic surgery section of the Zero to Finals surgery book.The audio in the episode was expertly edited by Harry Watchman.

This episode talks about what Pericardial Effusion is, it's etiology, clinical presentations including Ewart's Sign, Investigations to be done and the line of treatment for the same.It also includes Cardiac tamponade and the various signs associated with it (Kussmaul's Sign etc).

Evan Harmon MD, Cardiovascular Medicine Fellow, presents two rare cases of patients with myopericarditis following COVID 19 vaccine. This is followed by a discussion of the mRNA vaccine, who is at risk for myopericarditis, diagnostic testing and management. An expert panel led by Dr. Allan Klein, Director of the Pericardial Center discuss the case and issues surrounding the topic.

Dr. Brian Clothier and Cole VanEpps have a discussion about identification of Pericardial Tamponade in the prehospital setting, treatment options and causes of this life threatening emergency.

It's been 5 years since our last version of Pericardial Effusion was debuted, and it's time for an update! Remember: The presence of a pericardial effusion doesn't mean the patient is in tamponade, irrespective of the side of the effusion.  Don't forget to check out our Question Bank (3,200 q's with video narration answers), Fundamentals (one month US boot camp) and our On-Demand Courses (last one was on critical care ultrasound!)

Dr. Douglas Johnston joins Dr. Eric Roselli to highlight a new renaissance in the treatment of pericardial diseases.

Commentary by Dr. Valentin Fuster

Pericarditis treatment can be very challenging, however, the approach to surgical treatment has changed over the years with advances in imaging and earlier diagnosis. Dr. Doug Johnston, Vice Chairman of Thoracic and Cardiovascular Surgery and Surgical Director of the Pericardial Disease Center, talks about pericarditis (including recurring pericarditis, constrictive pericarditis), what it is, and when someone may need surgery to treat it. Dr. Johnston talks about what surgery involves, why Cleveland Clinic takes this approach and what recovery looks like.

Presented by the Research and Current Concepts Committee Uma Krishnamurti, MD, PhD, Chair Sinchita Roy-Chowdhuri, MD, PhD, Vice Chair Each Series in this 3 Part Series will introduce you to the 2020 award winners. Each interviewer are from the ASC Research and Current Concepts Committee. Part 1: Interviewers: Michiya Nishino, MD, PhD and He Wang, MD, PhD Bernard Naylor Excellence in Cytomorphology Award - Paper - Peritheliomatous Pattern: A Diagnostic Clue for Diagnosing Metastatic Melanoma in Cytology – First Author: Swikrity Upadhyay Baskota, MBBS, MD Cytotechnologist Scientific Presentation Award – Poster 15 – Prevalence of Tumors in Pleural, Pericardial and Peritoneal Serous Effusions: A Five-Year Institutional Study – First Author: Donna Russell, Med, CT(ASCP)HT Part 2: Interviewer: James McNulty, MS, CT(ASCP) Warren R. Lang, MD Resident Physician Award – Poster 50 – Anal Cytology and Concurrent Human Papillomavirus (HPV) Testing among Human Immunodeficiency Virus (HIV) – positive and HIV – negative Men – First Author: Robert Post, DO Innovative Cytotechnologist Practice Award – Poster 02 – Training in Cytopathology in Times of Social Distancing: A Comparison of Remote vs. Traditional Learning – First Author: Melissa McCrosson, CT(ASCP)cm1 Part 3: Interviewers: Diana Lin, MD and Dianna Ng, MD Advances in Thyroid Cytology Award – Platform 9 – Immune Profiling of Thyroid Lesions and its Application to Malignancy Prediction – First Author: George Xu, BA Quality Improvement in Cytology Award – Poster 107 - Quality Data Abstraction Utilizing Bethesda Pap Test reporting: Key Implementation Science indicators for National Gynecologic Cytology Benchmarks – First Author: Amy Spiczka, MS SCT, MB, HTL (ASCP)1 -------------------------------------------------------------------------------------------------------------------- Dr. Xin He was not available for this recording. He is the winner of the Geno Saccomanno, MD New Frontiers in Cytology Award – Poster 72 - Comparison of Molecular Testing Performed by Liquid Biopsy and Cytology Specimens in Non-small Cell Lung Cancer – First Author: Xin He, MD

Radi Zinoviev MD , Cardiology Fellow presents a case study of a young patient with Liddle’s Syndrome with long history of symptoms who presented at Cleveland Clinic for a second opinion. Dr. Zinoviev describes complicated pericarditis, the use of imaging and inflammatory markers to diagnose and guide management, and treatment strategies. Dr. Allan Klein leads a discussion following the case with Dr. Zinoviev, Dr. Christine Jellis, Dr. Alistair Phillips, Dr. Deborah Kwon and Dr. Rick Grimm.

Acute pericarditis, Chronic constrictive pericarditis and Cardiac Tamponade

This episode covers pericardial effusion and cardiac tamponade!

Cardio: 2. Harry and Sally talk through Pericarditis. This episode was vetted by Dr. Retesh Bajaj, Interventional Cardiology Fellow at Queen Mary University, London. Links: ECG of Pericarditis, multiple examples including Example 3: https://litfl.com/pericarditis-ecg-library/ Audio clip of Pericardial rub: https://www.youtube.com/watch?v=-DB_8zyg9W8

In this episode of the Cardiology section, we discuss the pericardium and the diseases associated with it.

Commentary by Dr. Valentin Fuster

athlete heart covid https://www.the-scientist.com/news-opinion/college-athletes-experienced-heart-damage-after-covid-19-study-67929 titiles like- “Images of the players’ hearts showed signs of inflammation consistent with myocarditis, a rare but potentially fatal condition.” “two dozen of Ohio State University players using cardiac magnetic resonance (CMR), they found evidence of myocarditis in 15 percent, while a further 30 percent had cellular damage or swelling “ The Ny york times said- https://www.nytimes.com/2020/09/16/well/move/is-coronavirus-affecting-the-hearts-of-college-athletes.html Is Coronavirus Affecting the Hearts of College Athletes? “In a new study of 26 college athletes who tested positive for coronavirus, four later showed signs of inflammation in their heart muscles.” and my favorite-- CNN says https://www.cnn.com/2020/09/14/health/covid-heart-inflammation-athletes-study/index.html Covid-19 study suggests to screen recovering athletes for heart inflammation before they return to play “As athletes recover from Covid-19, taking images of their hearts to screen for inflammation may help doctors determine when it could be safe to get back in the game, new research suggests.” Now lets look at this paper and see if this paper says what you think it says or at least does it say what the Big Ten thinks it says!! In the press release for the big ten return to football they say “The Big Ten Council of Presidents and Chancellors (COP/C) adopted significant medical protocols including daily antigen testing, enhanced cardiac screening and an enhanced data-driven approach when making decisions about practice/competition. “ they go on to say “All COVID-19 positive student-athletes will have to undergo comprehensive cardiac testing to include labs and biomarkers, ECG, Echocardiogram and a Cardiac MRI.” The thing I find funny is they say things like ‘data-driven approach but then say things like ‘a positive athlete can not return for a minimum of 21 days’ and athletes must get a cardiac MRI along with a bunch of other non evidence based and non data driven recommendations. BUT this podcast is about the cardiac MRI in athletes so let's look at that paper and why it is dead fricken wrong!! This is a perfect example of why school presidents should play doctor and realistically speaking, I as a doctor don’t want to be a school president. https://jamanetwork.com/journals/jamacardiology/fullarticle/2770645?guestAccessKey=ad3c4563-167f-452a-917f-7bfe15663b06&utm_source=For_The_Media&utm_medium=referral&utm_campaign=ftm_links&utm_content=tfl&utm_term=091120 The paper that has created this cardiac MRI craze is titled - Cardiovascular Magnetic Resonance Findings in Competitive Athletes Recovering From COVID-19 Infection it was in jama cardiology on sept 11 and they researchers at ohio state did CMR imaging in 26 competitive college athletes who previously had been diagnosed with COVID19. and they found “Four athletes (15%; all male individuals) had CMR findings consistent with myocarditis and Pericardial effusion was present in 2 athletes with CMR evidence of myocarditis.” the authors conclusions, “Cardiac magnetic resonance imaging has the potential to identify a high-risk cohort for adverse outcomes and may, importantly, risk stratify athletes for safe participation because CMR mapping techniques have a high negative predictive value to rule out myocarditis.4” they go on to say “cardiac magnetic resonance imaging evidence of myocardial inflammation has been associated with poor outcomes, including myocardial dysfunction and mortality.6 “ this sounds terrible!!! I will give you a second to grab a drink and sit down because I think in the next several minutes you will be both relieved and frustrated about what this article really says. music this was first released by anish koka on twitter but she was spot on and this sort of information needs widespread dissemination. As I said there were 26 athletes but out of those 12 had mild symptoms DURING the infection and 14 were asymptomatic during the infection. None of these pts had chest pain or required hospitalization not even a slightly elevated troponin from demand ischemia during their infection was reported and per the paper, “There were no diagnostic ST/T wave changes on electrocardiogram, and ventricular volumes and function were within the normal range” now the current return to play protocol is all expert opinion but in the article is cited as 2-week not activity and if asymptomatic then no diagnostic cardiac testing but if symptomatic then an electrocardiogram and transthoracic echocardiogram. The authors want you to look at this and say hey we might need to add CMRI lots look at their logic “Cardiac magnetic resonance imaging has the potential to identify a high-risk cohort for adverse outcomes and may, importantly, risk stratify athletes for safe participation because CMR mapping techniques have a high negative predictive value to rule out myocarditis.4” https://www.sciencedirect.com/science/article/pii/S0735109718388430?via%3Dihub and they site Cardiovascular Magnetic Resonance in Nonischemic Myocardial Inflammation: Expert Recommendations which the opening line says “This Journal of American College Cardiology Scientific Expert Panel provides consensus recommendations for an update of the cardiovascular magnetic resonance (CMR) diagnostic criteria for myocardial inflammation in patients with suspected acute or active myocardial inflammation” This is the first fault--remember these were healthy athlets THAT DID NOT HAVE SUSPECTED ACUTE OR ACTIVE MYOCARDIAL INFLMMATION!! you cant say well this test does really good at detecting a specific illness in this population so it must do a could job at detecting it in every population. That it like say well antibiotics work well to make people feel better when they have bacterial infections so they must work to make patients with cancer feel better. NO NO NO next they said, “Cardiac magnetic resonance imaging evidence of myocardial inflammation has been associated with poor outcomes, including myocardial dysfunction and mortality.6 “ and this comes from a paper titled “Prognostic value of cardiac magnetic resonance tissue characterization in risk stratifying patients with suspected myocarditis.” WITH SUSPECTED MYOCARDITIS!! this study was 670 patients who had CLINICALLY SUSPECTED myocarditis who then got a CMRI. just to get in to that study you had to have one of the following 1) acute chest pain syndromes with symptom onset

This episode covers pericardial effusion!

All we need to know about Pericardial diseases for the internal medicine board exam

This is a short, but sweet episode that reviews pericardial disease and treatments of pericarditis, pericardial effusion, restrictive pericarditis and tamponade. Please feel free to leave a rating or review for the podcast after listening! I love reading your thoughts and feedback! 

Echocardiography (Pericardial Disease) for the Internist-8 Dr RR Baliga's MUST KNOW FACTS PODCASTS for PHYSICIANS from chapter Echocardiography for the Internist in Baliga's Textbook of Internal Medicine with 1480 MCQs www.MasterMedFacts.com authored by Dennis A Tighe, MD, FACC, FACP, FASE Professor, University of Massachusetts Director, Cardiac Ambulatory Services, UMass Memorial Health Care & Martin St. John Sutton, MBBS, MD, FRCP Emeritus Professor, University of Pennsylvania Recipient of 2016 Lifetime Achievement Award from the American Society of Echocardiography   This podcast is not Medical Advice or Medical Opinion

Commentary by Dr. Julia Grapsa

Malignant Pericardial Effusion & Cardiac Tamponade + MCQ from chapter titled Emergencies in Hematology and Oncology in Baliga's Textbook of Internal Medicine available at MasterMedFacts.com authored by Thorvardur Halfdanarson,MD Professor of Oncology Mayo Clinic, Rochester, MN & Eric Engelman, MD Clinical Hematologist/Oncologist Dubuque, Iowa Not Medical Advice or Opinion  

Listen as Dr. London Smith (.com) and his producer Cameron discuss Pericardial Effusion with special guests Cameron, Dr. London, and DJ Dylan. Not so boring! http://www.londonsmith.com/jockdocpodcast/24-pericardial-effusion-cameron-dr-london-dj-dylan/ Performed by: London Smith, Cameron Clark, Cassie Walker, Dylan Walker. Written by: London Smith, Cameron Clark, Cassie Walker, Dylan Walker. Produced by: London Smith, Cameron Clark, Dylan Walker Cassie Walker. Created by: London Smith

Dr. Allan Klein, Director of the Cleveland Clinic Pericardial Disease Center introduces pericarditis cases, a discussion of various types of pericarditis including presentation, imaging, pathology, treatment and considerations. Robert Montgomery, MD, Cardiovascular Medicine Fellow presents a case of advanced pericardial constriction. Dr. Paul Cremer moderates a panel including cardiac surgeon Shinya Unai, MD, cardiologists and imaging specialists Dr. Christine Jellis and Dr. Deborah Kwon, and pathologist Dr. Carmela Tan addressing surgical treatment, and advanced imaging.

Dr. Allan Klein, Director of the Cleveland Clinic Pericardial Disease Center introduces pericarditis cases, a discussion of various types of pericarditis including presentation, imaging, pathology, treatment and considerations. Jay Ramchand, MD, Cardiovascular Medicine Fellow presents two cases of transient pericarditis. Dr. Paul Cremer moderates a panel including cardiac surgeon Shinya Unai, MD, cardiologists and imaging specialists Dr. Christine Jellis and Dr. Deborah Kwon, and pathologist Dr. Carmela Tan addressing surgical treatment, and advanced imaging.

This episode is all about the fibroelastic sac surrounding your heart- the pericardium! We discuss the continuum of pericarditis, pericardial effusions and cardiac tamponade- including symptoms/signs to look out for and an approach to management. As always, we have an associated infographic as well as relevant resources at www.theinternatwork.com.This episode was written by Dr. David Dorian (Internal Medicine Resident) and reviewed by Dr. Ken Melvin (Cardiologist), Dr. Rupal Shah (General Internist) and Dr. Nadine Abdullah (General Internist).

Grant Henderson, MD, Cardiovascular Medicine Fellow presents a case if woman with constrictive calcific pericarditis including review of symptoms, imaging and considerations. Following a presentation of the pathology by Dr. Carmela Tan, Dr. Allan Klein, Director of the Cleveland Clinic Pericardial Disease Center leads a discussion and with cardiac surgeon Dr. Douglas Johnston and Dr. Deborah Kwon, addressing surgical treatment, and advanced imaging.

Nikolaos Spilias, MD, Cardiovascular Medicine Fellow presents two cases of recurrent pericarditis, including presentation, imaging, treatment and considerations. Dr. Allan Klein, Director of the Cleveland Clinic Pericardial Disease Center leads a discussion and with cardiac surgeon Dr. Douglas Johnston and Dr. Deborah Kwon, addressing surgical treatment, and advanced imaging.

Back in the studio, joined by Simon Cook, one of our fabulous lecturers in Emergency and Critical Care here at the RVC. We talk to Simon about pericardial effusions and their management. We’ve hit 88 podcasts, 88 miles per hour allowed for time travel, not sure we are there yet. We hope that you enjoy.  Some papers of interest: https://www.ncbi.nlm.nih.gov/pubmed/28992908 https://www.ncbi.nlm.nih.gov/pubmed/28079972 https://www.ncbi.nlm.nih.gov/pubmed/24236526 We will have to wait a bit before Simon’s paper comes out in the Journal of Veterinary Emergency and Critical Care: Pericardial catheter placement in the management of pericardial effusion: 18 dogs Cook, Simon; Cortellini, Stefano; Humm, Karen R And looking forward to his findings from his current study. We will get him back into the studio to discuss If you have any comments about this podcast, please get in touch: email dbarfield@rvc.ac.uk; tweet @dombarfield. We would greatly appreciate your time to rate us on Apple podcast or Acast and kindly write us a review.

Back in the studio, joined by Simon Cook, one of our fabulous lecturers in Emergency and Critical Care here at the RVC. We talk to Simon about pericardial effusions and their management. We’ve hit 88 podcasts, 88 miles per hour allowed for time travel, not sure we are there yet. We hope that you enjoy.  Some papers of interest: https://www.ncbi.nlm.nih.gov/pubmed/28992908 https://www.ncbi.nlm.nih.gov/pubmed/28079972 https://www.ncbi.nlm.nih.gov/pubmed/24236526 We will have to wait a bit before Simon’s paper comes out in the Journal of Veterinary Emergency and Critical Care: Pericardial catheter placement in the management of pericardial effusion: 18 dogs Cook, Simon; Cortellini, Stefano; Humm, Karen R And looking forward to his findings from his current study. We will get him back into the studio to discuss If you have any comments about this podcast, please get in touch: email dbarfield@rvc.ac.uk; tweet @dombarfield. We would greatly appreciate your time to rate us on Apple podcast or Acast and kindly write us a review.

I had such a fun time chatting on the phone with Dan about medicine.  Total recorded time was 2 hours that I had to edit down to this current episode.  His story from childhood to how he became one of the administrators for a surgical group in one of the biggest hospital systems in California is enriching.  He is a true inspiration.  Thanks Dan! Physician Assistant Stats:* Physician Assistants practice medicine on teams with physicians and other healthcare workers. They examine, diagnose, and treat patients autonomously and as part of a team in all various specialties of medicine.   2017 Median Pay: $104,860 per year ($50.41 per hour)   Educational Degree: Masters Degree   Number of US jobs in 2016:106,200   10 Year Job Outlook: 37% growth, much faster then avg.     *Bureau of Labor Statistics, U.S. Department of Labor, Occupational Outlook Handbook, Physician Assistants, (visited August 5, 2018).     Terms Covered in Episode Navy A School   Corpsman - Enlisted medical specialist   Lipoma - Overgrowth of adipose tissue (fat) creating a benign tumor often located between skin and muscle layer.   Eugene Stead Jr. MD   CT Surgery - Cardiothoracic surgery deals with issues of the thorax, generally the heart and lungs.   Trauma Surgery - Surgical field dealing with acute traumatic injuries such as falls, motor vehicle crashes, gunshots, blunt and penetrating injuries, etc.   ICU (Intensive Care Unit, Critical Care Unit, or Intensive Therapy/Treatment Unit) - Part of the hospital with the sickest patients requiring the most intervention from both staff and equipment.  May consist of intubated, sedated, and ventilated patients.   Call - To be available on your “off time” for phone calls, patient visits, surgeries, emergencies, etc that varies by job.   Open Surgery - Traditional way of surgery going through the layers of the body to operate.   Endoscopic Surgery - Surgery utilizing cameras, smaller openings and temporary ports in the body to pass through instruments in a tight space allowing for less pain and quicker recovery.   Vein Harvest - Generally endoscopic removal of a vein to replace a coronary artery (cardiac bypass)   Bypass - Surgical procedure to restore blood flow to the heart after an obstruction occurs.   Cardiac Graft   BP (Blood Pressure) - Force of blood against the arterial walls.   Recovery - Phase after surgery when anesthesia is wearing off and patient is being monitored before being sent home with family or admitted to the hospital.   Punch Biopsy - Small round biopsy (cut) taken to identify the cause of abnormal tissue.   Hernia - Bulging of an organ (intestines) through an abnormal opening.   ENT Surgery - Ear, Nose, and Throat.  Various procedures involving the head.   MBA - Masters of Business   UCSF Neuroscience   Medicare - Government provided healthcare insurance to those over 65, young people with disabilities, and people with end stage renal disease.   401k - Retirement plan.   Western Governors University   Bedside Manner - approach or attitude towards a patient.   Neurosurgery - Surgery dealing with the Nervous System (brain and spine).   Trauma LVL 1 Center - Hospital able to provide total care for every aspect of injury.  Large facility with all types of staff including Residents.   Cerebral Stenosis - When artery inside the brain that becomes blocked by plaque or disease.   TPA (Tissue Plasminogen Activator) - Protein involved in the breakdown of blood clots.   Aneurysm - Ballooned and weaker area of an artery.   CVA (Cerebral Vascular Assault) - Stroke.  Damage to the brain from a loss of blood flow.   Ischemic CVA - loss of blood flow from a blockage.   Hemorrhagic CVA - loss of blood flow from a blockage a ruptured aneurysm.   Elective Surgery - Nonemergent scheduled surgery   Discectomy - Surgical removal of whole or part of a intervertebral disc.   Fusions - Surgery to join two or more vertebrae together.  Done for fractures, deformities, instabilities, slipped vertebrae, or herniated disk.   ACDF (Anterior Cervical Discectomy & Fusion) - Discectomy of the cervical spine (neck) with fusion to decompress the spinal cord and nerve roots of the cervical spine.   Neuroaxis (Neuraxis) - Central Nervous System   Tumor - Abnormal growth of cells   Resection - to surgically remove   Spine Stabilization - Surgery to stabilize the spine with more flexible materials then traditional fusion.   Angio - technique used to visualize inside blood vessels.   MRI (Magnetic Resonance Image) - Medical Imaging using magnets to see deep layers of the body.   Space Occupying Lesion - abnormal mass in the brain usually due to cancer, but may be abscess (infection) or hematoma (blood).   Glioblastoma - Rare very aggressive and fatal cancer of the brain or spine.   Code Yellow - Phrase used over PA system of hospital when Trauma Patient is coming to the ER.  To alert the hospital to assemble the Trauma Team and support staff to receive the patient.   Hypotensive - lower then normal blood pressure.   Chest Tube - tube placed in the chest cavity to evacuate blood, pus, or air.   Central Line - Larger then an traditional IV placed into a main vein of the body. Thoracotomy - Opening into the chest wall.   Finochietto (Rib Spreader) - Used to get a better window/view into the chest cavity the pushes the ribs aside.   Pericardial massage - Manually pumping the heart with a hand in the chest cavity.   Each and every episode of Maybe Medical is for educational purposes only, not to be taken as medical advice.  The opinions of those involved are of their own and not representative of their employer.

In today's VETgirl online veterinary continuing education podcast, we discuss whether you detect pericardial effusion and cardiac tamponade on chest radiographs in veterinary medicine.

In today's VETgirl online veterinary continuing education podcast, we discuss whether you detect pericardial effusion and cardiac tamponade on chest radiographs in veterinary medicine.

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 from the latest journal articles in the field.                                                 In our first manuscript this month, Cho and Associates investigate the need for readmission for Dofetilide reloading. The FDA labeling for Dofetilide loading states that Dofetilide must be initiated or reinitiated in hospital with continuous electrocardiographic monitoring.                                                 In this article, the authors retrospectively examine the hospital records for 138 patients admitted for Dofetilide reloading for atrial arrhythmias. Of these 138 patients, 102 were reloaded at a previously-tolerated dose, 30 with a dose higher than a previously tolerated dose, and 2 at a lower dose, with the prior dosage unknown in 4 patients.                                                 In 44 patients, or 31.9%, dose adjustment or discontinuation of Dofetilide was performed, although, torsades de pointes occurred in two patients admitted to increased Dofetilide dosage, no torsades de pointes was observed in patients loaded with the same dose of Dofetilide.                                                 This is 0 versus 6.7% or P = 0.05. In 30 out of 102 patients, 29.4% reloaded at a previously tolerated dose. Dofetilide dose adjustment was required. In 11 out of 30 patients or 36.7% admitted for an increase in dose, a dose adjustment or discontinuation was required.                                                 The authors therefore concluded that dosage adjustments or discontinuation were frequent, and that their observations support the need for hospitalization for Dofetilide reloading. In the next manuscript Tilman Maurer and Associates report a novel superolateral approach to creating a mitral isthmus ablation line.                                                 Because the creation of an endocardial mitral isthmus line with the end point of bidirectional block maybe challenging, the authors examine 114 patients with perimitral annular flutter without a prior mitral isthmus ablation line.                                                 The authors compared the initial group of 57 patients, group A, who underwent catheter ablation using a novel superolateral mitral isthmus ablation line connecting the left sided pulmonary veins with the mitral annulus along the base of the left atrial appendage visualized by selective angiography to another group of patients, 57 patients in groups B undergoing ablation using a conventional mitral isthmus ablation line connecting the left inferior pulmonary vein to the mitral annulus.                                                 The authors found that bidirectional block was achieved in 56 out 57 patients in group A, or 98.2%, and 50 patients in group B, or 87.7%, P=0.06. Ablation from within the coronary sinus was required significantly less for creation of a superolateral mitral isthmus ablation line compared to a conventional mitral isthmus ablation line, 7.0% versus 71.9%, P is less than 0.01.                                                 The need for epicardial ablation from within the coronary sinus in the total length of the mitral isthmus line, 29.3 versus 40.8 millimeters were predictors for unsuccessful bidirectional mitral isthmus blockade. Pericardial tamponade was observed in group A, but not in group B, 5.2% versus 0%, P=0.24.                                                 The authors, therefore, concluded that superolateral mitral isthmus ablation line has a higher acute success rate compared with conventional mitral isthmus ablation line with a low likelihood of needing ablation from within the coronary sinus.                                                 In our next paper, Cronin and Associates examine the relationship between right ventricular pacing frequency, and the incidence of ventricular arrhythmias leading to ICD shock.                                                 Using the altitude database, the authors examined 389 appropriate shocks, and 425,625 transmissions received from 8,435 patients over a mean follow-up of 15.0 months.                                                 Transmissions with 80 to 98% right ventricular pacing were associated with a hazard ratio of 1.56 for an appropriate shock in the subsequent week compared to less than 1% right ventricular pacing, P=0.04 using a time dependent Cox proportional hazard model, however, the authors found that greater than or equal to 98% right ventricular pacing trended towards a lower risk of appropriate shock. Hazard ratio 0.61.                                                 Lifetime cumulative percentage right ventricular pacing was similarly associated with an increased risk of appropriate shocks at 80 to 98% right ventricular pacing, but not greater than or equal to 98% right ventricular pacing.                                                 The authors, therefore, concluded that an increased frequency of right ventricular pacing is associated with an increased risk of appropriate ICD shocks until the right ventricular pacing is greater than or equal to 98%.                                                 In the next manuscript, Wesley O'Neal and Associates examined 12,241 patients from The Atherosclerosis Risk in Communities Study, ARIC study, the association of individual QT components, that is R-wave onset to R-wave peak, R-peak to R-wave end, ST-segment, T-wave onset to T-wave peak, and T-peak to T-wave end with the occurrence of sudden cardiac death.                                                 The authors identified a total of 346 cases of sudden cardiac death identified over a median followup of 23.6 years. The prolongation of the QT interval was associated with a 49% risk of sudden cardiac death. Of the components of the QT interval only the T-wave onset to T-peak component was associated with sudden cardiac death with each standard deviation increase, hazard ratio of 1.19.                                                 The authors found similar results when the QT interval components were included in the same model, thus the authors conclude that the risk of a sudden cardiac death is driven by prolongation of the T-wave onset to T-peak component.                                                 In the next article by Kalliopi Pilichou and Associates, the authors examined copy number variations or CNVs in arrhythmogenic cardiomyopathy patients. The author studied 160 arrhythmogenic cardiomyopathy proband genotype negative for 5 arrhythmogenic cardiomyopathy desmosome genes using conventional mutation screening.                                                 Using multiplex ligation dependent probe amplification, MLPA, 9 heterozygous copy number variations were identified in 11 or 6.9% of the 160 probands. Of these, the authors found that 5 had the least of the entire plakophilin-2 gene to a deletion of only the PRP2 [exon 00:08:45], 1 a deletion of the PRP2 exon 6211, and 1 a PRP2 duplication of the 5 UTR to exon 1. One the desmocollin 2 duplication of exon 7 to 9, and one large lesion of chromosome 18 comprising both DSC2 and desmoglein 2 genes.                                                 All probands were affected by moderate severe forms of disease and 10 or 32% of the 31 family members carrying one of these deletions met the diagnostic criteria for arrhythmogenic cardiomyopathy.                                                 The authors concluded that identifying the copy number variations may increase the yield of genetic testing. In family members carrying the copy number variations, but not displaying the phenotype other factors are likely involved.                                                 In the article by Rahul Samanta and Associates, the authors examined in 7 sheep a mean of 84 weeks post MI, the influence of intramyocardial adipose tissue on scar tissue identification during endocardial contact mapping, the authors found that endocardial electrogram amplitude correlated significantly with intramyocardial adipose tissue.                                                 Unipolar, Right = negative 0.48, bipolar R = negative 0.45, but not correlated with collagen. Unipolar, R = negative 0.36, bipolar, R = negative 0.43. Intramyocardial adipose tissue, dense regions of myocardium were reliably identified using endocardial mapping with thresholds of less than 3.7 millivolts and less than 0.6 millivolts respectively for unipolar, bipolar, and combined modalities.                                                 Unipolar mapping using optimal thresholding remained significantly reliable, an AUC of 0.76. During mapping of intramyocardial adipose tissue confined to punitive scar border zone regions. Bipolar amplitude range of 0.5 to 1.5 millivolts.                                                 The authors concluded that combined bipolar and unipolar voltage mapping with optimal thresholds may permit delineation of intramyocardial adipose dense regions of myocardium following infarction.                                                 In the next article by Kevin Leong and Associates, the authors examined the substraight in electrophysiologic mechanisms that contribute to the characteristic ECG of Brugada syndrome. The authors studied 11 patients with concealed type 1 Brugada syndrome and 2 healthy controls by performing noninvasive electrocardiographic imaging, or ECGI, and ECG recordings during an Ajmaline infusion.                                                 Following Ajmaline infusion the right ventricular outflow tract had the greatest increase in conduction delay and activation recovery interval prolongation compared to the right ventricle or the left ventricle. In controls there was minimal change in the JST point elevation, the conduction delay, or activation recovery intervals at all sites with Ajmaline.                                                 In Brugada syndrome patients, conduction delay in right ventricular outflow tract, but right ventricle or left ventricle correlated with a degree of JST point elevation. Pearson R 0.81.                                                 No correlation was found between the JST point elevation and activation recovery interval prolongation in the right ventricular outflow tract the right ventricle or the left ventricle.                                                  The authors, therefore, concluded that the degree of conduction delay in the right ventricular outflow tract and not prolongation or re-polarization time accounts for the ST or J-point elevation seen in type 1 Brugada syndrome pattern.                                                 In the next article by Jonas Diness and Associates, the authors investigate the role of inhibition with small conductance calcium activated potassium channels in atrial fibrillation termination.                                                 Since these channels are predominately expressed in the atria compared to ventricles, they are a particularly attractive drug target. With a total of 43 pigs atrial tachy pacing was performed until they developed sustained atrial fibrillation that could not be reverted by vernakalant administration.                                                 After the SK channel inhibitor AP14145 was administered, vernakalant resistant AF reverted to sinus rhythm and could not be re-induced by burst pacing. In open chest pigs both vernakalant and AP14145 significantly prolonged atrial refractory of this and reduced AF duration without affecting the ventricular refractory in this or blood pressure.                                                 The authors concluded that SK currents played a role in porcine atrial repolarization and their inhibition by AP14145 demonstrates an arrhythmic affects in a vernakalant resistant porcine model of atrial fibrillation.                                                 In our final article by Padmini Sirish and Associates, the authors examined the role of several ion transporters in action potential duration in cardiac function. The solute carrier SIC26A6, which is highly expressed in cardiomyocytes plays an important role in cardiac intracellular pH regulation.                                                 Using the SIC26A6 knockout mice, the authors found that ablation of SIC26A6 results in action potential shortening, reduced calcium transients, reduced sarcoplasmic reticulum calcium load, and decreased sarcomere shortening in the SIC26A6 knockout cardiomyocytes.                                                 Ablation of the SIC26A6 reduced fractual shortening and cardiac contractility in vivo. Intracelluar pH regulation is elevated in the SIC26A6 knockout cardiomyocytes consistent with the chloride bicarbonate exchange activities of SIC26A6.                                                 The SIC26A6 knockout mice exhibited bradycardia and fragmented QRS complexes supporting the role of SIC26A6 in the cardiac conduction system, therefore, the authors provided evidence that the role of SIC26A6 cardiac electrogenic chloride bicarbonate transporter in ventricular myocytes as well as intracellular pH regulation, excitability, and contractility.                                                 That's it for this month, but keep listening.  Suraj Kapa will be surveying all journals for the latest topics of interest in our field. Remember to download the podcast "On The Beat." Take it away Suraj. Suraj Kapa:                          Thank you very much Paul and welcome everybody back to "On The Beat," where we'll review hard hitting articles across the electrophysiologic literature. It is my pleasure to introduce you to 15 different articles published in the past month of September across all the journals in cardiovascular medicine.                                                 The first area that we will be focusing on is atrial fibrillation with a specific focus within the realm of anticoagulation, and we refer you to a paper published by [Kurshida Doll 00:16:55], entitled "Factors Associated With Anticoagulation Delay Following New-Onset Atrial Fibrillation," published in The American Journal Of Cardiology on October 15, 2017.                                                 In this publication Kurshida Doll, reviewed the frequency with which there is a delay in introduction of oral anticoagulation after a new diagnosis of atrial fibrillation, and the impact on overall outcomes. In a large electronic medical record they identify incident episodes of atrial fibrillation between 2006 and 2014.                                                 They used the CHADS2 score rather than the CHADS-VASc score to estimate overall risk, and then after this they reviewekud the outcomes of the patients. They found for those patients in whom oral anticoagulation would have been recommended, the median time to initiation was around five days, with an interquartile range of 1 to 43, with by far most patients receiving Warfarin with about 86%.                                                 Interestingly, about 98 strokes occurred between the time of new atrial fibrillation diagnosis, and the actual initiation of oral anticoagulation. Several factors led to this delay in oral anticoagulation including female gender, absence of hypertension, prior falls, and the presence of chronic kidney disease.                                                 However, ultimately, by 6 months over 90% of patients were on oral anticoagulants appropriately, though still a slightly higher proportion appropriately in men than woman.                                                 They noted that most patients with new diagnosis of atrial fibrillation and noted to have an elevated stroke risk started on oral anticoagulation within 1 week. Given these findings it is important to consider how we wait to introduce oral anticoagulation into patients after initial diagnosis given many initial diagnoses may be made by internists, or even in some cases by the patient themselves on a remote monitor or an ambulatory monitor it is important to consider how they are tied into the individual, who would feel most comfortable and who's most apt to prescribe oral anticoagulation.                                                 Changing gears within atrial fibrillation we next move on to cardiac mapping and ablation, and specifically focus on a paper published by Black-Maier et al, in the September edition of "Heart Rhythm" entitled "Risk Of Atrioesophageal Fistula Formation With Contact Force-Sensing Catheters."                                                 While atrioesophageal fistula formation is a relatively rare complication of atrial fibrillation ablation it can be life threatening, contact force catheters for ablation of atrial fibrillation have come into vogue as they are felt to improve procedural effectiveness and potentially reduce complications by improving individual understanding of contact with the myocardium and when contact is excessive.                                                 However, there's been little exploration of the actual risk of atrioesophageal fistula. An [inaudible 00:19:50] from the association they refused the mod database or the manufacturer and user facility device experience database for adverse event reports.                                                 Amongst almost 27,000 device reports they identified a total of 78 atrioesophageal fistula cases. About 1,200 of the reports were related to contact force-sensing catheters and about almost 1,500 were related to non contact force sensing catheters.                                                 Of the 78 atrioesophageal fistula cases reported the vast majority were the contact force-sensing catheters with a total number of 65, or about 5 times more than with non contact force-sensing catheters.                                                 Unfortunately, esophageal temperature increases were only mentioned in about 2.5% of cases in contact force and power settings were not consistently reported in order to come to any conclusions. They noted the overall mortality with atrioesophageal fistula in this population was around 56%, with really the vast majority surviving as a result of surgical repair as apposed to stenting or no intervention.                                                 While this data is somewhat skewed because it's based on self reported data by proceduralists, who are reporting back to the mod database, it is important to consider whether or not there is actually an increase complication rate associated with contact force-sensing catheters as these catheters do reflect a fundamentally different catheter than the non contact force-sensing catheters routinely used due to changes in the stiffness, and the mechanics of the catheter itself.                                                 It is important to consider when using any new catheter with any new options for monitoring, or that might alter the stiffness, or other mechanical properties of the catheter, whether or not application of similar power settings are relevant.                                                 While the data is potentially skewed in the status set it will be important to consider it going forward as to whether or not there are implications of some increased risk of complications, and how to mitigate these by altering our contact force and power setting decision making.                                                 Further study will be required in order to better understand these data and the implications. I would refer the readers also to an article published by [inaudible 00:22:02] in circulation where they reviewed the mechanism of atrioesophageal injury and also to another publication published in The Journal Of Cardiovascular Electrophysiology this past month by [inaudible 00:22:11], where they did a meta analysis of the overall benefit of contact force related catheters over non contact force related catheters.                                                 In that paper they demonstrated that based on this meta analysis there seems to be an overall benefit in terms of outcomes in contact force-sensing catheters without a difference in procedural complications. However, I would refer the reader to the fact that there are very limited randomized studies comparing contact force versus non contact force catheters.                                                 Next, also within the realm of cardiac mapping and ablation we reviewed a publication by Haldar, et al., entitled Resolving Bipolar Electrogram Voltages During Atrial Fibrillation Using Omnipolar Mapping, published in the last edition of Circulation Arrhythmia Electrophysiology. Also, reviewed by Dr. Wang in last months podcast.                                                 The importance of this article lays in an improved understanding of what we mean when we talk about voltage or substraight mapping. In his paper, Haldar, et al., tried to understand better what the bipolar electrogram might actually refer to when comparing traditional bipolar mapping versus omnipolar mapping.                                                 This becomes important as we consider a low voltage guided substraight modification for not just atrial fibrillation ablation, but also potentially for ventricular arrhythmia ablation. They sought to compare the use of peak-to-peak voltage for assessment of bipolar voltage with omnipolar peak-to-peak voltages in both sinus rhythm and atrial fibrillation.                                                 They demonstrated that in canines vertical orientation of a catheter relative to the underlying tissue consistently resulted in a higher bipolar voltage in both sinus rhythm and atrial fibrillation. Furthermore, they show that the max obtained ominipolar voltage were consistently larger than multi-horizontal and vertical voltages in both rhythms.                                                 Vector field analysis of these wave fronts during atrial fibrillation in particular, demonstrated the omnipolar electrograms can account for a collision in fractionation, and required an electrogram of voltages independent of these effects. Thus, they suggested that the omnipolar electrograms can use maximum voltages, and can separate the influence from directional factors, collision, or fractionation especially when compared with contemporary bipolar techniques.                                                 The implications of the study are several. First off, when performing substraight mapping we traditionally use what we can in terms of trying to get appropriate bipolar signal analysis. However, catheters have significantly evolved since the early studies of bipolar voltage mapping in terms of establishing voltage cutoffs.                                                 There are many different multipolar catheters with varying interelectrode spacing, but sometimes prefer parallel orientation to the underlying myocardium as opposed to vertical orientation. The fact that bipolar voltage can significantly vary based on both orientation of the catheter as well as the rhythm is important when considering whether a substraight actually exists in a specific location or not, and what "Normal voltage cutoffs," where specific patients should be."                                                 When we consider novel catheters with increasing complex design including introduction of mini electrodes as well as omnipolar electrodes, it is important to consider whether an assessment of "Normal voltage," should be the same. Further study will be required to better understand how to best analyze these results.                                                 Moving to a different form of management in atrial fibrillation we will next refer you to a paper by Borris [Madal 00:25:44] published in this last month's edition of Heart Rhythm, entitled Efficacy and safety of left atrial appendage closure with WATCHMAN in patients with or without contraindication to oral anticoagulation, 1-Year follow-up outcome data of the EWOLUTION  trial.                                                 The EWOLUTION trial was a prospective multi center registry looking at the outcomes of WATCHMAN patients, who had indication for closure based on European society of cardiology guidelines. They sought to evaluate a 1 year followup of these patients.                                                 The baseline CHADS-VASc score was on average about 4-1/2 with a mean age of over 73 years. Almost a third of the patients had prior transient ischemic attach or ischemic stroke. They noted that the vast majority of the patients had a successful WATCHMAN implantation with a 1,005 out of 1,025 patients having successful implantation, with only 3 of these 1,005 patients having any leak greater than 5 millimeters.                                                 The majority up to 87% had T-followup at least once after initial implantation. Interestingly, the vast majority only used antiplatelet therapy with only 8% having vitamin K antagonist used in the post WATCHMAN implantation period.                                                 There was a reasonably high mortality of 10% in the first year after implantation, though this was felt to typically reflect advanced age and other comorbidities. Also, interestingly almost 4% of patients had thrombus on their device, which was independent of the drug regimen used. In other words whether antiplatelet therapy or vitamin K antagonists.                                                 Overall, the ischemic stroke rate was relatively low at 1.1%, with a relative risk of 84% versus estimated historical data, and also with a relatively low major bleeding rate of only 2.6% and this predominately being non-procedure of device related.                                                 Thus, they concluded that LA closure with the WATCHMAN device had a high implant and sealing success, and it appeared to be safe and affective in reducing ischemic stroke risk given that the relative incidence was only 1.1%, despite the fact that the vast majority were not actually even using oral anticoagulation.                                                 There are trial ongoing in the United States to evaluate whether or not patients can be safely kept off of oral anticoagulation in the peri-implant period as in some countries standard of care is to place them on anticoagulants in the immediate post implantation period.                                                 However, two other things need to be noted in this real world analysis of outcomes with WATCHMAN. Almost 10% or 1 out of 10 patients died within 1 year of followup, thus whether or not better patient selection is required to understand those patients will receive maximal benefit from this invasive procedure might be considered.                                                 Further, more almost 4% had device related thrombus. What this means in terms of stroke risk especially over longterm followup needs to also be considered. I think overtime we'll get better understanding of what those risks might be for an endocardial system for a left atrial appendage occlusion.                                                 But, staying within the realm of stroke risk in atrial fibrillation, we next review the article by King, et al., published in The Journal Of American College Of Cardiology, in the September 2017 edition entitled, Left Atrial Fibrosis and Risk of Cerebrovascular and Cardiovascular Events in Patients With Atrial Fibrillation.                                                 Cardiac MRI to evaluate late gadolinium enhancements suggesting regional cardiac fibrosis and atrial fibrillation is slowly taking steam, but primarily as a method of assessing potential efficacy of atrial fibrillation ablation with greater amounts of delayed enhancement potentially suggesting an overall lower risk, or a lower likelihood of success of atrial fibrillation ablation.                                                 King, et al., sought to evaluate in a retrospective cohort study regarding the risk of cerebrovascular and cardiovascular major events associated with a degree of delayed enhancement in MRI. They reviewed 1,228 patients undergoing cardiac MRI to assess left atrial fibrosis between 2007 and 2015.                                                 They then staged these patients and stratified them according their [Utah 00:29:45] stage, which had been previously recorded for the degree of fibrosis seen. They demonstrated on followup that there was a significantly higher incidence of major cardiovascular and cerebrovascular events associated with higher degrees of late gadolinium enhancement with a relative risk ratio of about 1.67.                                                 However, the only individual component of these outcomes that remains significantly associated with advanced gadolinium enhancement was actually stroke or TIA, with a hazard ratio of 3.94, thus they concluded that severe LA late enhancement is associated with increased cerebrovascular events principally.                                                 This study is important in that it highlights another potential risk factor that may need to be considered when risk stratifying patients for their risk of stroke. We recognize that even some paroxysmal patients can have extensive left atrial fibrosis, and some persistent patients might not have a ton of atrial fibrosis.                                                 Whether this can further help risk stratified patients in terms of overall stroke risk, and might identify and help characterize low risk patients further needs to be considered.                                                 One of the key features of this evaluation needs to be also the mechanism. In theory patients with greater endocardial injury of the atrium might be more prone to clot formation, and thus it may seem reasonable to expect indeed when we have more left atrial fibrosis as suggested by delayed enhancement on MRI. There may in fact be a higher greater cerebrovascular event rate.                                                 Finally, changing gears a little bit within the realm of risk stratification and management for atrial fibrillation we focused on autonomics and specifically a publication by Stavrakis et al., in the last month edition of Jack Clinical Electrophysiology, entitled Low Level Vagus Nerve Stimulation Suppresses Postoperative Atrial fibrillation And Inflammation In A Randomized Study.                                                 The group, headed up by Sonny [Poe 00:31:42] have previously published on both tragus stimulation as well as low level of vagus nerve stimulation in patients undergoing atrial fibrillation ablation. In this particular study they sought to evaluate whether or not implantation of a low level of vagus nerve stimulator during cardiac surgery could reduce the risk of postoperative atrial fibrillation.                                                 They sutured a bipolar wire to the vagus nerve preganglionic fibers along the lateral aspect of the superior vena cava at the time of surgery. They then performed high frequency stimulation of 50% below the threshold for slowing the heart rate for 72 hours, and those randomized to the vagus nerve stimulation group.                                                 The secondary group was a sham cohort. They demonstrated amongst the 54 patients randomized to either group that the frequency of postoperative atrial fibrillation was almost a third in the low level of vagus stimulation group when compared with the control group.                                                 Interestingly, their frequency of atrial fibrillation was not only lower, but the level of inflammatory markers also decreased with both serum tumor necrose factor alpha and interleukin 6 levels being significantly lower in the low level vagus nerve stimulation cohorts.                                                 In line with prior data from atrial fibrillation ablation these data were suggesting that low level of vagus nerve stimulation can suppress postoperative atrial fibrillation and attenuate the inflammatory response.                                                 Also, in this past month there was a paper by [Yoo 00:33:09] et al., in The Journal Of The American Heart Association, specifically looking at the use of vagus nerve stimulation at the level of the tragus in patients with obstructive sleep apnea associated atrial fibrillation.                                                 Similar to prior work form the Oklahoma group, they demonstrated that in fact there is a beneficial effect on reduction of atrial fibrillation, and this is primarily mediated through attenuation of autonomic factors that mediate obstructive sleep apnea related atrial fibrillation.                                                 Moving away from atrial fibrillation, we next delve in cellular physiology first starting with an article published in Nature Scientific Report this past month, on very low density lipoprotein in metabolic syndrome, and how it modulates gap junctions and slows cardiac conduction.                                                 In the past year there have been multiple studies regarding specific cell types and how they might interplay with cardiac fibrosis, and risk of conduction slowing. In this publication we had all reviewed the effect of very low density lipoproteins, and their effect on cardiac conduction in, in vitro models.                                                 They demonstrated that primarily through down regulation of [conexion 00:34:21] 40 and conexion 43, very low density lipoproteins have significant impact on cardiac conduction with increased prolongation of the P-wave, PR-intervals, QR restoration, and QTC intervals.                                                 Thus, they concluded that very low density lipoproteins may contribute to the path of physiology of both atrial fibrillation and ventricular arrhythmias that can be seen in metabolic syndrome. This report is important because it highlights the fact that we can actually see other cell types including LDL causing a significant reduction in cardiac conduction and thus mediating arrhythmogenesis.                                                 In fact there was one other paper published just a couple weeks prior also in The Nature Of Scientific Reports by [Lee 00:35:04] et al., entitled Human Electronegative Low-Density Lipoprotein Modulates Cardiac Repolarization Via LOX-1-Mediated Alteration Of Sarcolemmal Ion Channels.                                                 They showed that LDL can actually result in QTC prolongation in patients with ischemic heart disease by specific mechanisms involving LOX-1. Recognition of the mechanisms behind which less traditional factors such as VLDL or LDL may mediate alterations in cardiac conduction are important when we consider our potential novel targets for treatment of arrhythmias in patients whether for prevention or for treatments.                                                 In light of this attempt to identify novel targets we next move on to another paper in the realm of cellular electrophysiology published by [Toib 00:35:52] et al., in The American Journal of Physiology, Heart and Circulatory Physiology, entitled Remodeling Of Repolarization And Arrhythmia Susceptibility In A Myosin-Binding Protein C Knockout Mouse Model.                                                 In hypertrophic cardiomyopathy there might be multiple mechanisms that might lead to increased risk of ventricular arrhythmias. These might be scar related due to the fact that patients can burn out from the hypertrophic cardiomyopathy overtime and get both endocardial, epicardial, and mid myocardial fibrosis, but what are the mechanisms that might mediate the development of ventricular arrhythmias and hypertrophic cardiomyopathy remain to be elucidated, and there's been very limited evaluation of the effect of repolarizing potassium currents on this risk.                                                 Thus, Toib, et al., studied myosin-binding protein C knockout mice to look at what happens with repolarizing potassium currents in his cohorts. They demonstrated that in these knockout mice there was a prolongation in the corrected QT interval when compared to the wild type mice with overt ventricular arrhythmias.                                                 They also demonstrated that there is action potential prolongation associated with a decrease for polarizing potassium currents, and a decreased MRNA levels of several key potassium channels subunits, thus, they concluded that in this specific subtype of hypertrophic cardiomyopathy needed by myocin combining protein C mutations that part of the ventricular arrhythmia risk might be due to a decrease in polarizing potassium currents in turn leading to increase in action potential and QT interval.                                                 The reason that this particular finding is important is in my highlight drug selection in specific types of hypertrophic cardiomyopathy. In my postulate for example the class 3 antiarrythmics drugs might actually increase risk in some subtypes of hypertrophic cardiomyopathy due to down regulation of potassium channel subunits.                                                 Consideration of this is critical when best evaluating how to mange and treat these patients. Changing gears to another method of channelopathy we focus within the realm of genetic channelopathies and specifically on Brugada syndrome.                                                 In this last month's edition of Heart Rhythm, Sierra, et al., published their series of longterm prognosis of drug induced Brugada syndrome. They reviewed a consecutive cord of 343 patients with drug induced Brugada syndrome, and compared their outcomes with 78 patients with a spontaneous type 1 pattern.                                                 The mean age of patients was around 41 years. Interestingly, about 4% of the patients had a clinical presentation of 7 cardiac deaths, and 25% had a clinical presentation of syncope. However, the majority of the patients were asymptomatic, around 71%.                                                 Most of the patients were female amongst the drug induced Brugada syndrome cohort. They demonstrated that there were less ventricular arrhythmias both induced string and electrophysiology study, and seen over followup of up to 62 months in the drug induced Brugada syndrome cohort as compared with the spontaneous type 1 cohort.                                                 Overall, the event rate in drug induced Brugada syndrome was 1.1% of [person year 00:38:54] versus 2.3% of person year in patients with spontaneous type 1 pattern.                                                 They suggested that presentation of sudden cardiac death or inducable ventricular arrhythmias at the time of VP study were independent risk factors associated with arrhythmic events in drug induced Brugada syndrome. However, if a patient was asymptomatic and had no inducible ventricular arrhythmias they had a significantly better prognosis with drug induced Brugada syndrome over a spontaneous type 1 pattern.                                                 Thus, they concluded that even in drug induced Brugada syndrome sudden cardiac death is possible. However, in asymptomatic patients without a prior clinical presentation of sudden cardiac death or inducible ventricular arrhythmias during electrophysiology study, they may be relatively safer than their spontaneous type 1 counterparts.                                                 This study highlights the importance of stratification of patients into the mechanism of how their genetic channelopathy presents whether as a spontaneous finding or as a finding in the setting of other events. Further prospective analysis, however, is needed to best guide how to manage these patients and in whom to put a defibrillator as I would note that almost 37% of these patients actually had an ICD placed with the vast majority without incident events.                                                 Speaking of implantable devices we next move to the realm of ICD pacemaker and CRT, and specifically we review the publication by Samar, et al., published in Jack Clinical Electrophysiology this past month on the diagnostic value of MRI in patients with implanted pacemakers and implanted cardiover defibrillators across the population.                                                 Does the benefit justify the risk of proof of concept study? Increasingly, MRIs are being done in patients with even Legacy defibrillators and permanent pacemakers. However, when assessing the benefit versus the risk it's important to understand did the MRI actually change outcomes, and this was a specific question that the authors tried to answer.                                                 They took patients with conventional or Legacy pacemakers or ICDs, and tried to evaluate what the actual benefit was on those patients in whom an MRI was done. They specifically asked four questions, one, did the primary diagnosis change, two, did the MRI provide additional information to the existing diagnosis, three, was the pre-MRI or tentative diagnosis confirmed, and four, did the patient management change?                                                 They noted there were no safety issues encountered in any of the 136 patients an MRI was performed. In 97% it was felt that MR added value to the patient diagnosis and managements, with 49% of investigators feeling that MR added additional valuable information to the primary diagnosis, and in nearly a third the MR actually changing the principle diagnosis and subsequent management of the patient.                                                 Increasing evidence suggesting that MRI can be safely performed even in Legacy pacemakers and ICDs, and the fact the MRI can wield important evidence related to diagnostics needs to be taken into consideration as investigators and other centers try to identify methodologies for safely performing MRIs in these patient cohorts.                                                 It seems thus far like MRI might justify risk of these procedures under controlled settings. Next, we move also within the realm of implantable cardioverted defibrillators, but to a different assessment published by Kawada et al., in this past months issue of Heart Rhythm where they sought to evaluate the comparison of longevity in clinical outcomes of implantable cardioverted defibrillator leads among manufacturers.                                                 They specifically sought to assess the longevity of [Lynox 00:42:35] SSD by [Atronic 00:42:36] leads compared with Sprint Fidelis by Matronic, Sprint Quattro by Matronic, and Endotac Reliance by Boston Scientific Leads. The reasoning for this was early failure of some of the biotronic Lynox leads has been reported. Thus, they retrospectively reviewed patients undergoing implantation with these different lead approaches between 2000 and 2013.                                                 They noted failure rates of the Lynox versus Spring Fidelis versus Endotac leads where 3.2% for a year, versus 3.4% for a year, versus 0.61% for a year respectively. No lead failure was notable with a followup [inaudible 00:43:13] in Sprint Quattro leads, thus, they felt that the survival probability of Lynox leads was comparable to Sprint Fidelis leads, and lower than that of Endotac or Sprint Quattro leads.                                                 They found that age was the primary predictor of Lynox lead failures with the patients less than 58 years old had significantly increased risk of lead failure compared with those greater than 58 years old, thus, they concluded that this was a first description of a lower survival rate for Lynox leads in an aging population.                                                 Early identification of leads that might be at risk of failure is critical in patient risk stratification. The finding that there might be other leads that might be at risk of failure highlights the importance of close monitoring of these leads in contribution to register data.                                                 I would note that within this study that it was primarily done at one center and the vast majority of patients actually received Lynox leads. Thus, further evidence was clinically required for more centers to understand what the mechanism of this risk is, and also whether the risk is born out consistently across multiple centers particularly because the vast minority got the one lead, but didn't have any lead failure encountered for.                                                 Further, speaking about defibrillators we focus on the different mechanism of failure, and specifically the publication by [Thogersen 00:44:38] et al., published in last months' edition of Circulation And Arrhythmia Electrophysiology entitled Failure To Treat Life Threatening Ventricular Tachy Arrhythmias In Temporary Implantable Cardioverted Defibrillators Implications For Strategic Programming.                                                 In this publication they did not so much focus on lead failure, but the failure the ICD due to potential strategic programming decision making on appropriately treating ventricular tachy arrhythmias. Their current consensus recommendations as far as using a generic rate threshold between 185 and 200 beats per minutes in primary prevention ICD patients, thus, they sought to determine in the case series what the relationship between program parameters and failure of modernizing ICDs to treat for VF actually worked.                                                 Between 2015 and 2017 at four institutions they reviewed cases where normally functioning ICDs failed to deliver timely therapy for VF. There were a small number of patients noted fitting this criteria with only 10 ambulatory patients. Five actually died from their untreated VF, whereas four had cardiac arrests through a witness requiring external shocks, and one was ultimately rescued by a delayed ICD shock.                                                 The main reason that they were not appropriately treated were that the ventricular fibrillation event did not satisfy the programmed detection criteria in nine out of ten patients. Seven of the patients had the slowest detection rates consistent with generic recommendations, but were never tested in the peer review trial for the manufacturers ICDs.                                                 Namely, the decision making on the appropriated generic rate threshold was tested on specific manufacturers ICDs, but didn't apply the decision making on programming on other manufactures ICDs. In some cases manufacturers specific factors were interacting with fast detection rates to withhold therapy such as enhancement in MIC wave oversensing.                                                 Thus, they demonstrated that in this population untreated VF despite recommendation programming, accounted overall for 56% of sudden deaths and 11% of all deaths in the overall cord of patients during the study period.                                                 Thus, over half of the cases where sudden death occurs in patients with ICDs appears to be due to untreated VF despite recommended programming. Thus, they concluded that these unanticipated interactions or complex decision making regrading generic program of parameters might in part lead to withholding of therapy inappropriately in ventricular fibrillation.                                                 This publication highlights the importance of thoughtful decision making when translating evidence based detection parameters both between manufacturers and applying them across individual patients.                                                 While the overall number of patients is quite low, mainly only ten patients who were affected by this event, the number of patients dying as a result of it is fairly high in terms of a percentage with 56% of sudden deaths occurring as a result of untreated VF from variation from recommended programming.                                                 Closer attention needs to be paid to understanding how to better assess which patients would benefit from the current generic rate thresholds as opposed to who will be harmed by it. It is possible that one size fits all approach will always result in some harm to some, while benefit to others as potentially cutting down the lower rate cutoff in some patients might lead to inappropriate therapies, which might be as life altering as untreated VF in many patients.                                                 Finally, keeping within the realm of defibrillation we review an article by [Layva 00:48:24] et al., published in last month's edition of The Journal of American College of Cardiology entitled Outcomes of Cardiac Resynchronization Therapy With or Without Defibrillation in Patients With Nonischemic Cardiomyopathy.                                                 There are several recent studies that have started to cast doubt on what the incremental benefit of defibrillation adage cardiac resynchronization therapy actually is in nonischemic cardiomyopathy.                                                 However, we also know that in patients with scar noted on MRI that there can be an increased risk of ICD therapy, thus, part of the difficulty that some individuals have is how we define the nonischemic cardiomyopathy cohorts. Namely, is all nonischemic cardiomyopathy crated equal and we can better risk stratify this population to subtypes some of whom might benefit from primary correction defibrillators and some of whom might not?                                                 Thus, in this study they aimed to determine whether CRTD is superior to CRTP in patients with nonischemic cardiomyopathy based on the presence or absence of left ventricular midwall fibrosis detected by cardiac magnetic resonance.                                                 There were a total of 68 patients who had midwall fibrosis, and 184 patients who had not, and all of them underwent the evaluation prior to CRT implantation. They noted that the presence of midwall fibrosis was an independent predictor of total mortality with a hazard ratio of 2.31 as well as total mortality or heart failure hospitalization.                                                 This sudden cardiac hazard ratio was about 3.75 with an increased risk attributable to the presence of midwall fibrosis. They also noted that total mortality or heart failure hospitalization, and total mortality or hospitalization for major adverse cardiac events was significantly lower in patients with CRT defibrillator than with CRT pacemaker in those with midwall fibrosis, but not in those without midwall fibrosis.                                                 These findings highlight that in some patients with nonischemic cardiomyopathy CRTD may be superior to CRTP, though these might be guided by the presence of abnormal substraights. The evaluation of what nonischemic cardiomyopathy means in an individual patient needs to be closely considered.                                                 Nonischemic cardiomyopathy is a blanket term for all those patients who do not have an ischemic cardiomyopathy and who may or may not have been fully evaluated for discrimination of another type of myopathy such as infiltrated myopathies for example sarcoidosis.                                                 The value of cardiac magnetic resonance imaging is being increasingly understood as it applies to both risk stratification, nonischemic cardiomyopathy, as well as the value in decision making as far as treatment of these patients. In a recent publication published this past month as well in Jack Electrophysiology, by [inaudible 00:51:13], et al., they reviewed the efficacy of implantable cardioverted defibrillator therapy in patients with nonischemic cardiomyopathy based on a meta analysis of existing trials.                                                 They demonstrated in a meta analysis of randomized controlled trials that compared to medical therapy ICD has significantly improved survival among patients with nonischemic cardiomyopathy with an injection fraction of less and equal to 35%. However, CRT defibrillator overall was not associated with statistically significant mortality death when compared to CRT pacemaker.                                                 These findings are actually complimentary to each other, but need to be considered in context. One of the indications for the recently published Danish study was the fact that not only is CRT being increasingly utilized appropriately in patients with nonischemic cardiomyopathies, but also guideline directed medical therapy has improved over the course of the last several years since the initial trials of defibrillator therapy as primary prevention.                                                 Furthermore, the trial was actually powered based on a 25% reduction in overall events. Thus, even if there's a smaller benefit it would not necessarily be powered to identify if this is statistically significant. One issue as stated is the fact that nonischemic cardiomyopathy might be a milieu of different causes in individual patients. Some of whom might be at high risk for sudden cardiac death and some of whom might not.                                                 The publication by Levya, et al., highlights that better attempts at risk stratification on the basis of either MRI or other modalities might be important in helping us further assess who actually benefits from ICD, however, when mixing in prior trials with more recent trials that existed at different areas of medical therapy, and different areas of appropriate use of devices such as CRT it is critical to consider whether or not the same cutoffs, the same power calculations still apply.                                                 It is doubtless that defibrillator therapy is needed in many patients with both ischemic and nonischemic cardiomyopathy even with improved therapies for these patients otherwise. However, this multitude of publications coming out to improve our assessment of the utility of ICDs should not necessarily call into question of whether or not ICDs are merited at all, but should call into question whether we understand and have come to the best form of risk stratification for those patients who would most benefit, and thus this is an opportunity for us to identify those patients better.                                                 Next, we will move to the realm of supraventricular tachycardia's and specifically an article published by [Yang 00:53:41], et al., in the last month's edition of Heart Rhythm, entitled Focal Atrial Tachycardia's From The Parahisian Region, Strategies From Mapping And Cather ablation.                                                 With focal atrial tachycardia's from the parahisian region can potentially be targeted from multiple different regions, the right atrial septum, the noncoronary cusp, and the right middle septum. However, the optical mapping and ablation strategy for these arrhythmias remains unclear, and thus they sought to investigate electrophysiology characteristics in optimal ablation sites for parahisian [inaudible 00:54:10] from these different areas.                                                 They reviewed 362 patients with atrial tachycardia's undergoing catheter ablation. They did DCG analysis and electrophysiology studies extensively on these patients. Overall, 91 patients had a parahistian origin. An ablation was successful in a majority of these up to 94.5%.                                                 The majority of these patients had their AT successfully eliminated from the noncoronary cusp with about 44 of the 91 having it targeted from this region, with the remaining 23 from the right atrial septum, and 19 from the right middle septum. They noted those who had an earliest potential at the distal HIS catheter tended to have their site of origin more successfully ablated from the noncoronary cusp.                                                 However, those with a greater [inaudible 00:54:55] in the proximal HIS catheter tended to more likely have successful ablation from the right atrial septum or right middle septum. The mean timing of the A potential in differentiating right and middle septum ATs from right atrial septum ATs, was that they attended to be later in right middle septum ATs, than right atrial septum ATs, or noncoronary cusp ATs.                                                 They noted that for atrial tachycardia's arising from the right atrial septum and right middle septum, an A to V ratio less than 1.22 predicted safe and successful ablation with a sensitivity of 88.4% and the specificity of 91.7%. Thus, they concluded that activation sequence and timing of the A and HIS catheter could provide clues for where the most likely successful site of ablation would occur for parahisian tachycardia's.                                       

This episode covers chapter 82 of Rosen's Emergency Medicine. Take a listen for all those juicy pericardial-pump-pearls!   List eight causes of pericarditis. Describe typical pain of pericarditis, expected lab work abnormalities, What is the typical sequence of ECG changes in pts with pericarditis? (the stages) Describe the treatment of pericarditis associated with: Uremia, Neoplasm, and SLE Outline the management of Dressler's syndrome. What is the pathophysiology of cardiac tamponade? Describe the mechanism of hypotension in pericardial tamponade and list 4 expected findings on physical examination. Describe the procedural steps in pericardiocentesis List 4 causes of pneumopericardium and one specific PEX finding List five causes of constrictive pericarditis. What is the pathophysiology of purulent pericarditis?  List 5 organisms responsible for infectious pericarditis? How is it managed? Describe the pathophysiology of hypertrophic cardiomyopathy Describe the clinical exam and ECG findings associated with HCM List 5 RFs for sudden death in HCM A pt with known hypertrophic cardiomyopathy presents to the ED with acute cardiogenic pulmonary edema causing mild hypoxia.  What is the general approach to management in the ED?  Explain your choices. List four causes of dilated cardiomyopathy. Describe ECG findings of dilated cardiomyopathy List 5 RFs for developing a dilated cardiomyopathy In what time frame would one expect peripartum DCM? List 5 causes of restrictive cardiomyopathy List 8 common pathogens responsible for myocarditis, and 3 non-infectious causes of myocarditis Describe the stages of viral myocarditis and the management at each stage     Wisecracks:   What are some functions of the pericardium? What are Chagas Disease and Trichinosis, list bizz-buzz features for each? What are the expected cardiac findings in Lyme disease and how is it treated? How does sarcoid affect the heart? Amyloidosis?  

This episode covers chapter 82 of Rosen's Emergency Medicine. Take a listen for all those juicy pericardial-pump-pearls!   List eight causes of pericarditis. Describe typical pain of pericarditis, expected lab work abnormalities, What is the typical sequence of ECG changes in pts with pericarditis? (the stages) Describe the treatment of pericarditis associated with: Uremia, Neoplasm, and SLE Outline the management of Dressler's syndrome. What is the pathophysiology of cardiac tamponade? Describe the mechanism of hypotension in pericardial tamponade and list 4 expected findings on physical examination. Describe the procedural steps in pericardiocentesis List 4 causes of pneumopericardium and one specific PEX finding List five causes of constrictive pericarditis. What is the pathophysiology of purulent pericarditis?  List 5 organisms responsible for infectious pericarditis? How is it managed? Describe the pathophysiology of hypertrophic cardiomyopathy Describe the clinical exam and ECG findings associated with HCM List 5 RFs for sudden death in HCM A pt with known hypertrophic cardiomyopathy presents to the ED with acute cardiogenic pulmonary edema causing mild hypoxia.  What is the general approach to management in the ED?  Explain your choices. List four causes of dilated cardiomyopathy. Describe ECG findings of dilated cardiomyopathy List 5 RFs for developing a dilated cardiomyopathy In what time frame would one expect peripartum DCM? List 5 causes of restrictive cardiomyopathy List 8 common pathogens responsible for myocarditis, and 3 non-infectious causes of myocarditis Describe the stages of viral myocarditis and the management at each stage     Wisecracks:   What are some functions of the pericardium? What are Chagas Disease and Trichinosis, list bizz-buzz features for each? What are the expected cardiac findings in Lyme disease and how is it treated? How does sarcoid affect the heart? Amyloidosis?  

Discussing the high yield pathophysiology of pericardial disease including acute pericarditis, constrictive pericarditis, and tamponade. We will hit the presentations, causes, diagnoses, and treatments of these important conditions.

TSRA Podcast: Cardiac - Pericardial Disease (Sahar Saddoughi and Hartzell Schaff) by TSRA

Pericardial and myocardial disease

Pearls, pitfalls and take home points from the NYU/Bellevue EM Residency weekly conference. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_9_0_Final.m4a Download Leave a Comment Tags: Pediatric Cardiology, Pericardial Tamponade Show Notes Vaillancourt S. et al. Repeated Emergency Department Visits Among ChildrenAdmitted With Meningitis or Septicemia: A Population-Based Study. Ann Emerg Med 2015; 65(6): 625-631. PMID: 25458981 EMCrit: Rapid Ultrasound for Shock and Hypotension – the RUSH Exam. Verma V et al. The utility of routine admission chest X-ray films on patient care. Eur J Intern Med 2011; 22(3): 286-8. PMID: 21570649 EMCrit: Opiate-Free ED with Sergey Motov Read More

Pearls, pitfalls and take home points from the NYU/Bellevue EM Residency weekly conference. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_9_0_Final.m4a Download Leave a Comment Tags: Pediatric Cardiology, Pericardial Tamponade Show Notes Vaillancourt S. et al. Repeated Emergency Department Visits Among ChildrenAdmitted With Meningitis or Septicemia: A Population-Based Study. Ann Emerg Med 2015; 65(6): 625-631. PMID: 25458981 EMCrit: Rapid Ultrasound for Shock and Hypotension – the RUSH Exam. Verma V et al. The utility of routine admission chest X-ray films on patient care. Eur J Intern Med 2011; 22(3): 286-8. PMID: 21570649 EMCrit: Opiate-Free ED with Sergey Motov Read More

Pearls, pitfalls and take home points from the NYU/Bellevue EM Residency weekly conference. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_9_0_Final.m4a Download Leave a Comment Tags: Pediatric Cardiology, Pericardial Tamponade Show Notes Vaillancourt S. et al. Repeated Emergency Department Visits Among ChildrenAdmitted With Meningitis or Septicemia: A Population-Based Study. Ann Emerg Med 2015; 65(6): 625-631. PMID: 25458981 EMCrit: Rapid Ultrasound for Shock and Hypotension – the RUSH Exam. Verma V et al. The utility of routine admission chest X-ray films on patient care. Eur J Intern Med 2011; 22(3): 286-8. PMID: 21570649 EMCrit: Opiate-Free ED with Sergey Motov Read More

In this VETgirl podcast, we review the diagnostic yield of cytologic analysis of pericardial effusion in dogs. Is it worth submitting fluid analysis and cytology for your hemorrhagic sample? The most common causes of canine pericardial effusion include neoplasia and idiopathic effusions. Coagulopathies, left atrial rupture, and septic pericarditis are much less common. Among neoplastic causes, cardiac hemangiosarcoma (typically right atrial or right AV groove) occurs most frequently followed by heart base tumors (chemodectomas), mesothelioma, and lymphoma. Prognosis for neoplastic causes is highly dependent on tumor type. Cytologic analysis is considered highly useful in providing a definitive diagnosis of infectious causes and cardiac lymphoma, but is of limited value in identifying other neoplastic causes. This is in contrast to the relatively high diagnostic ability of pericardial effusion cytology to identify neoplastic etiologies in humans (likely because of the types of neoplasia seen in humans). Additional testing of blood or pericardial parameters/biomarkers (Use of pericardial fluid pH to distinguish between idiopathic and neoplastic effusions. J. Vet. Intern. Med. 17 (4):525-529; 2003.

In this VETgirl podcast, we review the diagnostic yield of cytologic analysis of pericardial effusion in dogs. Is it worth submitting fluid analysis and cytology for your hemorrhagic sample? The most common causes of canine pericardial effusion include neoplasia and idiopathic effusions. Coagulopathies, left atrial rupture, and septic pericarditis are much less common. Among neoplastic causes, cardiac hemangiosarcoma (typically right atrial or right AV groove) occurs most frequently followed by heart base tumors (chemodectomas), mesothelioma, and lymphoma. Prognosis for neoplastic causes is highly dependent on tumor type. Cytologic analysis is considered highly useful in providing a definitive diagnosis of infectious causes and cardiac lymphoma, but is of limited value in identifying other neoplastic causes. This is in contrast to the relatively high diagnostic ability of pericardial effusion cytology to identify neoplastic etiologies in humans (likely because of the types of neoplasia seen in humans). Additional testing of blood or pericardial parameters/biomarkers (Use of pericardial fluid pH to distinguish between idiopathic and neoplastic effusions. J. Vet. Intern. Med. 17 (4):525-529; 2003.

Just diagnosis a peritoneal-pericardial diaphragmatic hernia (PPDH) incidentally on chest radiographs? Not sure if it need to be cut? PPDH is a developmental malformation that allows abdominal contents to slide through a hernia in the diaphragm directly into the pericardial sac. Clinical signs of PPDH, if there are any in your patient, can be attributed to compression of the heart by contents in the pericardial sac or adverse effects on the organs that are herniating. Check out this veterinary podcast to find out if medical versus surgical management is warranted!

Just diagnosis a peritoneal-pericardial diaphragmatic hernia (PPDH) incidentally on chest radiographs? Not sure if it need to be cut? PPDH is a developmental malformation that allows abdominal contents to slide through a hernia in the diaphragm directly into the pericardial sac. Clinical signs of PPDH, if there are any in your patient, can be attributed to compression of the heart by contents in the pericardial sac or adverse effects on the organs that are herniating. Check out this veterinary podcast to find out if medical versus surgical management is warranted!

Objectives: Pericardial adipose tissue (PAT) is associated with coronary artery plaque accumulation and the incidence of coronary heart disease. We evaluated the possible incremental prognostic value of PAT for future cardiovascular events. Methods: 145 patients (94 males, age 60 10 years) with stable coronary artery disease underwent coronary artery calcification (CAC) scanning in a multislice CT scanner, and the volume of pericardial fat was measured. Mean observation time was 5.4 years. Results: 34 patients experienced a severe cardiac event. They had a significantly higher CAC score (1,708 +/- 2,269 vs. 538 +/- 1,150, p < 0.01), and the CAC score was highly correlated with the relative risk of a future cardiac event: 2.4 (1.8-3.7; p = 0.01) for scores > 400, 3.5 (1.9-5.4; p = 0.007) for scores > 800 and 5.9 (3.7-7.8; p = 0.005) for scores > 1,600. When additionally a PAT volume > 200 cm(3) was determined, there was a significant increase in the event rate and relative risk. We calculated a relative risk of 2.9 (1.9-4.2; p = 0.01) for scores > 400, 4.0 (2.1-5.0; p = 0.006) for scores > 800 and 7.1 (4.1-10.2; p = 0.005) for scores > 1,600. Conclusions:The additional determination of PAT increases the predictive power of CAC for future cardiovascular events. PAT might therefore be used as a further parameter for risk stratification. Copyright (C) 2012 S. Karger AG, Basel

Mark Rosen, MD

The early diastolic sound of pericardial constriction occurs slightly earlier than the average third heart sound. Its frequency is somewhat higher, allowing you to hear it throughout the precordium using the diaphragm and the bell. Common causes of pericardial constriction include prior cardiac surgery and uremic pericarditis. Copyright 2011 by the Texas Heart Institute at St. Luke's Episcopal Hospital.