Rapid, irregular contraction of muscle fibers (typically of the heart)
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6 episodes with Fibrillation
3 episodes with Fibrillation
3 episodes with Fibrillation
2 episodes with Fibrillation
2 episodes with Fibrillation
2 episodes with Fibrillation
2 episodes with Fibrillation
2 episodes with Fibrillation
2 episodes with Fibrillation
We use our lunch hour to hang out with the best listeners out there. Going into a weekend of Winter Storms and lots of Football. Today we will talk about what is going to happen this season, why this new format will not work and finally, I'm going to pull some of my vinyl and show you what/and why I like what I like. Today is my Favorite Album of All Time, my favorite Album while in High School and My Favorite album out today.
Revoyez en 20 minutes avec Dr Jérôme Schwartz, cardiologue-rythmologue à Nancy, l'essentiel à savoir sur la fibrillation atriale et les nouvelles recommandations de l'European Society of Cardiology d'Août 2024. Au terme de ce podcast, vous aurez revu : ✅ Qui anticoaguler ? Nouveau score CHA2DS2-VA
Atrial fibrillation can be a tricky thing to manage in the ED. Sometimes it is not always clear if you should treat it, how you should treat it, or if it's even safe to treat. In this episode, Ray Isenburg and host Will Smith discuss the basics of AFib, how to treat it (both chemically and/or electrically), when is it safe to treat, and how to determine if this is something worth treating or if there is other pathology occurring that, once resolved, will resolve the heart rhythm.
Un nouveau podcast Ligne de MIR en collaboration avec la commission des Urgences Vitales de la SRLF ! Le Pr Guillaume Debaty, qui est urgentiste au SAMU de Grenoble, nous parle de la double défibrillation séquentielle. Aucun conflit n'est déclaré. Sommaire• Concepts physiologiques• Pour qui ? Comment ?• Les limites Références• Cheskes S, Verbeek PR, Drennan IR, McLeod SL, Turner L, Pinto R, et al. Defibrillation Strategies for Refractory Ventricular Fibrillation. N Engl J Med. 2022;387:1947-56.• Rahimi M, Drennan IR, Turner L, Dorian P, Cheskes S. The impact of double sequential shock timing on outcomes during refractory out-of-hospital cardiac arrest. Resuscitation. 2024;194.• Cheskes S, Drennan IR, Turner L, Pandit SV, Dorian P. The impact of alternate defibrillation strategies on shock-refractory and recurrent ventricular fibrillation: A secondary analysis of the DOSE VF cluster randomized controlled trial. Resuscitation. 2024;198.
4/13/24 - Host Doug Stephan and Dr. Ken Kronhaus of Lake Cardiology (352-735-1400) cover a number of topics, Including: the advantages of TeleHealth, how care of your teeth and gums can affect the possibility of Atrial Fibrillation, second-hand smoke found to increase the risk of Atrial Fibrillation, middle ageers need to get checked for Heart Disease, a regular exercise routine can provide Long Covid relief, a new AI Stethoscope is on the horizon, a recent study shows that there are no ill effects from taking Tylenol in pregnant mothers, younger generations are aging more rapidly than those born before 1950.
3/8/24 - Host Doug Stephan and Dr. Ken Kronhaus of Lake Cardiology (352-735-1400) cover a number of topics, Including: The miracle of a one year old girl who received a successful heart transplant, a new study shows that sweetened beverages can contribute to Atrial fibrillation, the FDA approves a non-evasive over-the-counter Glucose monitor, The FDA warns of fake eyedrops, Daylight Savings Time is ready to cause health issues again, Sleep apnea sufferers can expect health problems, too much Vitamin D can kill you, CDC says 5-day isolation period from COVID is no longer necessary.
The Plant-Based Bundle: 130+ ebooks and courses. $3,500+ total value. Only $50. Expires 11/27/23. https://bit.ly/chefajplantbasedbundle GET MY FREE INSTANT POT COOKBOOK: https://www.chefaj.com/instant-pot-download ------------------------------------------------------------------------------------ MY LATEST BESTSELLING BOOK: https://www.amazon.com/dp/1570674086?tag=onamzchefajsh-20&linkCode=ssc&creativeASIN=1570674086&asc_item-id=amzn1.ideas.1GNPDCAG4A86S ----------------------------------------------------------------------------------- Disclaimer: This podcast does not provide medical advice. The content of this podcast is provided for informational or educational purposes only. It is not intended to be a substitute for informed medical advice or care. You should not use this information to diagnose or treat any health issue without consulting your doctor. Always seek medical advice before making any lifestyle changes. Dr. Weiss, founder of Ethos Primary Care, embodies what it means to be a true primary care doctor. He listens deeply and compassionately, fully aware that your health is a direct result of how you eat, sleep, move, stress, and your connection to nature. He is the kind of doctor who will help you trade your prescriptions for plants. Deeply committed to helping people obtain their optimal health through living a mindful, whole plant food-based lifestyle for more than 30 years, Dr. Weiss has been helping people reverse and prevent disease and illness to live a more energized, fulfilled life. Dr. Weiss is also the founder of Ethos Farm Project, a nonprofit organization and semifinalist in the Rockefeller Foundation 2050 Food System Vision Prize competition. He has been featured in top media, including The New York Times, The New York Post, The Today Show, New Jersey Monthly, and the feature-length documentary, "Eating You Alive." The mission of Ethos Farm Project is to address the interconnected nature of how agriculture affects human health, planetary health, and our relationship with animals. To achieve this, his 388-acre historic farm in Long Valley NJ where he operates Ethos Primary Care from, produces truly nourishing food to feed the community, restoring the land, all while cultivating and empowering a new generation of farmers, doctors, and nurses through hands-on educational programming. Dr Weiss feels that he is fulfilling his purpose in life through the work he does as a Board Certified, Lifestyle Medicine physician and the work he does through his nonprofit, Ethos Farm Project. Connecting his life's passion for medicine and the environment, Dr. Weiss believes we need “all hands on deck” to combat the healthcare and environmental crises we now face as a species, in order to ensure a habitable planet for our children. Dr. Weiss is here monthly, on Chef AJ, to answer any and all medical questions you may have. An experienced primary care doctor, there is no question too simple or too complex for him to handle. To learn more about Dr. Weiss and all he is involved with, visit the following: https://www.ethosprimarycare.com/ https://www.ethosfarmproject.org/
Bonjour bonjour ! Enfin le retour tant attendu du podcast préféré du futur major de l'EDN (et des autres qui ont la flemme de bosser mais qui veulent se donner bonne conscience, on vous voit). Retour en fanfare donc, avec ce doux épisode concernant la fibrillation atriale, que tu auras 1 chance sur 3 d'expérimenter au cours de ta vie, surtout si tu aimes bien picoler, fumer, et manger la bonne charcut' de mamie (comment t'en vouloir ?) Allez sur ce, je te souhaite un excellent début de semaine, et accroche toi à ton slip parce que "L'externe" revient plus fort que jamais à coup de 3 épisodes par semaine, on ne change pas une équipe qui gagne ! Bisouuuuus
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The heart is the most important muscle in the body. It's the first muscle to show stress or nutritional inadequacy, and hormone imbalances. It's also the first muscle to respond. If the heart is "off" people feel an impending sense of doom, lethargy, hopelessness and decreased vitality. It's not a good feeling. Yes, you can do something about it. It's not just blood pressure meds, or decreasing activity. What if you could unlock genes, proteins, and energy to repair and optimize the heart? If the heart has no horse power as in the case of low blood pressure, people feel terrible. If the heart is overworking (high blood pressure), many times there are no symptoms but it's a risk factor for blowing your hydraulics (stroke). If the heart works too hard for too long, it enlarges and the valves don't work. If there is a deficiency in fat loving B vitamins or B vitamin cofactors then the heart gets out or rhythm (atrial fibrillation). Many times, just getting the B vitamin co-factors into the body and help the heart into normal rhythms. We even touch on aortic stenosis, heart fatigue, and adrenal exhaustion. Also learn about: 1. B vitamins that act like a heart regulator 2. G vitamins (co-factors) that help nerve relaxation (high blood pressure) 3. NHP- natural hormone pre-cursors for heart conditions 4. Oxygen transporters 5. Advanced oxidative medicine strategies If you have any medical questions go to https://www.westcliniconline.com/
“If you don't mind your mitochondria at night, it does not matter what you do the next day,” explains Dr. Michael Twyman, board certified cardiologist. Dr. Michael began working in traditional cardiology in 2012 and realized that there was a lack of focus on preventative measures to help stop people from having heart problems in the first place. In 2020, he opened his own clinic to address preventative heart health by applying quantum principles. In this episode, Dr. Michael shares his top tips for preventing heart attacks through healing mitochondrial dysfunction. There are up to 5,000 mitochondria per heart cell. With so many mitochondria fueling the heart, it stands to reason that when the mitochondria are not getting enough energy to function properly, then heart health will decline. There are many preventative measures one can take to protect their heart, but at the base level, it all comes down to sunlight and sleep. Simply by seeing the sunrise each day and getting good quality sleep, you will significantly lower your risk for heart attacks. Sleep is key, because during sleep the mitochondria undergo the repair process. Issues like congestive heart failure and atrial fibrillation are linked to sleep apnea, so it is critical to mind your circadian rhythm and make improving your sleep a top priority. Most people do not think about their heart health until something goes wrong. Instead of waiting for a heart attack to address your heart health, start taking preventative measures today. Quotes “My number one thing is, always see the morning sunrise.” (6:02-6:06 | Dr. Michael) “A lot of heart rhythm issues such as A. Fibrillation are often associated with obstructive sleep apnea.” (12:22-12:28 | Dr. Michael) “Sleep is not when you end your day. You have to think of sleep as when you begin your day.” (16:31-16:36 | Dr. Michael) “Before light bulbs were invented, the only type of light you had at night was red light from a fire, so you're just trying to recreate that type of experience.” (26:17-26:25 | Dr. Michael) “Since the heart is heavily dense in mitochondria, it stands to reason that if you could put more energy into mitochondria in the heart, things may work better.” (29:00-29:10 | Dr. Michael) Links Connect with Dr. Michael Twyman: Dr Twyman's Clinic: https://drtwyman.com/apollocardiology/ Instagram: @drtwyman To find a practitioner who understand the health principles of quantum biology: www.quantumbiologycollective.org To become a QBC member and get invites to live deep dives & access to our video library: www.quantumhealthtv.com To take our 8 week practitioner certification in the science of quantum biology so that you can add it to your existing area of expertise: www.appliedquantumbiology.com Follow on Twitter, Instagram & Facebook: @quantumhealthtv Podcast production and show notes provided by HiveCast.fm
Mathieu et Ian discutent de l'étude DOSE-VF et la double défibrillation en fibrillation ventriculaire réfractaire ! Les notes de l'épisodes sont disponibles https://francofoam.com/balado/e79-rvf-etude-dose-vf/ Poursuivez la discussion sur les réseaux sociaux ! Twitter https://twitter.com/Francofoam1 Facebook https://fr-fr.facebook.com/francofoam/ Instagram https://www.instagram.com/francofoam1 Écrivez-nous @ info@francofoam.com
Pour accéder à l'intégralité de ce podcast et écouter chaque semaine un nouvel épisode du Quart d'Heure Véto, c'est très simple, il vous suffit de vous abonner en cliquant sur ce lien :https://m.audiomeans.fr/s/S-yUNSBZSR Fe Ter Woort et ses collaborateurs ont effectués une étude prospective à partir de cas cliniques de chevaux présentant une fibrillation atriale afin de mettre en évidence un éventuel lien entre FA et hyperthyroïdie, comme cela est rapporté chez l'homme. L'hyperthyroïdie est un facteur prédisposant à la fibrillation auriculaire (FA) chez l'homme. La relation entre l'hormone thyroïdienne (TH) élevée et la FA chez les chevaux n'a pas été évaluée. Les objectifs de cette étude étaient d'Identifier : 1. Si des concentrations élevées d'hormone thyroïdienne étaient présentes chez les chevaux souffrant de FA 2. Si d'autres effets cardiovasculaires étaient observés chez les chevaux présentant une TH élevée et une FA 3. Si Le taux d'hormones thyroïdiennes affectait le taux de récidive. Notes et références Article de F. Ter Woort & al, Journal of Veterinary Cardiology, Volume 43, 2022, Pages 93-100 - Atrial fibrillatory rate as predictor of recurrence of atrial fibrillation in horses treated medically or with electrical cardioversion (OPEN ACESS) : https://www.sciencedirect.com/science/article/abs/pii/S176027342200090X Retrouvez toute la synthèse sur la Fiche Podcast : https://audmns.com/GFwKKHW Pour nous suivre : 1. Abonnez-vous à notre chaine pour profiter de l'intégralité des épisodes : Le Quart d'Heure Véto : décrypte et résume en moins de 15 min un article de biblio véto - Sur abonnement uniquement, Le Véto du Mois : Partagez le temps d'une interview l'expérience de vétérinaires emblématiques de notre milieu, des rencontres conviviales, comme si nous étions dans votre salon au coin du feu. Podcasts bonus au fil des inspirations... 2. Le Scope Nous partageons avec vous nos dernières découvertes, inspirations, pistes de réflexion, nouveautés… À découvrir et utiliser dès maintenant, TOUT DE SUITE, dans votre quotidien de vétérinaire, de manager, de vie personnelle, de chef d'entreprise… Et tout cela en moins de 5 minutes top chrono un à 2 mardis par mois ! Je souhaite recevoir mon Scope : https://vetmasterclass.com/lescope/ 3. Contactez-nous, suivez-nous et donnez nous votre avis ! Des sujets que vous souhaiteriez approfondir, des références à partager, ou nous faire part de vos feed-backs : Abonnez-vous à notre chaine, donnez nous des étoiles, un commentaire et partagez autour de vous ! Sur notre site : https://vetmasterclass.com/ Sur Facebook : https://www.facebook.com/VmHorse Sur Instagram : https://www.instagram.com/vetmasterclass/ Sur YouTube : https://www.youtube.com/channel/UC18ovcWk9e-mFiTL34OQ03g Sur Linkedin : https://www.linkedin.com/company/vetmasterclass-horse/about/ Belle journée à tous, Et continuez à vivre votre métier avec Passion !
Gwen Fosse is a Clinical Outreach Specialist at U of MI Congenital Heart Centre at Mott Children's Hospital. She has almost 50 years of experience working with patients affected by CHD and their families. In this episode, Gwen Fosse, RN shares about what SCA is, who is affected, what Project A.D.A.M. is, and what people can do to be #READY to help someone who might have an SCA. Gwen's Links:Project ADAM –· National: https://tinyurl.com/3bh5hpxc· Michigan: https://tinyurl.com/8vfd6bf3Michigan Dept of Health & Human Services – MI HEARTSafe Schools Program· https://tinyurl.com/2ppdv9tcData:· AHA info: https://tinyurl.com/mr3mv86x· AED App. https://tinyurl.com/ycxef3j5 · SCA Outcomes: https://tinyurl.com/3t62b9svPediatric Guideline· https://tinyurl.com/3xubxckjSchool Nurses· https://www.nasn.org/home· Cardiac Emergency Response Planning for Schools: https://tinyurl.com/5e9ubnhcAHA· https://www.heart.org/· CPR and First Aid https://cpr.heart.org/en/CPR – Hands-Only resources:· http://heart.arizona.edu/learn-cpr· www.heart.org/handsonlycpr (AHA 2012)· The Michigan Way - https://tinyurl.com/vf3brvj5SCA conditions info.:· SADS Foundation: https://sads.org/· Medication cautions: https://crediblemeds.org/Heart to Heart with Anna SCA episodes:Saving a Life from Sudden Cardiac Death: https://tinyurl.com/bdcwu9ufJackie Renfrow's show (about Long Q-T Syndrome): https://tinyurl.com/58b7w338Championship Hearts: https://tinyurl.com/8dy2m2ztNonprofit organizations providing AEDs and heart screenings to the community:Championship Hearts Foundation – https://www.champhearts.orgLiving for Zachary – https://tinyurl.com/b6575u7sVia Heart Project – https://viaheartproject.org/ CARES: https://tinyurl.com/h43tdsd3European Parliament Roberta Metsola's speech about SCA – https://tinyurl.com/2fhuybceAmerican Red Cross OSupport the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite
Pour accéder à l'intégralité de ce podcast et écouter chaque semaine un nouvel épisode du Quart d'Heure Véto, c'est très simple, il vous suffit de vous abonner en cliquant sur ce lien : https://m.audiomeans.fr/s/S-yUNSBZSR Rikke Buhl et ses collaborateurs ont essayé de déterminer si la mesure du taux de fibrillation atriale (AFR), correspondant au nombre de fibrillation par minute, que l'on peut obtenir à partir de l'ECG de surface, pourrait être un marqueur prédictif pour la récidive de la FA après traitement ou pour les chances de réussite du traitement médical ou électrique. Le taux de récidive de la fibrillation atriale (FA) chez les chevaux après cardioversion en rythme sinusal (RS) est relativement élevé. Le taux de fibrillation atriale (AFR), correspondant au nombre de fibrillation par minute, peut-être obtenu à partir de l'ECG de surface. Il est considéré comme un biomarqueur du remodelage électrique et pourrait être utilisé pour prédire la réussite de la cardioversion de la FA et la récurrence de la FA. L'objectif de l'étude est d'évaluer si l'AFR était associé à la réussite du traitement et pourrait prédire la récurrence de la FA chez les chevaux. Notes et références Article de R.Buhl - Atrial fibrillatory rate as predictor of recurrence of atrial fibrillation in horses treated medically or with electrical cardioversion - Equine Vet J. 2022;00:1–10 (OPEN ACESS) : https://beva.onlinelibrary.wiley.com/doi/10.1111/evj.13551 Retrouvez toute la synthèse sur la Fiche Podcast : https://audmns.com/IsBMcrq Pour nous suivre : 1. Abonnez-vous à notre chaine pour profiter de l'intégralité des épisodes : Le Quart d'Heure Véto : décrypte et résume en moins de 15 min un article de biblio véto - Sur abonnement uniquement, Le Véto du Mois : Partagez le temps d'une interview l'expérience de vétérinaires emblématiques de notre milieu, des rencontres conviviales, comme si nous étions dans votre salon au coin du feu. Podcasts bonus au fil des inspirations... 2. Le Scope Nous partageons avec vous nos dernières découvertes, inspirations, pistes de réflexion, nouveautés… À découvrir et utiliser dès maintenant, TOUT DE SUITE, dans votre quotidien de vétérinaire, de manager, de vie personnelle, de chef d'entreprise… Et tout cela en moins de 5 minutes top chrono un à 2 mardis par mois ! Je souhaite recevoir mon Scope : https://vetmasterclass.com/lescope/ 3. Contactez-nous, suivez-nous et donnez nous votre avis ! Des sujets que vous souhaiteriez approfondir, des références à partager, ou nous faire part de vos feed-backs : Abonnez-vous à notre chaine, donnez nous des étoiles, un commentaire et partagez autour de vous ! Sur notre site : https://vetmasterclass.com/ Sur Facebook : https://www.facebook.com/VmHorse Sur Instagram : https://www.instagram.com/vetmasterclass/ Sur YouTube : https://www.youtube.com/channel/UC18ovcWk9e-mFiTL34OQ03g Sur Linkedin : https://www.linkedin.com/company/vetmasterclass-horse/about/ Belle journée à tous, Et continuez à vivre votre métier avec Passion !
09/30/22 - Host Doug Stephan and Dr. Ken Kronhaus of Lake Cardiology (352-735-1400) cover a number of topics, including: more reasons to ponder about getting the new COVID booster and fall flu shots, 60-thousand die from the flu in an average year, indicators are pointing to a tough 2022/23 flu season, how getting wet in the rain relates to getting a cold, studies now show that getting a good amount of sleep can help prevent COVID and finally, Dr. Ken provides a look at fish oil supplements and how they can help with Atrial fibrillation.
Performing good CPR, and delivering a shock as soon as possible to a patient in Ventricular Fibrillation or pulseless V-Tach are the two most critical interventions that have been shown to increase survival from sudden cardiac arrest. To aid in the rapid delivery of a shock, an Automated External Defibrillator (AED) should be used in settings where a full monitor/defibrillator isn't available. Research has demonstrated significantly better out of hospital cardiac arrest survival outcomes in communities with robust public CPR training and public access/first responder AEDs. Why an AED makes a difference. The general use of AED including: indications for use; attaching the AED pads; following verbal prompts; and safely administering a shock. Following the Adult Cardiac Arrest algorithm while using an AED. Contraindications to AED use. 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!
Electrical signals to the heart keep it beating at a regular rhythm. If something happens to disrupt the signals, such as a heart attack or illicit drug use, the fibers of the heart muscle can start fibrillating, or quivering. Fibrillation prevents the heart from pumping blood and oxygen effectively to the body's major organs. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app
10/15/21 - Host Doug Stephan and Dr. Ken Kronhaus of Lake Cardiology (352-735-1400) begin with a truly in-depth discussion of recently released studies that warn against daily use of low dose Aspirin. Dr. Ken offers his recommendation, and as usual, one size does not fit all. Then, Doug asks Dr. Ken if it's possible to take too much fish oil and speculation that too much could lead to Atrial fibrillation (A-fib), an irregular and often very rapid heart rhythm (arrhythmia) that can lead to blood clots in the heart. Finally, the who, what, when and why of getting a COVID booster shot.
Our guests are John, a patient with an extraordinary story to tell, and Dr. John Mandrola, a cardiac electrophysiologist from Louisville, KY. Dr. Mandrola is cardiology editor on Medscape where he writes a regular column and produces a weekly podcast. He is also the co-author of The Haywire Heart: How Too Much Exercise Can Kill You and What You Can Do To Protect Your Heart. https://www.amazon.com/Haywire-Heart-exercise-protect-heart/dp/1937715671 GUEST: John Mandrola, MD: https://twitter.com/drjohnm (Twitter) and https://drjohnm.org/ (Website) LINKS: The Haywire Heart (Amazon https://amzn.to/3kT5pJV (link)) Note: The Accad and Koka Report participates in the Amazon Affiliate program and may earn a small commission from purchases completed from links on the website, WATCH ON YOUTUBE: https://youtu.be/7dArQkG8EE0 (Watch the episode) on our YouTube channel Support this podcast
Our guests are Thomas Wingert, a patient, Bogdan Enache, an electrophysiologist at Centre Hospitalier Princesse Grace in Monaco, and Saurabh Jha, an Associate Professor of Radiology at the Perelman School of Medicine and the University of Pennsylvania. SHOW NOTES Point/Counterpoint on Halting the Implantation of Subcutaneous ICD. Editorial by B. Enache and J. Mandrola in JACC Electrophysiology.Watch the episode on our YouTube channel
Our guests are Thomas Wingert, a patient, Bogdan Enache, an electrophysiologist at Centre Hospitalier Princesse Grace in Monaco, and Saurabh Jha, an Associate Professor of Radiology at the Perelman School of Medicine and the University of Pennsylvania. SHOW NOTES Point/Counterpoint on Halting the Implantation of Subcutaneous ICD. Editorial by B. Enache and J. Mandrola in JACC Electrophysiology.Watch the episode on our YouTube channel
Bienvenue sur RARE à l'écoute, la chaîne de Podcast dédiée aux maladies rares. Pour le troisième épisode sur les amyloses cardiaques, nous recevons le Pr Thibaud Damy, cardiologue, professeur des universités, praticien hospitalier au sein du service de cardiologie de l'hôpital Henri-Mondor à Créteil et responsable du centre de référence national des amyloses cardiaques. Nous abordons aujourd'hui l'organisation de la prise en charge des amyloses cardiaques en France, la prise en charge de l'amylose ATTR, et le suivi recommandé pour les patients atteints d'amylose cardiaque. Si vous désirez vous informer et aller plus loin dans la connaissance de cette pathologie, nous vous donnons rendez-vous sur notre site internet www.rarealecoute.com. L'orateur n'a reçu aucune rémunération pour la réalisation de cet épisode. Invité : Pr Thibaud Damy – Hôpital Henri-Mondor - Créteil http://www.reseau-amylose-chu-mondor.org/index.php/78-reseau-amylose-chu-henri-mondor/24-site-internet-du-centre-de-reference-des-amyloses-cardiaques L'équipe : Virginie Druenne - Programmation Cyril Cassard - Animation Hervé Guillot - Production Crédits : Sonacom
Well Said has invited Dr. Nicholas Skipitaris, Director of Cardiac Electrophysiology for Lenox Hill Hospital and the Western Region, Northwell Health and Assistant Professor of Cardiology, Zucker SOM as we explore exactly what Atrial Fibrillation is and dive into the symptoms, medications and strategies for combating this condition.
We're talking Atrial Fibrillation today with our special guest, Dr. John D Day. John D. Day, MD, graduated from medical school at Johns Hopkins University. He did his residency and cardiac electrophysiology fellowship training at Stanford University. Dr. Day is an electrophysiologist at the Intermountain Medical Center Heart Institute in Salt Lake City, Utah. He previously served as president of the Heart Rhythm Society and currently serves as the Utah Governor of the American College of Cardiology. He is recognized as an international thought leader on atrial fibrillation management. Dr. Day is board certified in cardiology, and cardiac electrophysiology. He has published more than 100 manuscripts, abstracts, and book chapters and regularly lectures both nationally and internationally on heart rhythm disorders. Dr. Day is the former editor-in-chief of the Journal of Innovations in Cardiac Rhythm Management. In 2017, Dr. Day published The Longevity Plan: Seven Life-Transforming Lessons from Ancient China, with HarperCollins as publisher. The Longevity Plan was an Amazon number one bestseller and was named best books of 2017 by the Huffington Post and won the Nautilus Book Award Gold Medal for the best book of 2017. 2:07 What is Atrial Fibrillation? 2:58 How does someone develop Atrial Fibrillation? 6:33 How is Atrial Fibrillation treated? 9:43 Biomarkers 12:13 Anti-Inflammatory drugs and Atrial Fibrillation 13:50 Gut Microbiome and Atrial Fibrillation 15:15 More about The AFib Cure “Executive Medicine Moment” At Executive Medicine of Texas we understand that true health can only be found when you treat the patient as a whole. That’s why our Executive Physical Exams are second to none in the amount of testing and information we gather prior to making a wellness plan for our patients. Learn more about how you can take charge of your health at http://www.EMTexas.com You can learn more about Dr. John D Day: https://drjohnday.com/ Buy the book: https://www.amazon.com/AFib-Cure-Medications-Control-Health-ebook/dp/B089FK6W3D/ref=pd_rhf_dp_p_img_5?_encoding=UTF8&psc=1&refRID=4N3DNN35XSP1FN2DCB56 Website: StayYoungAmerica.com Twitter: @StayYoungPod Facebook: @Stay Young America! Join us next time as we always bring you information you can use
Dan Pak stayed active for many years and like most active people never thought that his heart could be an issue . Follow Dan's story as he tells how he was first diagnosed with AFib ( Atrial fibrillation ). How he wouldn't let this stop him from his goals . Plus Dan tells us about the procedure he needed to help him . As well as how active he became on social media and interviews to help get the word out that Heart health is important . Please do not try any of these activities without first consulting your doctor to make sure its ok for you and your Heart . Some links for you to check out to see the full story of Dan's journey . Your Heart may be glad you did . https://stittsvillecentral.ca/stittsvilles-dan-pak-running-for-his-life-and-the-ottawa-heart-institute/https://ottpak.blogspot.com/ https://ottawa.ctvnews.ca/a-runner-s-racing-heart-danny-pak-gives-back-to-the-university-of-ottawa-heart-institute-by-taking-part-in-vital-research-studies-1.5285183 Twitter@ottpak Instagram@ottpak https://raceroster.com/events/2021/34303/tamarack-ottawa-virtual-race-weekend-2021/pledge/participant/10752232
Join Us Live in 2021 for a Focused, Evidence-Based Course That's Designed to Update You on Over 30 Leading-Edge EM Topics.20 CME Credits | No PowerPoint | 8 Top Destinations | San Francisco, CA - June 3-6, 2021San Diego, CA - June 8-11, 2021New York, NY - June 16-19, 2021Kauai, HI - June 22-26, 2021Vancouver, BC, Canada - July 20-23, 2021Las Vegas, NV - October 2-5, 2021New Orleans, LA - October 13-16, 2021 (Jazz & Heritage Festival)Key West, FL - November 29-December 3, 2021Register @ https://courses.ccme.org/course/ema/registerThe goal of the course is straightforward - an exceptional and unique educational experience held in world-class locations at great times of the year. All of the course destinations have been the site of prior Emergency Medicine & Acute Care courses and, as such, we know they'll provide the environment for a fulfilling educational experience as you take a break from shifts and enjoy the company of family and friends.Experience the Course Series Enjoyed byOver 50,000 of Your Colleagues!
✨ Si tu souhaite réussir ta première séance de SUP yoga, télécharge cet audio gratuit qui te guidera à travers 10 points clefs. https://mailchi.mp/4830af5a98f4/nk2ewgtfw9 ——————— c'est une histoire que je n'ai jamais voulu gardé secrète que je vous raconte aujourd'hui pour que mon expérience puisse servir aux autres. A 22 ans, alors que je suis une jeune athlète prometteuse, j'accepte l'implantation un défibrillateur cardiaque dans ma poitrine. Je suis en pleine ascension sportive, mais ma carrière ne tient qu'à un fil (et ma vie aussi d'ailleurs !) quand en décembre 2005 on me diagnostique une tachycardie ventriculaire à 280-300 pulsations minutes. Tout bascule, au même moment je perd mon père d'un cancer foudroyant. Je dois réapprendre à vivre avec mon ange gardien et trouver la force de continuer à vivre pour ma passion : la planche à voile. Dans cet épisode on parle de : la façon dont j'ai accueilli la nouvelle de l'implantation comment surmonter la peur du choc électrique savoir se reconstruire après l'implantation garder la foi en ses capacités physiques rester fidèle à son intuition, sa passion s'adapter malgré les difficultés de la vie pour continuer de réaliser ses rêves Outil cité dans cet épisode : Audio gratuit pour réussir ta première séance de SUP yoga: Si tu souhaite maitriser le pouvoir transformationnel du SUP yoga pour toi et tes futurs élèves, inscris-toi à la liste d'attente de la future SUP YOGA TEACHER TRAINING en mai 2021. APODEC, l'association des porteurs de défibrillateurs en France Si tu as apprécié cet épisode, n'hésite pas à laisser une note et un commentaire sur iTunes, Apple Podcast ou la plateforme d'écoute de ton choix ! Cela aide le podcast à se faire connaitre et ça me fait plaisir de te lire ! ————————————— ✨ Plus de contenu sur mon site internet ✨ Suivez mon tour du monde en voilier à la recherche des plus beaux spots de glisse ✨ Mon actualité sur instagram ✨ Ma page facebook "Avec du coeur tout est possible »
10/23/20 - Host Doug Stephan and Dr. Ken Kronhaus of Lake Cardiology (352-735-1400) begin the news that common mouthwash kills the Coronavirus bacteria and could be the key to prevention. Dr. Ken's not so sure, until further testing, but it couldn't hurt. The latest update says that we could have a vaccine by the end of November. Word is that the latest mutation COVID 2 is less lethal than the original. Next, we meet Dr. Jon Davidson, Division Chief of the Department of Interventional Radiology at University Hospitals Cleveland Medical Center. He is also an Associate Professor at The Case Western Reserve University School of Medicine. His focus is: 1. State of affairs with COVID 2. Importance of masks until vaccine is available 3. The importance of reaching a balance between total lockdown and throwing caution to the wind as it pertains to the virus 4. The politicization should decrease after the election. Next, Dr. Ken says: "Sugar rots the body, from top to bottom." Plus, lots more great tips and ideas to help you maintain your Good Health.
Dr RR Baliga's Internal Medicine Podkasts for Physicians: GOT KNOWLEDGE DOC Podkasts about Long-Term Risk of HF with Chemotherapy with Trastuzumab Long-Term Risk of Heart Failure in Breast Cancer Patients After Adjuvant Chemotherapy With or Without Trastuzumab. JACC Heart Fail 2019;7:217-224. Not Medical Advice or Opinion
Emergent treatment of rapid atrial fib/flutter with Dr. Dave Zull. Please see below for Evidence based annotated articles Arrigo M. New Onset Atrial Fibrillation in critically ill patients and it’sassociation with mortality. Int J Cardiol 266:95-99, Sept 2018Bosch, NA, et al. Atrial Fibrillation in the ICU CHEST 154:1424-1434. Dec 2018Nice review of A fib in the critically ill patient. Emphasis first on correcting precipitants like sympathomimetics, electrolytes, volume and intercurrent illness. Esmolol implied to be best rate control drugDeSouza IA, et al. Pharmacologic Cardioversion of recent onset Atrial Fibrillation and Flutter in the Emergency Department. Ann Emerg Med 76:14-30. July 2020Looking at 360 patients with acute a fib. Ibutilide converted 50% of A fib and 75% of A flutter patients. Two patients had VT as a complication, but none received Magnesium prophylaxis.Nikki, AHA, et al. Early or Delayed Cardioversion in recent onset Atrial Fibrillation. N Engl J Med 380:1499-1508, Apr 2019Oral H, et al. Facilitating Transthoracic Cardioversion of atrial Fibrillation with Ibutilide pretreatment. N Engl J Med 340:1849, Jun 199972% converted to NSR with electrical cardioversion without pretreatment whereas 100% converted with Ibutilide pretreatment before electicityPatsilinakos S, et al. Effect of high doses of Magnesium on converting Ibutilide to a safe and more effective agent. Am J Cardiol 106:673, Sept 2010Magnesium sulfate 4-5 gm infused over one hour before Ibutilide prevents TorsadesSleeswijk ME, et al. Efficacy of Magnesium-Amiodarone step-up scheme in critically ill patients with new onset atrial fibrillation. J Intensive Care Med 23:61, Jan/Feb 2008Magesium infusion followed by Amiodarone infusion in A fib with RVR in the ICU. Half had acceptable rate or rhythm control with Mag alone. At the end of 24 hours 90% of patients converted to NSR.Stiell, Ian, et al. Electrical vs Pharmacologic cardioversion for emergency department patients with acute Atrial Fibrillation. RAFF2 Lancet 395:339-349, Feb 2020Canada’s aggressive protocol for conversion of acute A fib in the ER. IV Procoinamide infusion converted 50% to NSR. Electrical cardioversion worked in 92%. Only 3% of new A fib patients required admissionTercius AJ, et al. Intravenous Magnesium sulfate enhances the ability of intravenous Ibutilide to successfully convert atrial fibrillation or flutter. Pacing Clin Electrophysiol 30:1331, Nov 2007Vinson DR, et al. Ibutilide effectiveness and safety in the Cardioversion of atrial fibrillation and flutter in the community emergency department. Ann EmergMed71:96, Jan 2018Wyse DG, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation (AFFIRM trial). N Engl J Med 247:1825-33, Dec 2002Internists and cardiologist love to quote the AFFIRM trial as proof that attempts to convert are fruitless and we stick to rate control only. These patient were all in chronic a fib and of course we would never convert these patients unless there is life threat. This study has NO application to acute a fib less than 48 hoursZimetbaum P. Atrial Fibrillation. Annal Intern Med. March 2017Everything you ever wanted to know about atrial fibrillation
Voyage dans le temps et l’espace mondial dans ta quiétude dominicale hebdomadaire pour prendre le temps et ton laissé passer pour l’été. Dans ce climat de torpeur typique de la transition juillet août, il est important de pouvoir contempler sereinement ces mouches vertes venir pondre dans ta merguez sous-cuite. Quel chance, ces petites bites, au […] L’article Crossover – 2 aout 2020 – Opération Défibrillation est apparu en premier sur Radio Campus Tours - 99.5 FM.
Voyage dans le temps et l’espace mondial dans ta quiétude dominicale hebdomadaire pour prendre le temps et ton laissé passer pour l’été. Dans ce climat de torpeur typique de la transition juillet août, il est important de pouvoir contempler sereinement ces mouches vertes venir pondre dans ta merguez sous-cuite. Quel chance ces petites bêtes au […] L’article Crossover – Opération Défibrillation est apparu en premier sur Radio Campus Tours - 99.5 FM.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.28.225755v1?rss=1 Authors: Lopez, G., Nicolas, A., Roman, G., Godinez, R., Castro, M. A. Abstract: With an aperiodic, self-similar distribution of two-dimensional arrangement of atrial cells, it is possible to simulate such phenomena as Fibrillation, Fluttering, and a sequence of Fibrillation-Fluttering. The topology of a network of cells may facilitate the initiation and development of arrhythmias such as Fluttering and Fibrillation. Using a GPU parallel architecture, two basic cell topologies were considered in this simulation, an aperiodic, fractal distribution of connections among 462 cells, and a chessboard-like geometry of 60x60 and 600x600 cells. With a complex set of initial conditions, it is possible to produce tissue behavior that may be identified with arrhythmias. Finally, we found several sets of initial conditions that show how a mesh of cells may exhibit Fibrillation that evolves into Fluttering. Copy rights belong to original authors. Visit the link for more info
See all the Healthcast at https://www.biobalancehealth.com/healthcast-blog/ Heart Disease, Blood Flow, SA node, Right Atrium, Left Atrium, ventricular contraction, neurologic malfunction of the heart Before I can explain a common neurologic malfunction of the heart, I should explain the way the heart beats and the way the heart increases and decreases how fast it beats. The heart has an amazing spontaneous electrical generator called the SA node. It is located in the Right atrium and generates the beat of the heart that causes the atrium to contract and send blood to the ventricle through another node of electrical tissue called AV node which then causes the ventricle to contract. This amazing conduction system causes a coordinated contraction that amazingly causes blood to pump from the atria to the ventricles and then out to the lungs or the aorta to the body. When the heart is working properly you can put a stethoscope on the chest and hear the Lub-Dub that is associated with human and animal life. Lub is the sound of the atrial contraction and Dub is the sound of the ventricular contraction. 99.9% of the time we completely ignore this automatic activity in our chest. Only when the heart becomes sick or develops an electrical short do we have symptoms that cause us to pay attention to the heart's rhythm. What speeds up the heart or slows it down? The heart isn't an isolated independent pacemaker. It is controlled by the autonomic nervous system, the sympathetic nervous system and the parasympathetic system. When these two systems are balanced the sympathetic system speeds up the heart to accommodate exercise, anxiety and fear, and to respond to the adrenal outpouring of adrenaline. The parasympathetic system is the opposite of the sympathetic system and is the “brakes” of the heart rate, which takes over when we are relaxing , quiet and at rest. The trouble begins when we are under the severe stress of modern life that makes us “sympathetic dominant”. Under the control of the sympathetic system people have a fast heart rate all the time which doesn't allow the heart to rest and relax its muscle. Over time the heart is overworked and gets faster and faster. The owner of that heart becomes out of breath easily and is unable to exercise for any period of time because the heart cannot fill completely in between beats and therefore cannot deliver oxygen to the muscles. Today we are talking about the rhythm abnormality called atrial fibrillation. It can be caused by chronic stress, and chronic fast heart rate called tachycardia, combined with a genetic weakness, that progresses from a fast, regular beat to heart beats that are irregular and uncoordinated, making the heart fail to push out enough blood and oxygen to the body. The atria may beat twice and miss a beat to the ventricles which feels like your heart is “falling” out of your chest. Fibrillation means uncoordinated muscle contraction. The big risk of atrial fibrillation is that the uncoordinated heart activity will literally act as a whirlwind and shake the blood up without moving it through the chambers, which causes a high risk of blood clots, stroke and heart failure. The other and more deadly risk is that the fibrillation will be so uncoordinated that it will prevent oxygenated blood from reaching the vessels that feed the heart muscle, which results in a heart attack and instant death. Generally, if you have symptoms of AF you will seek evaluation from a doctor and receive medication or other treatment. The symptoms of AF include: Palpitations, which are sensations of a racing, uncomfortable, irregular heartbeat or a flip-flopping in your chest. Reduced ability to exercise Dizziness. Chest pain Shortness of breath Habits and situations that worsen AF include: Caffeine Alcohol Fatty diet Sugar Dehydration Heat Cold Hypoglycemia High altitude and aerobic exercise tight neck muscle and headaches lack of sleep Even if you avoid these situations and activities, you may still progress from tachycardia to intermittent atrial fib to chronic atrial fib. This is typical if the high stress lifestyle that pushed your body over to AF is continued. I can tell you that you cannot push through this disease…it will only get worse. What can you do yourself if you have Atrial Fibrillation? Increase your sleep and avoid alcohol and caffeine Take up meditation and or yoga Stop stressful work or activities Listen to relaxing music Take the following supplements: Magnesium glycinate Replenish your potassium by eating tomatoes, bananas, oranges and avocados CoQ 10 200-600 mg/day D-ribose 2-3 times a day L-Carnitine The Sinatra foursome is : Co Q 10, D-ribose, L-carnitine, and magnesium The treatments that doctors can offer patients include medications to slow the heart rate like beta blockers eg: Metaprolol or drugs like digoxn to make each contraction stronger. Other medications that have a normalizing effect on the heart rhythm include NSAIDS and antidepressants at low dose. Antiarrhythmic drugs are reserved for constant AF and is an alternative to ablation directly to the area that is an additional node that has overcome the beat of the SA node or the SA node itself, that is accompanied by placement of a pacemaker. There are alternative treatments like electrical stimulation of the Vagus nerve which slows the heart. There are more non-medicine treatments being rolled out monthly. The most amazing things that have come use in the last few years is your very own EKG that you can do yourself in one minute. It works with your iphone and can be sent to your cardiologist. It is helpful in diagnosing how often the abnormal beat occurs. This is important in deciding whether a blood thinner should be instituted to prevent blood clots and strokes. The name of the EKG I use is Kardia. The latest Applewatch has the ability to count your heart rate and rhythm, so you can always be monitored! As always, we hope that this information is useful for you when discussing your health concerns with your physician. Remember an informed consumer is more likely to be a healthy consumer. Stay healthy, be healthy.
With Doralisa Morrone & Raffaele De Caterina – University of Pisa, Italy. Link to paper Link to editorial
Did you over-indulge during the Super Bowl festivities, Christmas, or the last family holiday? You’re not the only one – holiday heart syndrome and atrial fibrillation (afib) is not uncommon after eating too much. Food can help you proactively manage your health – or it can lead to missed heart beats. In addition to explaining more about afib, today’s guest talks about figuring out what fuels your body the best and creating your own personal diet. Mellanie True Hills is the CEO and founder of StopAfib.org, a patient advocacy organization to help those living with atrial fibrillation. Their mission is “to rid the world of strokes from afib and to give people living with afib their lives back.” Key points What is atrial fibrillation? What does it feel like? Afib lead to stroke, heart failure and other health issues Cure to jet lag How to avoid afib: it can be related to diet, weight, sleep, etc. Exercise safely for the heart Holiday heart syndrome: overindulging during super bowl, Christmas, Thanksgiving, etc. Quest to find information can bring about food bullying when people don’t agree with recommendations or ideas or their pet diet may be less than ideal Nutrition research is a difficult area to study – there are confounders Don’t stress out over research that flip flops, food research is going to change Fab quotes “The heart needs water in order to function properly.” “Make sure you’re doing all the healthy kinds of behaviors.” “Sleep is really crucial for your heart health.” “Competitive athletes have 5x the risk for afib as the rest of the population” “Holiday heart syndrome can come as a shock when the heart goes out of order. It’s really crucial to get help.” “Nutrition research is not necessarily held to the same kind of standard as drug and device.” “Very often doctors don’t know about nutrition; they’re not really in the position to provide help.” “Figure out what fuels your body the best and create your own personal diet.” Links Website: https://stopafib.org/ Facebook Instagram & Twitter: @stopafib Food Bullying: How to Avoid Buying BS Embrace your Heart
Registered Nurse and proud septuagenarian, Barbara Blaser, was the guest speaker at my Northern California myotonic dystrophy support group. With her healthcare background and deep knowledge of medicinal herbs, she spoke about the use of herbal tinctures, edibles, and lotions to help relieve muscle pain, anxiety, insomnia, gastrointestinal problems, and more. Barbara's nursing career was predominantly in the mental health field. But at some point in her 60s she had an esophagectomy and due to complications, she developed septicemia. She turned to natural herbal healing to help her pain, anxiety, and GI problems. Handouts that Barbara provided at the support group meeting are culled from this website.
Preventing Strokes in Atrial Fibrillation -2 2019 ACC/AHA/HRS Update Dr RR Baliga's MUST KNOW FACTs PodCasts for Physicians from Journal of Am Coll Cardiology 2019;74:104-132
Preventing Strokes in Atrial Fibrillation -1 2019 ACC/AHA/HRS Update Dr RR Baliga's MUST KNOW FACTs PodCasts for Physicians from Journal of Am Coll Cardiology 2019;74:104-132
Please bear with me as this is a work in progress*** I suffer from atrial fibrillation as well as supraventricular tachycardia and I am a survivor of multiple strokes - all due to PTSD, stress and life behaviors that were not good for me at all. I am really excited to share my experiences. I also want to share what I did after I learned more about what happened to me in order to curb my stress anxiety and how I turned my dire health situation into the life I have always wanted. View my products at www.luxiouslemon.com
With Freek Verheugt, Heartcenter, Onze Lieve Vrouwe Gasthuis (OLVG) - Netherlands. Link to paper Link to editorial
In this podcast, Dr. Joshua Buckler, a cardiologist with Minneapolis Heart Institute at Ridgeview Heart Center, provides an overview of growing issue of atrial fibrillation, and the increased need for its awareness and the modalities to evaluate and treat it. Objectives: Upon completion of this podcast, participants should be able to: Identify risk factors for atrial fibrillation. Express the importance of screening for atrial fibrillation. Recognize when a patient needs to be referred for atrial fibrillation. CME credit is only offered to Ridgeview Providers for this podcast activity. Complete and submit the online evaluation form, after viewing the activity. Upon successful completion of the evaluation, you will be e-mailed a certificate of completion honoring you 1.25 CME/CEU credits within 2 weeks. You may contact the accredited provider with questions regarding this program at rmccredentialing@ridgeviewmedical.org. Click on the following link for your CME credit: CME Evaluation: "Atrial Fibrillation (Podcast)" (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.) The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition.” FACULTY DISCLOSURE ANNOUNCEMENT It is our intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented. Planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed no conflict of interest exists with the presentation/educational event. SHOW NOTES: CHAPTER 1: We understand around 10% about an Atrial Fibrillation (A-Fib or AF), which makes understanding it a challenge. The majority of AF starts in the left atrium likely due to left atrial stretch secondary to mitral regurgitation or hypertension. This then leads to loss of connectivity and communication of the atrial cells, leading to micro reentry circuits. A lot of the AF comes from the pulmonary vessels where they connect to the LA. Why does this happen? Currently, we are unsure. AF comes down to the irregularity of atrial contraction fighting to get through AV node, resulting in irregularities of the ventricular action. AF runs about 300-500 bpm. Those high irregular rates through the AV node can result in symptomatic patients trying to maintain cardiac function over prolonged periods of time. Second, is the loss of AV synchronization - which is how the atrium and ventricle work in concert together. Lastly, is stroke risk. AF is so important, because it is grossly under-recognized and the implications of stroke and heart failure (HF), which can be catastrophic. The literature seems to support that individuals with AF seem to have a lower quality of life. The statistics are staggering, that a patient with AF has a 5x risk of stroke, 3x risk of heart failure, 3x risk of myocardial infarction or dementia. There has been a 5-6 fold increase in rates of AF since 1999. AF is commonly found with patients who are obese, diabetics, those who use alcohol and untreated obstructive sleep apnea. Dr. Buckler believes that entry point into the healthcare system is crucial for the success of AF patients. Establishing a one call system with curbside to the cardiologist for patients experiencing new onset AF. Obesity is a direct risk factor for AF. The "Legacy trial" was performed in Adelaide, Australia. It looked at losing 10% of body weight dramatically reduces AF following cardiac ablation. Patients with smaller weight fluctuations, around 2% of body weight, did better post-ablation, than those with higher weight fluctuations of around 5% increase in body weight. CHAPTER 2: AF is similar to diabetes. It affects everything. It's affected by everything and no one wants to deal with it. There is a large multidisciplinary approach to the treatment of AF due to the complex nature of the disease process. There is a large push to get the AF patient into the sleep clinic, as OSA and AD are closely intertwined. Furthermore, there is independent data that if OSA is treated, so is the patient's AF. Dr. Buckler believes in a team approach to the successful management of AF. He notes that is the PMD can start the workup by getting thyroid testing, sleep study, setting up the echo and placing the patient on anticoagulation as well as a rate limiting medication is a good start. Most cardiologists believe a rhythm control strategy is the way to go for treating most AF patients. The utilization patterns of AF patients is problematic. Most AF patients are costing the healthcare system around $8,700 per year/per patient. Dr. Buckler mentions a study that if some AF are ablated early in their disease state, the short-term cost far outweigh the costs downstream if they have recurrent AF. Addressing risk factor modifications, including OSA, obesity, ETOH, DM, smoking, are instrumental in the care of the AF patient. Believe it or not, endurance athletes have higher rates of AF. Whereas, high endurance women athletes actually have lower rates of AF. Something to chew on. Ablation has a high likelihood of success with initial treatment successful upwards of 90% of the time. The network of AF patient and how they enter the system is highly complex and intertwined coming down to primary care, emergency medicine, hospital medicine and cardiology. Building in pathways to the neurologist is critical for those individuals who may have experienced a cryptogenic stroke from undiagnosed AF. CHAPTER 3: How do we screen for AF? Holter monitors are still being used which seem to be of low yield. The ZIO patches are also used as well, but for around 14 days - but what if the patient does not have an episode of AF? Even 30-day monitors are good, but not great, as the average time period a patient will have an episode is around 42-43 days. So maybe we should consider an implantable cardiac monitor or better yet, what about consumer wearable's. What are consumer wearable you may ask well they are the: apple watch which have been FDA cleared not approved for AF detection or another device called Kardia single lead EKG machine that can tell you if you are in AF or other dysrhythmias. Some non-western medicine approaches to the treatment of AF are yoga, acupuncture and biofeedback. Ultimately, Dr. Buckler believes that across the country no one has a truly good data set that documents the burden of AF patients. Furthermore, AF patient's generally have longer lengths of stay when hospitalized. Some interesting modalities not quite ready for prime-time at the ED entry point may be, TEE, cardio version, or CTA, evaluating for left atrial appendage clot then cardio version which might be promising. Dr. Buckler believes that every AF patient should be seen by cardiology, at least once. Cardiology should be the repository for AF. Optimally, the idea would be to offer that service within 48-hours. Also, would like the patient to get through risk factor management more efficiently. The check list once again -- everyone needs a sleep study, echo, thyroid testing, etc.
September is National Atrial Fibrillation Awareness Month. Atrial fibrillation (also called AFib or AF) is a quivering or irregular heartbeat (arrhythmia) that can lead to blood clots, stroke, heart failure and other heart-related complications. According to the American Heart Association, at least 2.7 million Americans are living with AFib.
MedAxiom HeartTalk: Transforming Cardiovascular Care Together
Lead administrator and physician from Bellin Health share their journey of navigating the corridor from volume to value-based healthcare and address these important questions:•What does volume-to-value mean for you?•How are physicians reacting to this new population health model?•Why have you decided to focus on understanding cost of care?•From a population health perspective, what focus areas are you targeting for 2019?Andrea Werner, MSW is Senior Vice President for Cardiovascular and Pulmonology; Neurosciences, Orthopedics, and Sports Medicine; and Pathology and Radiology for Bellin Health in Green Bay, Wisconsin. James Rider, MD is the Director of Cardiovascular Research, Nuclear Cardiology, and the CHF program for Bellin Health in Green Bay, Wisconsin. Lori Walsh, MHSA is Vice President - Membership and Senior Consultant for MedAxiom.
Presented by Marius Myrstad, Norway Link to the original presentation and slides on ESC 365
Dr. Behzad Elahi interviews Dr. Devin I. Rubin on his article, Needle Electromyography and Histopathologic Correlation in Myopathies. Fibrillation potentials and short-duration MUPs predict pathologic changes of muscle fiber necrosis, splitting, and/or vacuolar changes (as seen with inflammatory myopathies and muscular dystrophies). Absence of fibrillation potentials suggests other myopathologic changes (e.g., congenital myopathy). Muscle Nerve 59:315-320, 2019.
Dr. Behzad Elahi interviews Dr. Devin I. Rubin on his article, Needle Electromyography and Histopathologic Correlation in Myopathies. Fibrillation potentials and short-duration MUPs predict pathologic changes of muscle fiber necrosis, splitting, and/or vacuolar changes (as seen with inflammatory myopathies and muscular dystrophies). Absence of fibrillation potentials suggests other myopathologic changes (e.g., congenital myopathy). Muscle Nerve 59:315-320, 2019.
Dr. Behzad Elahi interviews Dr. Devin I. Rubin on his article, Needle Electromyography and Histopathologic Correlation in Myopathies. Fibrillation potentials and short-duration MUPs predict pathologic changes of muscle fiber necrosis, splitting, and/or vacuolar changes (as seen with inflammatory myopathies and muscular dystrophies). Absence of fibrillation potentials suggests other myopathologic changes (e.g., congenital myopathy). Muscle Nerve 59:315-320, 2019.
Host Doug Stephan and Dr. Ken Kronhaus of Lake Cardiology (352-735-1400) discuss who need and who don't need Statin Drugs. Then, Dr. Ken reviews Sleep Disorders and how CPAP Machines can provide real help. Next, news reveals a link between Bacon and Colorectal Cancer. Did you know that your heart rate, at rest, can influence your longevity? An in-depth look at Atrial Fibrillation is next. Plus, lots more information about maintaining your Good Health.
Dans cette 24e baladodiffusion, les Drs Luc Lanthier et Gabriel Huard discutent d’anticoagulation pour les sujets en fibrillation auriculaire qui subissent une angioplastie coronarienne (étude AUGUSTUS), en plus de réviser la littérature médicale de mars 2019. Quiz clinique (1 min 41), étude principale (2 min 05), critique (25 min 00), autres articles (31 min 30), … Continuer la lecture de « BC 024 – Anticoagulation post-angioplastie coronarienne chez les sujets avec fibrillation auriculaire (étude AUGUSTUS) »
Podcast summary of articles from the March 2019 edition of Journal of Emergency Medicine from the American Academy of Emergency Medicine. Topics include pediatric joint infections, atrial fibrillation, intranasal ketamine for headache, cannibus induced cardiomyopathy, mercury toxicity, and board review on acute compartment syndrome. Guest speakers are Dr. Colin Crowe and Dr. Michael Gottlieb.
Apple was part of a study conducted on over four hundred thousand people, in order to find out if the Apple Watch can detect irregular heartbeats. The results were amazing. Once you hear this, you might turn around and get yourself an Apple Watch!
Apple was part of a study conducted on over four hundred thousand people, in order to find out if the Apple Watch can detect irregular heartbeats. The results were amazing. Once you hear this, you might turn around and get yourself an Apple Watch!
From Essentials of Emergency Medicine NYC 2017, Reuben Strayer explains how the pulse ox might be the most useful bit of tech in the ED. Pearls: The pulse ox waveform is an excellent indicator of mechanical heart rate and peripheral perfusion. For patients breathing room air, pulse oximetry can be used to monitor for hypoventilation. Nail polish has minimal impact on the accuracy of pulse oximetry. If you are unable to get a good pulse ox waveform by adjusting or repositioning the probe, be concerned that the patient is poorly perfused. “The respiratory rate is the most vital of the vital signs.” Experienced doctors look at a patient who seems well, but understands that they’re not truly well, because they subconsciously notice tachypnea. Subconsciously is the only way to notice tachypnea, because respiratory rate is often not measured accurately. Since we don’t always have access to reliable respiratory rate, Strayer’s go-to vital sign is the oxygen saturation. “Reusable pulse oximeter probes are gross.” One study found that even when these probes are cleaned by standard procedure, ⅔ had bacteria cultured from them. Strayer recommends using single use probes in your department. Wilkins MC. Residual bacterial contamination on reusable pulse oximetrysensors. Respir Care. 1993 Nov;38(11):1155-60. PubMed PMID: 10145923. Data is conflicting about the effect of nail polish on pulse oximetry readings, but overall it is felt that the impact is minimal. Earlier data suggested that nail polish decreased sat readings by 2-10%, but more recent studies found minimal effect. If it seems that the waveform is affected by nail polish, you can remedy the situation by turning the probe 90 degrees, so it goes sideways through the finger. Yamamoto LG, et al. Nail polish does not significantly affect pulse oximetry measurements in mildly hypoxic subjects. Respir Care. 2008 Nov;53(11):1470-4. PubMed PMID: 18957149. As long as a patient is breathing room air, pulse ox can monitor ventilation and function as a hypoventilation alarm. Significantly hypercapnic patients saturate less than 95% when they’re breathing room air. So if you need to monitor a patient for hypoventilation, such as due to intoxication or procedural sedation, the pulse ox will do a great job of telling you if the patient is still breathing. If you need to give supplemental oxygen, then use capnography to monitor respirations. The pulse oximeter does so much more than provide oxygen saturation. It provides the photoplethysmogram (PPG) which is a waveform that tells you the “mechanical” heart rate. While telemetry gives the electrical heart rate, what really matters to your organs is the mechanical rate. This can be especially helpful during transvenous or transcutaneous pacing. When you have reliable tracing, the pulse ox heart rate is more reliable than the telemetry heart rate. The pulse ox can measure the peripheral perfusion index which is a more sensitive and earlier indicator of hypoperfusion than blood pressure. This is a numerical value which indicates the strength of the pulsations read by the pulse oximeter. It is based on the amplitude of the pulse ox waveform and expressed as a number between 1 (low) and 10 (high). The perfusion index dips before the stroke volume drops and long before the heart rate rises. Many monitors will report the perfusion index in tiny print after the word PERF. Lima AP, Beelen P, Bakker J. Use of a peripheral perfusion index derived from the pulse oximetry signal as a noninvasive indicator of perfusion. Crit Care Med.2002 Jun;30(6):1210-3. PubMed PMID: 12072670. van Genderen ME, et al. Peripheral perfusion index as an early predictor for central hypovolemia in awake healthy volunteers. Anesth Analg. 2013 Feb;116(2):351-6. PubMed PMID: 23302972. What if you don’t have a reliable pulse ox tracing? Most of the time this is because the probe is poorly positioned, the patient is moving too much, or there’s a lot of ambient light. If you’ve corrected for these problems and you still don’t have a good tracing, you should be concerned that the patient is poorly perfused. One study of 20,000 anesthesia cases showed that pulse ox failure was directly related to worsening physical status. Moller JT, et al. Randomized evaluation of pulse oximetry in 20,802 patients: I. Design, demography, pulse oximetry failure rate, and overall complication rate. Anesthesiology. 1993 Mar;78(3):436-44. PubMed PMID: 8457044. How does the pulse ox measure oxygen saturation and what is the best way to position the oximeter probe on the finger? One side of the pulse ox puts emits visible (red) light and infrared light. On the other side is the detector. The percent oxygen saturation is calculated based on the different way in which oxyhemoglobin absorbs visible and infrared light compared with deoxyhemoglobin. The pulse ox measures carboxyhemoglobin as if it were oxyhemoglobin, giving a falsely elevated pulse ox reading for a victim of carbon monoxide poisoning. The best spot for a peripheral pulse ox is a place with a lot of capillaries and arterioles, like the fingertips, earlobes, nose, or forehead. Functionally, it doesn’t seem to matter whether the emitter is on the dorsum, volar aspect, or even side of the finger. For convenience sake, most find it ergonomically superior to have the cord and emitter on the dorsum of the finger. Mannheimer PD. The light-tissue interaction of pulse oximetry. Anesth Analg.2007 Dec;105(6 Suppl):S10-7. Review. PubMed PMID: 18048891 Vegfors M, Lennmarken C. Carboxyhaemoglobinaemia and pulse oximetry. Br JAnaesth. 1991 May;66(5):625-6. PubMed PMID: 2031826 DeMeulenaere, Susan. "Pulse oximetry: uses and limitations." The Journal for Nurse Practitioners 3.5 (2007): 312-317. Link. Chan ED, et al. Pulse oximetry: understanding its basic principles facilitates appreciation of its limitations. Respir Med. 2013 Jun;107(6):789-99. PMID: 23490227
An echocardiogram technician told me I have a beautiful heart and that got me going. What makes for good heart health? What role do genetics, lifestyle, and environment play? Dr. Erica Pitsch talks about the Framingham Heart Study, John talks about congestive heart failure and Mended Hearts, and Saurabh shares how yoga and meditation help his stress level and coping with myotonic muscular dystrophy.
Dr. Percy Francisco Morales is a fellowship-trained electrophysiologic cardiologist who felt that he could help more people by developing an alter ego and creating online content. As physicians, we tend to answer the same questions again and again, so he thought it would be helpful for patients if he made an atrial fibrillation FAQ and thus Dr. A Fib was born. We discuss the risks associated with a fib, management options, why coumadin is becoming a thing of the past, and new procedures. www.drafib.com
The Apple Watch was built with the intention of being a health and fitness gadget. Most wearable devices can take our pulse and measure our blood pressure. Apple took this to the next level when it introduced a new feature this year. In this episode of Komando on Demand, Kim takes a look at the new Apple Watch Series 4 and its new ability to take an ECG. But how reliable is it? Kim talks to Sergei Shatillo P.A., who works with heart transplant recipients at the Mayo Clinic, about common heart ailments and how the Apple Watch Series 4 can impact people's lives.
MedAxiom HeartTalk: Transforming Cardiovascular Care Together
Four years after starting an effective A-fib clinic, Bradley Hubbard, MD, of Michigan Heart, shares his journey: first steps, lessons learned, and advice to those looking to start an A-fib clinic. Dana Carpenter is Communication Consultant for MedAxiom.Contact: HeartTalk@medaxiom.com For more information: https://www.medaxiom.com
For this episode, we bring in an expert and an esteemed guest to answer all of your burning questions about resuscitation of cardiac arrest. Part man, part mystery, but wholly dedicated to furthering excellence in out of hospital care: Dr. Walt Lubbers, MD. Some background: Walt is an Emergency and Prehospital Medicine physician who holds board certification in both EM and EMS. He's also an Assistant Professor of Emergency Medicine and Attending Physician at University of Kentucky Medical Center. If that wasn't enough, he's also the Medical Director of several EMS agencies throughout Central and Eastern Kentucky.
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 for this month's issue. We'll also hear from Dr. Suraj Kapa reporting on new research from the latest journal articles in the field. In our first article, Barry Maron associates report on the long term clinical course of hypertrophic cardiomyopathy patients following ICD therapy for ventricular arrhythmias. They studied a cohort of 486 high-risk hypertrophic cardiomyopathy patients with ICDs from eight international centers. Of these 486 patients over 6.4 years, 94 patients or 19% experienced appropriate ICD interventions, terminating VT or VF. Of the 94 patients receiving appropriate ICD therapy, 87 were asymptomatic or only mildly symptomatic at the time of appropriate ICD interventions. Of these 87 patients, 74 or 85% remained in classes one or two without significant change in clinical status of the subsequent 5.9 years up to 22 years. Among the 94 patients, there was one sudden death in three patients who died from non arrhythmic hypertrophic cardiomyopathy related processes. Post ICD intervention, freedom from hypertrophic cardiomyopathy, mortality was 100% at one year, 97% at five years, and 92% at 10 years, distinctly lower than the risk of ischemic or non ischemic cardiomyopathy in ICD trials. Hypertrophic cardiomyopathy patients with ICDs interventions reported the heightened anxiety and expectation of future shocks. However, they did not affect general psychological well-being or quality of life. The authors concluded that in hypertrophic cardiomyopathy, unlike ischemic heart disease, prevention of sudden death with ICD therapies unassociated with a significant increase in cardiovascular morbidity and mortality, nor transformation into heart failure deterioration, ICD therapy does not substantially impair overall psychological and physical well-being. In our next article, Abdulla Damluji and associates examined the cost of hospitalizations for cardiac arrest using the US nationwide inpatient sample from 2003 to 2012. Using the log transformation of inflation adjusted costs the authors examined 1,387,396 patients who were hospitalized after cardiac arrest. They had a mean age of 66 years. Inpatient procedures included coronary angiography in 15%, PCI in 7%, intra-aortic balloon pump in 4.4%, therapeutic hypothermia in 1.1%, and mechanical circulatory support in 0.1% of patients. Notably the rates of therapeutic hypothermia increased from 0 in 2003 to 2.7 in 2012, p less than 0.001. Both hospital charges inflation adjusted costs linear increased over time. In a multi-variant analysis predictors of inflation adjusted costs included large hospitals size, urban teaching hospital, and length of stay. Among co-morbidities, atrial fibrillation or fluid and electrolytes imbalance were the most common associated with cost. The authors found that during the period between 2003 and 2012 post cardiac arrest, hospitalizations had a steady rise and associated healthcare costs likely related to increase length of stay, medical procedures and systems of care. In our next paper, Peter Huntjens and associates examined intrinsic interventricular dyssynchrony as a predictor of human dynamic response to cardiac resynchronization. The authors use a cardiovascular computational model CircAdapt to characterize the isolated effect of intrinsic interventricular or intraventricular activation on resynchronization therapy response that is the change in LV dP/dt max. The simulated change in LV dP to dt max had a range of 1.3 to 26.5% increased considerably with increasing inter ventricular dyssynchrony. In contrast, the isolated effect of intra ventricular dyssynchrony was limited with the change in the LV dP/dt max range and the left ventricle from 12.3 to 18.3% in the right ventricle from 14 to 15.7%. Secondly, electrocardiographic imaging derived activation characteristics of 51 CRT candidates were used to create individual models of ventricular activation in CircAdapt. The model predicted change in LV dP/dt max was close to the actual value in left bundle branch block patients with 2.7% difference between measured and simulated when only intrinsic interventricular dyssynchrony was personalized. Among non left bundle branch block patients a change in LV dP/dt max was systematically over predicted by CircAdapt with a 9.2% difference between measured and simulated. Adding intra ventricular activation to the model did not improve the accuracy of response prediction. The authors found that computer revealed intrinsic interventricular dyssynchrony is the dominant component of the electrical substrate driving the response to CRT. In the next paper Kenji Kuroki and associates examined the use of voltage limit adjustment of substrate mapping and fast Fourier transform analysis of local ventricular bipolar electrograms during sinus rhythm to predict VT isthmuses. They performed these studies and nine post infarction patients who underwent catheter ablation for total of 13 monomorphic ventricular tachycardias. Relatively higher voltage areas on electroanatomical map or defined as high voltage channels, which were further classified as full or partial if the entire or more than 30% of the high voltage channel was detectable. 12 full high voltage channels were identified in seven of nine patients. Relatively higher fast Fourier transform areas were defined as high frequency channels, which were located on seven of 12 full high voltage channels. Five VT isthmuses or 71% were included in the seven full high voltage channels positive in high frequency channel positive sites. While no VT isthmuses were found in five full high voltage channel positive but high frequency channel negative sites, high frequency channels were identical to 9 out of 16 partial high voltage channels. Eight VT isthmuses or 89% were included in nine partial high voltage channel positive in high frequency channel positive sites, whereas no VTs isthmuses were found in the seven partial high voltage channel positive and high frequency channel negative sites. All high voltage channel positive in high-frequency channel positive sites predicted VT isthmus with a sensitivity of 100% and specificity of 80%. The authors concluded that based on this small series that combined use of voltage, limited adjustment and fast Fourier transform analysis may be useful method to detect VT isthmuses. In the next study, John Whitaker and associates examined the use of lesion index, LSI index, a proprietary algorithm combining contact force, radio-frequency application duration, and RF current. Cardiac CT was used to assess atrial tissue thickness. Ablation lines two to three per animal were created in the right atrium in seven mini pigs with point lesions using 25 watts of energy. Two weeks after the ablation, serial sections of targeted atrial tissue or examine histologically to identify gaps and transmural ablation. LSI guidelines had a lower incidence of histological gaps. Four gaps in the 69 catheter moved or 5.8% compared to ablation using LSI plus two millimeter lines in which there is seven gaps in 33 catheter moves or 21.2% and using LSI plus four millimeter lines in which there are 15 gaps in 23 moves or 65.2% p less than 0.0. The change in LSI was calculated retrospectively is a distance between two adjacent lesions above the mean LSI of the two lesions. Changing LSI values of 1.5 or less were associated with no gaps in transmural ablation. The authors concluded that in this mod of chronic atrial ablation delivery of uninterrupted transmural linear lesions may be facilitated using LSI to guide catheter movement. When change in LSI between adjacent legions is 1.5 millimeters or lower, no gaps in atrial linear lesions should be expected. In our next paper, Matthew Bennett and associate examined whether their response to antitachycardia pacing in patients with ICD could further discriminate ventricular from super ventricular arrhythmias in patients receiving ATP in the RAFT trial. The RAFT trial randomized 1,798 patients with New York Heart Association class two or three heart failure, left ventricular ejection fraction less than or equal to 30%, in QRS duration 120 millisecond or greater, to an ICD plus or a minus cardiac resynchronization. Beginning with 10,916 ATP attempts for 8,150 tachycardia episodes in 924 patients, the author's excluded tachycardias where ATP terminated the episode or were the specific etiology tachycardia was uncertain. In this study, they analyzed 3,676 ATP attempts delivered to 2,046 tachycardia episodes in 541 patients. The authors found that a shorter difference between the post pacing interval is PPI minus TCL, was more likely to be associated with VT than SVT, mean of 138.1 milliseconds for VT and 277.4 milliseconds for SVT p, less than 0.001. A PPI minus TCL value of less than or equal to 300 milliseconds had a sensitivity in 97.4% and a specificity of 28.3% for VT. The authors concluded that specifically the PPI minus TCL following antitachycardia pacing may help distinguish ventricular from supraventricular arrhythmias. In the next study, Shailee Shah and Amr Barakat and associates examined the outcomes after repeat AF ablation. The authors examined 137 patients out of a total of 10,378 patients undergoing Afib ablation who had had initial long-term success defined from recurrent arrhythmias for greater than 36 months off anti-arrhythmic drugs in subsequent underwent repeat ablation for recurrent atrial fibrillation. The median arrhythmia free period that define long-term success was 52 months. In redo-ablations reconnection of at least one of the pulmonary veins was found in 111 or 81% of patients. Additional non PV ablations were performed in 127 or 92.7% of patients. After a mean follow-up of 17 months, 103 patients or 75% were arrhythmia-free, 79 off anti-arrhythmics, and 24 on arrhythmics. The authors found that repeat ablations with re-isolation to the point of veins and modifying the atrial substrate had a good success rate. In the next article Qiongling Wang and associates hypothesized that genetic inhibition of CaMKII oxidation in a mouse model of Duchenne muscular dystrophy can alleviate abnormal calcium homeostasis thus preventing ventricular arrhythmias. The authors tested whether the selective loss of oxidation of the CaMKII effects ventricular arrhythmias in the mouse model of Duchenne muscular dystrophy. Genetic inhibition of ox-CaM kinase II by knocking replacement of the regulatory domain methionines with valines, which we'll call MMVV, prevented ventricular tachycardia in the mdx mice. Confocal calcium imaging of ventricular myocytes, isolated from the mdx MMVV mice revealed normalization of intra-calcium release events compared to myocytes from the mdx mice. Abnormal action potentials as assessed by optical mapping mdx were also alleviated by genetic inhibition of ox-CaMK II. Knockout of the NADPH oxidase regulatory sub-unit P 47 Fox normalized elevated ox-CaMK II, repaired intracellular calcium hemostasis and rescued inducible ventricular arrhythmias in the mdx mice. The authors concluded that inhibition of ROS or ox-CaMK II protects against pro-arrhythmic intracellular calcium handling, preventing ventricular arrhythmias in a mouse model of Duchenne muscular dystrophy. In the next article, Kyohei Marume and Teruo Noguchi and associates examined whether the combination of QRS duration of 120 milliseconds or greater in late gadolinium enhancement is a precise prognostic indicator for the primary endpoint of all cause death and a composite of sudden cardiac death or aborted sudden cardiac death in 531 patients with dilated cardiomyopathy. They also analyzed the association between the combination of late gadolinium enhancement and increased QRS duration in these end points among patients with a class one indication for implantable defibrillator. The author's divided study patients in three groups according to late gadolinium enhancement in QRS duration. Two negative indices that is late gadolinium enhancement negative and narrow QRS, one positive index with either late gadolinium enhancement positive or wide QRS or two positive indices late gadolinium positive and wide QRS and followed them for 3.8 years. Multiple variable Cox regression analysis identified to positive indices as significant predictors of all cause death. A hazard ratio of 4.29 p equals 0.026. Among the 317 patients with a class one indication for ICD, the five year event rate of sudden cardiac death or aborted sudden cardiac death was lowest in the two negative indices groups, 1.4%. With propensity score matching cohorts the two negative indices group had a significant lower event rate of sudden cardiac death or aborted sudden cardiac death than to two other groups hazard ratio 0.2, p equals 0.046. The authors concluded that the combination of late gadolinium enhancement in wide QRS provides additional prognostic stratification compared to late gadolinium enhancement status alone. In the next study, Matthew Sulkin and associates examined whether a novel local impedance measurement on an ablation catheter identifies catheter tissue coupling and is predictive of lesion formation. The author's first studied explanted hearts, 10 swine, and then in vivo 10 swine, using an investigational electro anatomical mapping system that measures impedance from an ablation catheter with mini electrodes incorporated into the distal electrode. Rhythmia and Intellanav, Boston Scientific. Explanted tissue was placed in a warmed 37 degree celsius saline bath mounted on a scale, and the local impedance was measured 15 millimeters away from the tissue to five millimeters of catheter tissue compression at multiple catheter angles. Lesions were created for 31 and 50 watts from 5 to 45 seconds for an N of 70. During in vivo valuation of the local impedance measurements of the myocardium 90 and blood pool 30 were guided by intracardiac ultrasound while operators were blinded to the local impedance data. Lesions were created with 31 and 50 watts for 45 seconds in the ventricle with an n of 72. The local impedance of myocardium, which was 119.7 ohms, was significantly greater than in blood pool 67.6 ohms the p of less than 0.01. Models that incorporate local impedance drop to predict lesion size had better performance that models incorporate force time integral r squared of 0.75 versus r squared of 0.54 and generator impedance drop r squared of 0.2 versus r squared of 0.58. Steam pops displayed a significantly higher starting local impedance and a larger change in local impedance compared to successful RF applications, p less than 0.01. The authors concluded that local impedance recorded for miniature electrodes provides a valuable measure of catheter tissue coupling and the change in local impedance is predictive of lesion formation during RF ablation. In the next paper, Boaz Avitall and associates found that the rising impedance recorded from a ring electrode placed two millimeters from the cryoballoon signifies ice formation covering the balloon surface and indicates ice expansion. The authors studied 12 canines in a total of 57 pulmonary veins, which were targeted for isolation. Two cryoapplications were delivered per vein with a minimum of 90 and a maximum 180 second duration. Cryoapplications was terminated upon reaching a 500 ohm change from baseline. Animals recovered 38 plus or minus six days post procedure, and the veins were assessed electrically for isolation. Heart tissue was histological examined. Extra cardiac structures were examined for damage. Pulmonary vein isolation was achieved in 100% of veins if the impedance reached 500 ohms in 90 to 180 seconds. When the final impedance was between 200 and 500 ohms within 180 seconds of freeze time, pulmonary vein isolation was achieved in 86.8%. For impedance of less than 200 ohms pulmonary vein isolation was achieved in 14%. No extra cardiac damage was recorded. The authors found that impedance rise of 500 ohms at less than 90 seconds with a freeze time of 90 seconds resulted in 100% pulmonary vein isolation. In our final papers Sally-Ann Clur and associates examined left ventricular isovolumetric relaxation time as the potential diagnostic marker for fetal Long QT Syndrome. Left ventricular isovolumetric contraction time, ejection time, left ventricular isovolumetric relaxation time, cycle length, and fetal heart rate were measured using pulse doppler wave forms in fetuses. Time intervals were expressed as percentage of cycle length, and the left ventricular myocardium performance index was calculated. Single measurements were stratified and compared between Long QT Syndrome fetuses and controls. Receiver operator curves were reformed for fetal heart rate in normalized left ventricular isovolumetric relaxation time. A linear mixed effect model including multiple measurements was used to analyze fetal heart rate, the left ventricular iso volume metric relaxation time, and the left ventricular myocardial performance index. There were 33 Long QT fetuses in 469 controls. In Long QT fetuses the left ventricular isovolumetric relaxation time was prolonged in all groups, p less than 0.001, as was the left ventricular isovolumetric relaxation time. The best cutoff to diagnose Long QT syndrome was the normalized left ventricular isovolumetric relaxation time greater than equal to 11.3 at less than or equal to 20 weeks, giving a sensitivity in 92% and a specificity of 70%. Simultaneous analysis of the normalized left ventricular isovolumetric relaxation time and fetal heart rate improved the sensitivity and specificity of Long QT Syndrome, AUC of 0.96. The normalized left ventricular isovolumetric relaxation time, the left ventricular myocardial performance index, and fetal heart rate trends differed significantly between Long QT Syndrome fetuses and controls throughout gestation. The authors concluded that left ventricular volumetric relaxation time is Prolonged QT fetuses. Findings of a prolonged normalize left ventricular isovolumetric relaxation time, and sinus bradycardia can improve the prenatal detection of fetal Long QT Syndrome. 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 podcasts On the Beat. Take it away Suraj. Suraj Kapa: Thank you, Paul and welcome back to On the Beat were we will be summarizing hard-hitting articles across the entire electrophysiologic literature. Today we'll be starting within the realm of atrial fibrillation where we're review an article within the realm of anticoagulation and stroke prevention. Quon et al. published in last month's issue of JACC cardiac electrophysiology on anticoagulant use and risk of ischemic stroke and bleeding in patients with secondary atrial fibrillation. It is well known that use of anticoagulation in atrial fibrillation can reduce overall thromboembolic outcomes. However, its role in secondary atrial fibrillation is unclear. Thus, the authors sought to evaluate the effects anticoagulant use on stroke and bleeding risk. Amongst those where atrial fibrillation occurred in the setting of acute coronary syndrome, pulmonary disease, or sepsis. Amongst around 2300 patients evaluated retrospectively there was no evidence of a lower incidence of ischemic stroke among those treated with anticoagulants compared to those who are not. However, anticoagulation was associated with a higher risk of bleeding in those with new onset AF associated with acute pulmonary disease. The authors suggest as a result that there is unclear overall benefit for long-term anticoagulation in patients with presumed secondary atrial fibrillation. The difficulty in assessing this is how to define secondary atrial fibrillation. However, in many studies patients who developed in the setting of acute illness still had a high risk of developing quote unquote clinically significant AF in long-term follow-up. However, this was not necessarily absolute as many patients not necessarily develop AF that could be considered clinically significant. Thus, the clinical question that arises is: how long should we treat a patient with anticoagulation when they have presumed secondary atrial fibrillation. These data seem to suggest that there may be no net overall benefits. In other words, all-comers with secondary atrial fibrillation should not necessarily be forever treated with anti-coagulation. However, this slightly requires clinical trials to evaluate further. Next we delve into the realm of cardiac mapping and ablation where we view an article by Gaita et al. entitled 'Very long-term outcome following transcatheter ablation of atrial fibrillation. Are results maintained after 10 years of follow-up?', published in Europace last month. While pulmonary vein isolation is a widely accepted approach for treatment of atrial fibrillation, most reported studies review outcomes in terms of freedom of AF over a relatively short time period, generally two to five years. However longer term follow up is inconsistently reported. Gaita et al. sought to review 10 year outcomes amongst 255 patients undergoing ablation in a single center. They noted 52% remainder arrhythmia-free amongst a mixed cohort of both paroxysmal and persistent patients while 10% progressed to permanent atrial fiBrillation. They found that absence of increases in blood pressure, BMI, and fasting glucose was protective against an arrhythmia recurrence. These findings suggest that in a relatively small cohort of patients limited to a single center that even long-term outcomes after pulmonary vein isolation are generally quite good, exceeding 50%. However, future freedom from atrial fibrillation is heavily tied to control of other risk factors. In other words, if a patient is going to have poor control of diabetes, blood pressure, or gain weight, the benefit of their pulmonary vein isolation over long-term follow-up is likely less. These data thus highlight both the potential long-term benefit of PVI, but also the importance of counseling patients regarding the need for continued management and control of future and existing risk factors. Staying within the realm of atrial fibrillation we next review an article by Weng et al. entitled 'Genetic Predisposition, Clinical Risk Factor Burden, and Lifetime Risk of Atrial Fibrillation' published in last month's issue of circulation. The probability of detecting atrial fibrillation in patients based on clinical factors and genetic risk is unknown. Weng et al. sought to clarify whether a combination of clinical and polygenic risk scores could be used to predict risk of developing atrial fibrillation over long-term followup in the Framingham Heart Study. Amongst 4,600 individuals, 580 developed incident atrial fibrillation and had an overall lifetime risk of developing atrial fibrillation of 37%. Those are the lowest risk tertile based on clinical risk factor burden and genetic predisposition had a lifetime risk of 22% versus 48% in the highest. Furthermore, a lower clinical risk factor burden was associated with delayed atrial fibrillation onset. In order to identify patients with atrial fibrillation, before negative sequelae such as stroke occur, patient and physician understanding of risk and monitoring needs is necessary. The fact is that it will be great to identify every single patient who has atrial fibrillation before they have a negative sequela of that atrial fibrillation such as ischemic stroke. However, performing continuous monitoring of all patients with potential negative sequelae of atrial fibrillation is extraordinarily difficult. The reason is it's excessively costly. We cannot monitor the entire population irrespective of whatever the risk factors are. However, if we're able to identify the highest risk cohorts early on before the atrial fibrillation onsets, this may offer opportunities for use of newer cheaper monitors. The work by Weng et al. suggests one such possible approach combines clinical and polygenic risk scores. Actionability of these data, however, remains to be seen and further validation other cohorts is necessary to clarify generalized ability. The next article we review is published in last month's issue of the Journal of American College of Cardiology by Lopes at al. entitled 'Digoxin and Mortality in Patients With Atrial Fibrillation. Lopes et al. sought to evaluate the impact of the Digoxin on mortality in patients with atrial fibrillation and the association with the Digoxin serum concentration and heart failure status. They value this association in over 17,000 patients. At baseline 32% were receiving Digoxin. Baseline Digoxin use did not associate with risk of death, but even in these patients a serum concentration of greater than 1.2 nanograms per milliliter was associated with a 56% increase in mortality risk. For each .5 nanogram per milliliter increase in oxygen concentration the hazard ratio increased by 19% for overall mortality. This was irrespective of heart failure status. Furthermore, in patients who are newly started in Digoxin over the follow-up period, the risk and death and sudden death was higher. These data suggests a significant risk associated with Digoxin use for management of atrial fibrillation irrespective of heart failure status. Furthermore, serum valleys above 1.2 require close consideration of dose de-escalation. Whether there is any optimal dose, however, from the study is unclear. These data amongst a host of prior data strongly suggest again strategic use of Digoxin principally for the management of atrial fibrillation. Moving on within the realm of atrial fibrillation, we review an article published in last month's issue of Circulation Research by Yan et al. entitled Stress Signaling JNK2 Crosstalk with CaMKII Underlies Enhanced Atrial Arrhythmogenesis. In this more acellular based study the mechanism underlying atrial arrhythmogenesis associated with aging was evaluated. Yan et al. sought to figure out whether the stress response JNK in calcium mediated arrhythmias might contribute to atrial arrhythmogenesis in aged transgenic mouse models. They demonstrated significant increased activity of JNK2 and aging atria, those furthermore associated with rhythmic remodeling. This association was mediated through CaMKII and ryanodine receptor channel function, with activation of the former leading to increased calcium leak mediated by the ladder. This in turn related to increase atrial fibrillation likelihood. Identifying novel targets for atrial fibrillation therapy is critical. Given atrial fibrillation is a complex disease process related to a multitude of risk factors it can be assumed that the contribution of any single factor may be mediated through distinct mechanisms. Aging in particular as well regarded, but considered to be non-modifiable risk factor for atrial fibrillation. Identifying genes or pathways, the immediate aging associated fibrillation, may take the risk of aging as no longer a non-modifiable thing. The finding of the significance of JNK2 and associate downstream effects with AF risks and aging hearts may hold potential in offering unique therapeutic targets. Finally, within the realm of atrial fibrillation, we're viewing article by Chen et al. in last month's issue of the Journal of the American Heart Association entitled Association of Atrial Fibrillation With Cognitive Decline and Dementia Over 20 Years: The ARIC-NCS Study. Multiple studies have suggested a significant association between atrial fibrillation risk of dementia. However, these studies have limited time follow-up and were often done and predominantly white patients. Thus, the authors sought to use the data from ARIC, the Atherosclerosis Risk in Communities Neurocognitive Study, to assess the risk of cognitive decline associated with atrial fibrillation. Amongst over 12,000 participants, a quarter of whom are black and half of whom are white, they noted 2100 patients developed atrial fibrillation and 1,150 develop dementia over a 20 year follow up period. There was a significantly greater risk of cognitive decline amongst those who developed atrial fibrillation. In turn incident atrial fibrillation for the follow-up period was associated with a higher risk of dementia even after adjusting for other clinical and cardiovascular risk factors such as incidents that ischemic stroke. These data further strengthened prior evidence of a direct link between atrial fibrillation and risk of cognitive decline and dementia. Understanding this long-term risk raises the need to additionally identify approaches to prevent this occurrence, which in turn is dependent on understanding the underlying mechanisms. The finding that the risk of cognitive decline dementias independent of ischemic stroke events raises concern that either subclinical micro-embolic events or other factors may be playing a role in this risk and in turn raises question as to how best to prevent them. Until better understood, however, the question of whether the association is causal remains to be seen. Changing gears yet again, we now delve into the realm of ICDs, pacemakers and CRT. Published in last month, issue of Heart Rhythm Tarakji et al. published a paper entitled 'Unrecognized venous injuries after cardiac implantable electronic device transvenous lead extraction.' Overall risk of transvenous lead extraction includes that of potentially fatal venous laceration. The authors sought to evaluate the incidence of venous injury that may be unrecognized based on microscopic study of extracted leads. Amongst 861 leads obtained from 461 patients they noted 80 leads or almost 9%. Amongst 15% of patients showed segments vein on the lead body, most of which were transmural including the tissue layer. However, in terms of clinical significance, only 1% had need for emergent surgical intervention for clinically significant venous laceration. Risk factors for having the entire vein on the lead included age of lead, ICD leads, and the use of the laser sheath. These findings suggest that there may be a high incidence of subclinical venous injury after lead extraction though rarely resulting clinically apparent sequelae. As would be expected, venous injury, including transmural removal of portions of the vein traversed by the lead, was more common amongst older leads, which generally more often require laser sheets and ICD leads. The question is however, whether this carries any direct clinical implications. One they may be considered is the potential additive risk of an advancing new lead through the same venous channel, particularly in the setting of potential transmural venous injury that already exists. Next in last month's issue of Heart Rhythm we review an article by Sharma at al. entitled 'Permanent His-bundle pacing as an alternative to biventricular pacing for cardiac resynchronization therapy: A multicenter experience.' The use of resynchronization therapy for treatment of patients with heart failure and wide QRS has been shown to offer morbidity and mortality benefits. However, many patients maybe non-responders, and recent studies on His bundle pacing of suggested potential clinical benefits. His bundle pacing essentially only requires one pacing catheter attached within the region of the His bundle Sharma et al. sought to evaluate the safety and success rates of His bundle pacing for patients who have either failed standard resynchronization therapy or in whom most tried as a primary intervention. They noted His bundle pacing was successful in 90% of patients with reasonable myocardial and His bundle capture thresholds. Patients in both groups exhibits significant narrowing of QRS morphology and improvement in left ventricular ejection fraction from a mean of 30 to 43%. However, a total of seven patients had lead related complications. These database on a retrospective analysis of two types of patients, those failing standard biventricular therapy, and those on whom his bundle pacing was attempted as a primary modality suggest overall safety and efficacy in a handful of experienced centers. The promise of His bundle pacing is that a may allow for more effective resynchronization than standard approaches. The high rate of success suggests that His bundle pacing maybe both safe and reasonable to pursue. However randomized trials across more centers are needed to fully prove its benefit, particularly as a primary modality of treatments. Next we review ICDs and chronic kidney disease. In last month's issue of JAMA cardiology by Bansal at al. entitled 'Long-term Outcomes Associated With Implantable Cardioverter Defibrillator in Adults With Chronic Kidney Disease.' While the benefit of ICDs in patients with low EF is widely recognized, modifying factors that may increase risk of death are not as well defined. These include things like advanced age and chronic kidney disease. Bansal et al. sought to evaluate long-term outcomes and ICD therapy in patients with chronic kidney disease. In retrospective study of almost 5,900 ambulatory patients amongst whom 1550 had an ICD, they found no difference in all cause mortality. However, ICD placement was associated with an increased risk of subsequent hospitalization due to heart failure or any cause hospitalization. In light of recent studies such as DANISH the robust sense of ICD benefit is being questioned. One of the thoughts for the absence of similar benefit to prior studies lies in the improving care of ambulatory heart failure patients. In patients with chronic kidney disease several questions rises to the risk with ICD, including infectious risk in dialysis patients and the concomitant mortality risk with renal dysfunction. The author suggested in retrospective study, no incremental benefit of ICDs in patients with chronic kidney disease and perhaps some element of added risk is related to hospitalization. However, this study has several limitations. It is retrospective and many patients received ICDs may have been perceived to be sicker in some way. Thus care must be taken in interpretation, but consideration of randomized studies to adjudicate benefit are likely necessary. Finally, within the realm of devices, we reviewed an article by Tayal et al. entitled "Cardiac Resynchronization Therapy in Patients With Heart Failure and Narrow QRS Complexes.' publishing the Journal of American College of Cardiology last month. Several parameters have been stressed to identify benefit of resynchronization therapy in patients with wide QRS include cross correlation analysis with tissue doppler imaging. However, many patients may have evidence in mechanical dyssynchrony even in the absence of an apparent wide QRS thus Tayal et al. sought to evaluate the benefit of resynchronization therapy amongst 807 patients with heart failure and a narrow QRS mean criteria in a randomized study. Of the 807 46% had delayed mechanical activation. Those without delay mechanical activation had underwent we standardization therapy and were associated with worse overall outcomes likely due to new delayed mechanical activation potentially related to CRT pacing. These data support the absence of a role for resynchronization therapy in patients with a narrow QRS. This is expected as resynchronization therapy likely offers the most benefit in patients with mechanical dyssynchrony that results from electrical dyssynchrony. Since by its very nature resynchronization therapy relies on non physiologic cardiac pacing thus compared to normal cardiac activation the nature of resynchronization pacing is desynchronization. These data support the absence of a role for resynchronization therapy in patients with heart failure and narrow QRS complexes. Moving on to cellular electrophysiology we review an article by Kozasa et al. published in last month's issue of Journal of Physiology entitled 'HCN4 pacemaker channels attenuate the parasympathetic response and stabilize the spontaneous firing of the sinoatrial node.' Heart rate is controlled by an interplay between sympathetic and parasympathetic components. In turn HCN4 abnormalities have been implicated in congenital sick sinus syndrome. The authors sought to clarify the contribution of HCN4 to sinus node autonomic regulation. They created a novel gain-of-function mouse where the HCN4 activity could be modulating from zero to three times normal. They then evaluated ambulatory heart-rate variability and responsive heart rate to vagus nerve stimulation. They found HCN4 over-expression did not increase heart rate, but attenuated heart-rate variability. It also attenuated bradycardic response to vagus nerve stimulation. Knockdown of HCN4 in turn lead to sinus arrhythmia and enhanced parasympathetic response. These data suggest HCN4 attenuates sinus node response to vagal stimuli thus stabilizing spontaneous firing of the node. The clinical application of this remain to be seen but are maybe important in that they highlight a mechanism for a heretofore poorly understood mechanism for how exactly HCN4 abnormalities may lead to sick sinus syndrome. Within the realm of ventricular arrhythmias we highlighted a number of articles published this past month. The first article we review was published in last month's issue of JACC clinical electrophysiology, entitled characterization of the electrode atomic substrate and cardiac sarcoidosis: correlation with imaging findings of scarring inflammation published by [inaudible 00:41:40] et al. In patients with cardiac sarcoidosis one of the questions is how to define the electronic atomic substrate, particularly before we entered the electrophysiology laboratory. Both active inflammation and replacement fibrosis maybe be seen in patients. The authors evaluated in 42 patients with cardiac sarcoidosis, the association between an abnormal electrograms and cardiac imaging findings including PET and Computed Tomography, as well as Cardiac MRI. They noted that amongst these 40 patients, a total of 21,000 electrograms were obtained, and a total of 19% of these were classified as abnormal. Most of the abnormalities occurred in the basal paravalvular segments and intraventricular septum. They further noted that many of these abnormalities in terms of electrograms were located outside the low voltage areas, particularly as it relates to fractionation. In about 90% of patients they notice late gadolinium enhancements and they noted abnormal FDG uptakes suggesting active inflammation in about 48%. However, it should be noted that only 29 of the 42 patients underwent cardiac imaging. Segments with abnormal electrograms tended to have more late gadolinium enhancement evidence scar transmurality, and also they noted that the association of abnormal PET scan did not necessarily occur with abnormal electrograms. Thus, they concluded that in patients with cardiac sarcoidosis and ventricular tachycardia pre-procedural imaging with cardiac MRI could be useful in detecting electroanatomic map abnormalities that may in turn be potential targets for substrate ablation. However, they were more likely associated with more scar transmurality and lower degrees of inflammation on PET scanning. These data are important in that they highlight potential non-invasive means by which to understand where substrate might occur in patients with the cardiac sarcoidosis. It is well recognized that cardiac sarcoidosis is associated with increased risk of ventricular arrhythmias. These risks have increased ventricular arrhythmias, might be targetable with ablation. Newer therapies might even offer non invasive means by which to perform ablation in patients best. Thus if we could identify non based on mechanisms of identifying the substrate, this will be even more critical. The critical findings of this particular paper lie in noting that most of the abnormalities still is in intra ventricular sePtum in basal segments, and also that it is MRI in late gadolinium enhancement and associates more with the abnormal electrograms. Interestingly, the absence of inflammation correlating with the presence of more abnormal electrograms suggests that it is not so much the act of inflammation as being reflected in the endocardial map, but the existence of scar. Next, again within JACC clinical electrophysiology we review an article by Porta-Sánchez et al. entitled 'Multicenter Study of Ischemic Ventricular Tachycardia Ablation With Decrement Evoked Potential Mapping With Extra Stimulus.' The authors sought to conduct a multicenter study of decrement evoked potential base functional tech ventricular tachycardia substrate modification to see if such mechanistic and physiologic strategies could result in reduction in VT burden. It is noted that really only a fraction of the myocardium in what we presume to be substrate based on the presence of low voltage areas are actually involved in the initiation and perpetuation of VT. Thus if we can identify the critical areas within the presumed substrate for ablation, this would be even a better way of potentially honing in on our targets. They included 20 consecutive patients with ischemic cardiomyopathy. During substrate mapping fractionated late potentials were targeted and an extra stimulus was provided to determine which display decrements. All patients underwent DEEP focus ablation with elimination being correlated with VT non-inducibility after radio-frequency ablation. Patients were predominantly male, and they noted that the specificity of these decrement evoked potentials to detect the cardiac isthmus for VT was better than that of using late potentials alone. They noted 15 of 20 patients were free of any VT after ablation of these targets over six months of follow-up, and there was a strong reduction in VT burden compared to six months pre ablation. They concluded that detriment evoked potential based strategies towards ablation for ventricular tachycardia might identify the functional substrate and those areas most critical to ablation. They in turn regarded that by its physiologic nature it offers greater access to folks to ablation therapies. This publication is important in that it highlights another means by which we can better hone in on the most critical regions for substrate evaluation in patients with ventricular tachycardia. The fact is more extensive ablation is not necessarily better and might result in increased risk of harm if we think about the potential effects of longer ablations or more ablation lesions. Thus if we could identify ways of only targeting those areas that are most critical to the VT circuits, we could perhaps short and ablation procedural time, allow for novel ways of approaching targeted ablation with limited amounts of ablation performed, or perhaps even improve overall VT outcomes by knowing the areas that are most critical to ensure adequate ablation therapy provided. However, we need to understand that this is still a limited number of patients evaluated in a non randomized manner. Thus whether or not more extensive ablation performed might have been better is as of yet unclear Staying within the realm of ventricular tachycardia we review an article published in last month's issue of Heart Rhythm by Winterfield et al. entitled the 'Impact of ventricular tachycardia ablation on healthcare utilization.' Catheter ablation of atrial tachycardia has been well accepted to reduce recurrent shocks in patients with ICDs. However, this is a potentially costly procedure, and thus effect on overall long-term health care utilization remains to be seen. The authors sought to evaluate in a large scale real world retrospective study the effect of VT ablation on overall medical expenditures in healthcare utilization. A total 523 patients met study inclusion criteria from the market scan database. After VT ablation median annual cardiac rhythm related medical expenditures actually decreased by over $5,000. Moreover the percentage of patients with at least one cardiac rhythm related hospitalization an ER visit decreased from 53 and 41% before ablation respectively, to 28 and 26% after ablation. Similar changes we're seeing in number of all cause hospitalizations and ER visits. During the year before VT ablation interestingly there was an increasing rate of healthcare resource utilization, but a drastic slowing after ablation. These data suggests that catheter ablation may lead to reduced hospitalization in overall healthcare utilization. The importance of these findings lies in understanding why we do the things we do. We can provide a number of therapies to patients, but we seek two different effects. One is the individual effect of improving their particular health. The second thing is trying to avoid increasing healthcare expenditures on a population level and making sure resources are utilized. If we can reduce recurrent hospitalizations and overall healthcare expenditure in patients by providing a therapy in addition to provide individual benefit, this is the optimal situation. These data suggests that VT ablation might provide such a benefits, that in fact it reduces overall healthcare utilization while improving overall outcomes. Next and finally within the realm of ventricular arrhythmias, we review more on the basic side the role of Titin cardiomyopathy leads to altered mitochondrial energetics, increased fibrosis and long-term life-threatening arrhythmias, published by Verdonschot et al. in last month's issue of European Heart Journal. It is known now that truncating Titin variants might be the most prevalent genetic cause of dilated cardiomyopathy. Thus, the authors sought to study clinical parameters and long term outcomes related to Titin abnormalities in dilated cardiomyopathy. They reviewed 303 consecutive and extensively phenotype dilated cardiomyopathy patients who underwent cardiac imaging, Holter monitoring, and endomyocardial biopsy and in turn also underwent DNA sequencing of 47 cardiomyopathy associated genes. 13% of these patients had Titin abnormalities. Over long-term followup they noted that these patients had increased ventricular arrhythmias compared to other types of dilated cardiomyopathy, but interestingly, they had similar survival rates. Arrhythmias in those Titin abnormal patients were most prominent in those who were subjected to an additional environmental trigger, including viral infection, cardiac inflammation, other systemic disease or toxic exposure. They also noted the cardiac mass was relatively reduced in titan admirable patients. They felt that all components of the mitochondrial electron transport chain we're simply up-regulated in Titin abnormal patients during RNA sequencing and interstitial fibrosis was also augmented. As a result, they concluded that Titin variant associated dilated cardiomyopathy was associated with an increased risk of ventricular arrhythmias, and also with more interstitial fibrosis. For a long time we have reviewed all non ischemic cardiomyopathy as essentially equal. However, more recent data has suggested that we can actually hone in on the cause. In turn, if we hone in on the cause, we might be able to understand the effects of specific therapies for ventricular arrhythmias based on that underlying cause. Patchy fibrosis might not be as amenable, for example, to ablation as discreet substrate that we might see in infarct related VT. Understanding the relative benefit in very specific types of myopathies might hold benefit in understanding how to, one, risk stratify these patients, and two, understand what type of therapy, whether pharmacologic or ablative, might result in greatest benefit to the patients. Changing gears entirely now to the role of genetics, we review multiple articles in various genetic syndromes published this past month. First, we reviewed an article by Providência et al. published in the last month's issue of heart entitled 'Impact of QTc formulae in the prevalence of short corrected QT interval and impact on probability and diagnosis of short QT syndrome.' The authors sought to assess the overall prevalence of short corrected QT intervals and the impact on diagnosis of short QT syndrome using different methods for correcting the QT interval. In this observational study they reviewed the sudden cardiac death screening of risk factors cohorts. They then applied multiple different correction formulae to the ECGs. They noted that the prevalence of individuals with the QTc less than 330 and 320 was extremely low, namely less than .07 and .02% respectively. They were also more frequently identified using the Framingham correction. The different QTc correction formulae could lead to a shift of anywhere from 5 to 10% of individuals in the cohort overall. They further noted, that based on consensus criteria, instead of 12 individuals diagnosed with short gut syndrome using the Bazett equation, a different number of individuals would have met diagnostic criteria with other formulae, 11 using Fridericia, 9 with Hodges, and 16 using the Framingham equation. Thus, they noted that overall the prevalence of short QT syndrome exceedingly low and an apparently healthy adult population. However, reclassification as meeting criteria might be heavily dependent on which QT correction formula is used. The importance of these findings is that not all QTs are created equal. Depending on how you compute the QT interval in which formula to use may affect how you actually risk characterize a patient. Unfortunately, these data do not necessarily tell us which is the right formula, but this highlights that it might be relevant to in the future evaluate the role of different formulae and identifying which is the most necessary to classify a patient. Moving on to an article published in last month's issue of the journal of clinical investigation by Chai et al. we review an article entitled 'Physiological genomics identifies genetic modifiers of Long QT Syndrome type 2 severity.' Congenital Long QT Syndrome is a very well recognized, inherited channelopathy associated life-threatening arrhythmias. LQTS type 2 is specifically caused by mutations in casein to encoding the potassium channel hERG. However, even with the mutation not all patients exhibit the same phenotype. Namely some patients are more at risk of life threatening arrhythmias in spite of having the same mutation as others who do not exhibit the same severity phenotype. The authors sought to evaluate whether specific modifiable factors within the remaining genetic code might be modifying the existing mutation. Thus, they sought to identify contributors to variable expressivity in an LQT 2 family by using induced pluripotent stem cell derived cardiomyocytes and whole exome sequencing in a synergistic manner. They found that patients with severely effected LQT 2 displayed prolonged action potentials compare to sales from mildly effected first-degree relatives. Furthermore, stem cells derived from patients were different in terms of how much L-type calcium current they exhibited. They noted that whole exome sequencing identified variants of KCNK17 and the GTP-binding protein REM2 in those patients with more severe phenotypes in whom greater L-type calcium current was seen. This suggests that abnormalities or even polymorphisms in other genes might be modifying the risk attributed to by mutations in the primary gene. This showcases the power of combining complimentary physiological and genomic analysis to identify genetic modifiers and potential therapeutic targets of a monogenic disorder. This is extraordinarily critical as we understand on one level that when we sequence a monogenic disorder that there might exist variants of uncertain significance, namely they have not been classified as disease causing, but could be. In turn, we also recognize that mutations in a family might effect different relatives differently. However, why this is has been relatively unclear. If we can understand and identify those patients who are most at risk of dangerous abnormal rhythms, this will be useful in how much to follow them, and what type of therapy to use in them. The fact that other genes might modify the risk even in the absence of specific mutations, suggests that novel approaches to characterizing the risk might help for the risk modified patients classification in general. Clinical use, however, remains to be seen. Moving on from long QT, we evaluate 'The Diagnostic Yield of Brugada Syndrome After Sudden Death With Normal Autopsy' noted in last month's issue of the Journal of American College of Cardiology and published by Papadakis et al. It is well known, the negative autopsies are not uncommon in patients, however, families might be wondering how at risk they are. Thus, the authors sought to assess the impact of systematic ajmaline provocation testing using high right precordial leads on the diagnostic yield Brugada syndrome in a large cohort of Sudden Arrhythmic Death syndrome families. Amongst 303 families affected by Sudden Arrhythmic Death Syndrome evaluation was done to determine whether or not there was a genetic inherited channelopathy cause. An inherited cardiac disease was diagnosed in 42% of the families and 22% of relatives Brugada syndrome was the most prevalent diagnosis overall amongst 28% of families. Ajmaline testing was required, however, to unmask the Brugada Syndrome in 97% of diagnosed individuals. Furthermore, they use of high right precordial leads showed a 16% incremental diagnostic yield of ajmaline testing for diagnosing Brugada syndrome. They further noted that a spontaneous type 1 regard or pattern or a clinically significant rhythmic event developed in 17% of these concealed regardless syndrome patients. The authors concluded the systematic use of ajmaline testing with high right precordial leads increases the yield of Brugada Syndrome testing in Sudden Arrhythmic Death Syndrome families. Furthermore, they noted that assessments should be performed in expert centers or patients could also be counseled appropriately. These findings are important and one of the big questions always becomes how aggressively to test family members of patients or of deceased individuals who experienced sudden arrhythmic death. Many of these patients have negative autopsies, and genetic autopsy might not be possible due to lack of tissue or blood products that can be adequately tested. The data here suggest that amongst a group of 303 sudden arrhythmic death, families that Brugada Syndrome is by far the most frequent diagnosis. If an inherited cardiac disease was identified. In turn, it is not ECG alone or echo alone that helps identify them, but requires drug provocation testing in addition to different electrode placements. Whether or not this will consistently offer benefit in patients in general or my result in overcalling remains to be seen next within the realm of genetic predisposition. We view an area where we don't know if there's a genetic predisposition in article published by Tester et al. entitled Cardiac Genetic Predisposition in Sudden Infant Death Syndrome in last month's issue of the journal of american college of cardiology. Sudden Infant Death Syndrome is the leading cause of post-neonatal mortality and genetic heart diseases might underlie some cases of SIDS. Thus the authors sought to determine the spectrum and prevalence of genetic heart disease associated mutations as a potential monogenic basis for Sudden Infant Death Syndrome. They study the largest cohort to date of unrelated SIDS cases, including a total of 419 individuals who underwent whole exome sequencing and targeted analysis for 90 genetic heart disease susceptibility genes. Overall, 12.6% of these cases had at least one potentially informative genetic heart disease associated variants. The yield was higher in those mixed European ancestry than those of European ancestry. Infants older than four months were more likely to host a potentially informative gene. Furthermore, they noted that only 18 of the 419 SIDS cases hold a [inaudible 01:01:26] or likely pathogenic variant. So in other words, only 4% of cases really had a variant that they could say was distinctly pathogenic or likely pathogenic. Thus, overall, the minority of SIDS cases have potentially informative variant in genetic heart disease susceptibility gene, and these individuals were mostly in the 4 to 12 month age group. Also, only 4% of cases had immediately clinically actionable variance, namely a variant, which is well recognized as pathogenic and where we could actually say that a specific therapy might have had some effect. These findings can have major implications for how best to investigate SIDS cases in families. It might suggest that SIDS cases where the individual was older, nearly 4 to 12 months of age might have a greater yield in terms of identifying variance. While this might not affect the deceased in fit, it might affect, families are planning on having another child in whom a variant can be identified. Finally, within the realm of genetics, we review an article published in last month's issue of Science Advances by Huang. et al. entitled 'Mechanisms of KCNQ1 Channel Dysfunction in Long QT Syndrome Involving Voltage Sensor Domain Mutations'. Mutations that induce loss of function of human KCNQ1 underlie the Long QT Syndrome type 1. While hundreds of mutations have been identified the molecular mechanism by which they result in impaired function are not as well understood. The authors sought to investigate impact of 51 specific variants located within the voltage sensor domain and emphasized effect on cell surface expression, protein folding, and structure. For each variant efficiency of trafficking of the plasma membrane, impact of proteasome inhibition, and protein stability were evaluated. They noted that more than half of the loss of function mutations were seen to destabilized structure of the voltage sensor domain, generally accompanied by mistrafficking and degradation by the proteasome. They also noted that five of the folding defective Long QT Syndrome mutant sites were located in the S0 helix, where they tend to interact with a number of other loss of function mutation sites in other segments of the voltage sensor domain. They suggested these observations reveal a critical role for the S0 helix as a central scaffold to help organize and stabilized KCNQ1 overall. They also note the importance of these findings is that mutation-induced destabilization of membrane proteins may be a more common cause of disease functioning in humans. The importance of these findings lies in better understanding why specific mutations lead to appa
An interview with Sumeet Mainigi, MD, on this all too common, often undetectable and potentially life-threatening condition.
Podcast summary of articles from the March 2018 edition of Journal of Emergency Medicine from the American Academy of Emergency Medicine. Topics include flecainide for afib, neutropenic fever in healthy pediatric patients, bupivacaine toxicity, ACE inhibitor induced visceral angioedema, cannabinoid hyperemesis syndrome and board review on hip dislocations. Guest speaker is Dr. Albert Hong from the Metrohealth Emergency Medicine Residency.
A Fib is the most common arrhythmia that is encountered in the ED. Knowing how to manage it when it is causing problems is important! Join the EM GuideWire Team as they discuss a-fib with RVR management with esteemed Cardiologist (and friend of us in the ED), Dr. Laszlo Littmann.
Dans cette douzième baladodiffusion, les Drs Luc Lanthier et Gabriel Provencher discutent d’anticoagulation pour les sujets en fibrillation auriculaire qui subissent une angioplastie coronarienne, en plus de réviser la littérature médicale de novembre 2017. Quiz clinique (4 min 25), étude principale (5 min 05), critique (26 min 56), autres articles (40 min 00), réponse au … Continuer la lecture de « BC 012 – Anticoagulation post-angioplastie coronarienne chez les sujets avec fibrillation auriculaire (étude RE-DUAL PCI) »
Here are 7 health conditions that you won’t think about that may suggest that you have a sleep-breathing disorder. 1. Nighttime urination 2. Atrial Fibrillation 3. Panic attacks at night 4. Seizures 5. GI problems 6. Skin problems 7. Infertility Bonus: Cancer -------------------------- Show Notes Joshua Thomas interview Josh Ax: Eat Dirt: Why Leaky Gut May Be the Root Cause of Youkr Health Problems and 5 Surprising Steps to Cure It doctorstevenpark.com/7conditions
Acupuncture and herbs restore normal sinus rhythm to the heart.
In Karen's favourite episode to date, Sarah takes us on a sunny joy ride - surfing the waves of ECGs and riding the highs and lows of life itself! Join us for the most bizarre, surreal yet surprisingly practical explanation of ECGs you will ever experience. Email us questions at humerushacks@gmail.com Like our Facebook page 'Humerus Hacks' Follow us on Twitter @humerushacks
Cardiovascular health with acupuncture for hypertension and atrial fibrillation
Want more of this show? Subscribe in iTunes: HERE Subscribe in Google Play: HERE Read our massive post on EKG Interpretation for Nurses here: https://www.nrsng.com/interpret-ekgs-heart-rhythms/ The post EKG08: VTach and VFib (Ventricular Tachycardia and Fibrillation) appeared first on NURSING.com.
Cardiac surgery can vary from being routine elective surgery to time-critical emergency surgery. The term encompasses a broad range of procedures carried out on patients from neonates to nonagenarians. In the 63 years since the first open heart surgery was performed using cardiopulmonary bypass enormous advances have been made in the field such that an average person presenting for coronary bypass grafting in 2016 can expect a very low chance of peri-operative morbidity or mortality. When things go wrong however they can go badly wrong and at the worst possible moment (see Murphy’s Law). This talk focuses on describing common complications encountered in the postoperative period, with a focus on anticipation, prevention and planning for rapid recognition and successful management of potentially life threatening complications.
Never miss another interview! Join Devin here: http://bit.ly/joindevin. Read the full Forbes article and watch the interview here: http://bit.ly/2czVfcP. Subscribe to this podcast on iTunes by clicking here: http://bit.ly/ymotwitunes or on Stitcher by clicking here: http://bit.ly/ymotwstitcher. ----------------------- “Somebody ought to do something about that.” If you’re like me, you’ve said that–if only to yourself–on occasion. The most successful people in the world seem to be the ones who don’t. Instead, they do something. Most of us aren’t willing to give up our careers to “do something” to solve a social problem, especially if there is no good answer to the partner question, “What’s in it for me?” Mellanie True Hills, a professional speaker who has earned the National Speakers Association’s Certified Speaking Professional designation, recognized a problem and created a nonprofit to address it without giving up her career. Hills launched her nonprofit, American Foundation for Women’s Health, which in turn runs StopAfib.org, after having a near-death experience resulting from atrial fibrillation or “Afib.” StopAfib.org is a patient-to-patient organization that works to help those experiencing Afib to advocate for themselves with the healthcare community to get the best possible outcomes. StopAfib.org operates on an annual budget of approximately $500,000, she says. The revenue comes from donations from individuals, corporations and foundations. With a small staff, the organization has been able to drive significant impact by partnering with other organizations and advocating at the national level. For instance, Hills was a driving force in the creating and national recognition of Atrial Fibrillation Awareness Month. ----------------------- Read the full Forbes article and watch the interview here: http://bit.ly/2czVfcP. Need a corporate social responsibility speaker? Learn more about Devin Thorpe at http://devinthorpe.com.
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This week the Humerus Hacks girls team up with special guest Dr Bridget to talk about ticklish atria, shocking rhythms and aggressive ECGs.
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Commentary by Dr. David Wilber
AFIBEDIA Dr. Randall Wolf the professor of surgery at university of Texas, Cincinnati and Tokyo the inventor of the WOLF MINIMAZE This is a weekly podcast called AFipedia
Edward H. Livingston, MD discusses atrial fibrillation with Eric N. Prystowsky, MD, author of Treatment of Atrial Fibrillation, and talks about new technologies to facilitate screening for atrial fibrillation with Leslie Saxon, MD.
Dr Abraham discusses The Champion study concerning wireless monitoring in chronic heart failure.
A series of independent, unsupported programs developed by theheart.org featuring discussions with world renowned cardiologists on the importance of the latest clinical trial findings and cardiology news.
The number of Americans suffering from atrial fibrillation is soaring and the treatment varies from medication to a variety of surgical procedures. We'll discuss the latest options. A new study shows that if you want to lower your blood pressure, walking is good, but fast walking is better. Your triglyceride level helps a doctor predict the risk of heart disease. And this week two big studies indicated there may be a much better way of measuring triglycerides than the one they have been using. “Heart therapy strains efforts to limit costs.? The New York Times, July 7, 2007http://www.nytimes.com/2007/07/07/health/07heart.html?ex=1185336000&en=d636fe3ce0c28ce3&ei=5070 Fast walking is better for improving systolic blood pressure in older adults. www.medpagetoday.com, posted July 12, 2007http://www.medpagetoday.com/PrimaryCare/ExerciseFitness/tb/6145 “Blood triglycerides seen as heart attack predictor.? Reuters, July 17, 2007http://today.reuters.com/news/articlenews.aspx?type=healthNews&storyid=2007-07-17T215724Z_01_N17274797_RTRUKOC_0_US-HEART-TRIGLYCERIDES.xml “Nonfasting Triglycerides and Risk of Myocardial Infarction, Ischemic Heart Disease, and Death in Men and Women.? Journal of the American Medical Association, Vol. 298 No. 3, July 18, 2007http://jama.ama-assn.org/cgi/content/short/298/3/299 “Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women.? Journal of the American Medical Association, Vol. 298 No. 3, July 18, 2007http://jama.ama-assn.org/cgi/content/abstract/298/3/309?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=fasting+compared+with+nonfasting+triglycerides+and+risk&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
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