Podcasts about cardiac arrhythmia

NEJM 1991;324:781-788Background A hallmark of post-myocardial infarction (MI) care in the 1980's was the monitoring and suppression of premature ventricular contractions (PVCs) via use of antiarrhythmic drugs. The practice was based on pathophysiologic rationale that PVC burden is a strong risk factor for sudden and non-sudden cardiac death following MI and thus, suppression must reduce death. PVC reduction was a seductive surrogate endpoint that was easy to measure and declare victory on, but it had never been tested in a proper RCT. The Cardiac Arrhythmia Suppression Trial (CAST) was sponsored by the National Heart, Lung and Blood Institute (NHLBI) and sought to test the hypothesis that suppression of asymptomatic or mildly symptomatic PVCs with antiarrhythmic therapy with encainide, flecainide, or moricizine after MI would reduce death due to arrhythmia.Patients Patients were eligible for enrollment 6 days to 2 years post MI with an average of ≥6 PVCs per hour on ambulatory monitoring of at least 18 hours duration, and no runs of VT of ≥15 beats at a rate of ≥120 bpm. An ejection fraction (EF) of ≤55% was required within 90 days of MI or ≤40% if recruited after 90 days. There was a run-in phase. Patients were only enrolled in the main trial if they had at least 80% suppression of PVCs and at least 90% suppression of runs of VT during an initial, open-label titration period. Initial open-label drug assignment was based, in part, on the EF. Flecainide was not given to patients with an EF of ≤30%. Moricizine was only used as a second line drug in patients with an EF of ≥30%.Baseline characteristics Baseline characteristics of the patients enrolled in the trial are not provided in the main manuscript and cannot be inferred from the results, tables or figures presented.Procedures Patients in whom arrhythmias were suppressed were randomly assigned to receive either the effective drug or its matching placebo. A detailed description of study procedures is not presented in the main manuscript. Compliance with the study drug was assessed in follow-up visits and based on pill counts of tablets returned but the schedule of these visits is not provided. Concomitant drug therapy was assessed at the time of the last visit, according to a standardized checklist.During the trial, patients could be instructed to discontinue the study drug based on the occurrence of the following events: ventricular tachycardia, significant increase in arrhythmia burden, disqualifying ECG changes including significant QT prolongation or bradycardia, new or worsened congestive heart failure, the need for treatment with an antiarrhythmic agent outside the entry criteria for the study, or any number of other adverse medical events divided into cardiovascular or non-cardiovascular events.Endpoints The primary endpoint of the study was death or cardiac arrest with resuscitation due to arrhythmia. The site PI was responsible for classifying each death without knowledge of the patient's assigned treatment. Secondary endpoints included cardiovascular and non-cardiovascular causes of death, disqualifying ventricular tachycardia without arrest, syncope, pacemaker implantation, recurrent MI, congestive heart failure, angina pectoris or coronary artery revascularization.Results Observation began on the day of randomization to blinded therapy and was censored on April 18, 1989, the date when the use of encainide and flecainide was discontinued by the Data and Safety Monitoring Board because the data indicated it was unlikely that benefit could be demonstrated, and it was likely that the drugs were harmful. The original CAST trial manuscript reports data on patients assigned to the encainide and flecainide groups. Moricizine use was continued and would be reported separately in the revised CAST II trial.1498 participants were randomized to receive either encainide, flecainide or their matching placebo and followed for an average of 10 months. Compliance with the assigned treatments was estimated to be >90% in 70% of all patients and was similar in the active-drug and placebo groups. Antiarrhythmic therapy significantly increased the relative risk of the primary endpoint of death or cardiac arrest due to arrhythmia (RR 2.64; 5.7% vs 2.2%; p=0.0004) and was associated with a number needed to harm (NNH) of approximately 29. It also increased the risk of all deaths and cardiac arrests (RR 2.38; 8.3% vs 3.5%; p=0.0001; NNH = 20); even those not associated with arrhythmia (2.3% vs 0.7%; p=0.01).Conclusions The CAST trial unexpectedly demonstrated that treatment of asymptomatic or mildly symptomatic PVCs in post-MI patients, with encainide and flecainide, increased death and cardiac arrests. From a chronological standpoint, it is the first major trial in cardiovascular medicine (perhaps all of medicine) that “reversed” a standard medical practice. In this case, one that was instituted and broadly adopted on the basis of pathophysiologic reasoning and one that targeted a surrogate endpoint. Thus, more than anything it highlights the importance of testing interventions in properly conducted RCTs prior to adoption and basing the analysis on hard outcomes that are meaningful to patients and society. How many practices in modern medicine are supported by high quality RCTs? It may be as low as 30-40%. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.02.546740v1?rss=1 Authors: Yoshinaga, D., Feng, R., Prondzynski, M., Shani, K., Tharani, Y., Milosh, J., Walker, D., Carreon, K., Boss, B. M., Parker, K. K., Pu, W. T., Bezzerides, V. J. Abstract: BACKGROUND: N-terminal-acetyltransferases catalyze N-terminal acetylation (Nt-acetylation), an evolutionarily conserved co-translational modification. Nt-acetylation regulates diverse signaling pathways, yet little is known about its effects in the heart. To gain insights, we studied NAA10-related syndrome, in which mutations in NAA10, which catalyzes Nt-acetylation, causes severe QT prolongation, hypotonia, and neurodevelopmental delay. METHODS: We identified a missense variant in NAA10 (c.10C greater than A; p.R4S) that segregated with severe QT prolongation, arrhythmia, cardiomyopathy, and sudden death in a large kindred. We developed patient-derived and genome-edited human induced pluripotent stem cell (iPSC) models and deeply phenotyped iPSC-derived cardiomyocytes (iPSC-CMs) to dissect the mechanisms underlying NAA10-mediated cardiomyocyte dysfunction. RESULTS: The NAA10-R4S mutation reduced enzymatic activity, decreased expression levels of NAA10/NAA15 proteins, and destabilized the NatA complex. In iPSC-CM models of NAA10 dysfunction, dysregulation of the late sodium and slow rectifying potassium currents caused severe repolarization abnormalities, consistent with clinical QT prolongation and increased risk for arrhythmogenesis. Engineered heart tissues generated from mutant NAA10 cell lines had significantly decreased contractile force and sarcomeric disorganization, consistent with the cardiomyopathic phenotype in the identified family members. Diastolic calcium levels were increased with corresponding alterations in calcium handling pathways. We identified small molecule and genetic therapies that reversed the effects of NAA10 dysregulation of iPSC-CMs. CONCLUSIONS: Our study defines novel roles of Nt-acetylation in cardiac ion channel regulation and delineates mechanisms underlying QT prolongation, arrhythmia, and cardiomyopathy caused by NAA10 dysfunction. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

THIS EPISODE COVERS THE FOLLOWING TOPICS AND MORE:How POTS is identifiedSymptoms of POTSMedical and Non-Medical TreatmentsHorizontal Options (horizontal exercise etc.)How POTS effects childrenMovement and ConditioningStaying optimistic and learning to manage this condition.  ABOUT OLEG KOVALENKO, M.D.Dr. Oleg Kovalenko is a Board-Certified Physician at Pediatrics Associates' Miami Lakes East Cardiology department. He grew up in Kherson Ukraine and attended Dnepropetrovsk State Medical Academy in Dnepr, Ukraine. He completed his pediatric residency at the West Virginia University Charleston Division, WV. His Cardiology Fellowships include Rainbow Babies Children's Hospital in Cleveland, Ohio, University of Michigan, CS Mott and Children's Hospital in Ann Arbor, Michigan. Dr. Kovalenko is fluent in English, Russian and Ukrainian. He is married to Natalia and his hobbies include running, ballroom dancing and soccer. His special areas of Medical Interest are: Pediatric Cardiology, Cardiac Arrhythmia, Inherited Arrhythmias, Sudden Cardiac Death Prevention and Fetal Cardiology. 

In this episode Dr Sharon Man joins Dr Cristina Cusu once again to continue discussion on cardiac syncope, discussing cardiac arrhythmia in context of syncope. Narrow complex tachycardia, broad complex tachycardia, bundle branch block, AV block all discussed in this episode and we finish with other investigations like ECHO or EP studies. Enjoy listening. 

Dr. Halley Alexander talks with Dr. Shóbi Sivathamboo about the incidence of serious cardiac arrhythmias detected by subcutaneous cardiac monitors in patients with chronic drug-resistant epilepsy. Read the full article in Neurology.

Dr. Shobi Sivathamboo discusses the incidence of serious cardiac arrhythmias detected by subcutaneous cardiac monitors in patients with chronic drug-resistant epilepsy. Show references: https://n.neurology.org/content/early/2022/04/06/WNL.0000000000200173"

Dr. Mark Keezer discusses the risk of sudden death and cardiac arrhythmia in patients utilizing lamotrigine to treat epilepsy.  Show references:https://n.neurology.org/content/early/2022/03/08/WNL.0000000000200164

Dr. Halley Alexander talks with Dr. Mark Keezer about the risk of sudden death and cardiac arrhythmia in patients utilizing lamotrigine to treat epilepsy. Read the full article in Neurology.

Natasha Drapeau is the Executive Vice President of BioSig Technologies, pioneers in advanced biomedical signal processing solutions that will unlock the future of bioelectronic medicine, starting with the PURE EP™ System and their work on common and complex cardiac arrhythmia. Approximately more than half of patients diagnosed with this heart rhythm disorder have AFib. The BioSig noninvasive technology works with all the systems generating data to get an entire cardiac picture for diagnosis and performing a cardiac ablation procedure. Natasha explains, "What we're focusing on with our technology is really to prevent that signal distortion. That's happening both through our different hardware architecture and the software algorithms. We focus on delivering a much cleaner, more detailed cardiac picture displayed to the physician in real-time." "But also, we're uncovering a lot of diagnostic data that was simply not there before. We have side-by-side comparisons because we have other technology in support at the same time as PURE EP. I believe we have an opportunity there to give that better, more comprehensive cardiac picture to physicians, and that could lead to a transformation of care." @BioSig_Tech #MedTech #MedicalTechnology #Afib #AtrialFibrillation #AfibAwareness #Electrophysiology #Epeeps #GlobalEP #AF #Ablation #Cardiology #CardioTwitter #HeartHealth #BioelectronicMedicine BioSig.com Listen to the podcast here

Natasha Drapeau is the Executive Vice President of BioSig Technologies, pioneers in advanced biomedical signal processing solutions that will unlock the future of bioelectronic medicine, starting with the PURE EP™ System and their work on common and complex cardiac arrhythmia. Approximately more than half of patients diagnosed with this heart rhythm disorder have AFib. The BioSig noninvasive technology works with all the systems generating data to get an entire cardiac picture for diagnosis and performing a cardiac ablation procedure. Natasha explains, "What we're focusing on with our technology is really to prevent that signal distortion. That's happening both through our different hardware architecture and the software algorithms. We focus on delivering a much cleaner, more detailed cardiac picture displayed to the physician in real-time." "But also, we're uncovering a lot of diagnostic data that was simply not there before. We have side-by-side comparisons because we have other technology in support at the same time as PURE EP. I believe we have an opportunity there to give that better, more comprehensive cardiac picture to physicians, and that could lead to a transformation of care." @BioSig_Tech #MedTech #MedicalTechnology #AFib #AtrialFibrillation #AfibAwareness #Electrophysiology #Epeeps #GlobalEP #AF #Ablation #Cardiology #CardioTwitter #HeartHealth #BioelectronicMedicine BioSig.com Download the transcript here

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The Sports Orthopods discuss Jamal Murray's ACL tear and how it compares to Dexter Fowler's in terms of where they are in their respective careers.  We also talk James Wiseman's meniscus tear and try to understand the deliberation that was reported by...

Part 2Magnesium, Potassium and Cardiac Rhythms – Carolyn Dean MD NDEvidence-based scientific research on the relationship between potassium, magnesium and cardiac arrhythmias date back to the early 1950’s – probably even before that but my Google wouldn’t take me that far!It’s said that most everybody’s heart will beat irregularly during the day at least once or twice.  But when the heart sustains an irregular rhythm it’s a sign that there is in imbalance in the electrical activity of the heart.Atrial fibrillation is the most commonly diagnosed heart arrhythmia, reaching epidemic proportions. In the United States, AFib hospitalizations increased by 23 percent be- tween 2000 and 2010.62 The number of people in 2010 with AFib was about 5.2 million, and this is predicted to increase to about 12.1 million cases in 2030. I believe the increase in AFib parallels the increase in magnesium deficiency in the population.The standard of care within the allopathic medical community has been developed to identify a-fib with an increased risk for heart failure, clots, and strokes. But that’s only if you already have heart disease. I believe that a significant portion of the population does not have a heart problem –they have a mineral deficiency problem!The heart has four chambers; the top two are atria and the bottom two are ventricles. What causes the atria to fibrillate? In a healthy heart, the electrical impulses in the atria are coordinated by the proper balance and interaction of several minerals that function as electrolytes: magnesium, calcium, sodium, and potassium. It seems logical that an imbalance of these minerals is the cause and balancing them to support the structure and function of the heart is an excellent strategy.But 2020 the medications that are used to treat AFib can themselves cause heart disease, which may just increase the likelihood of maintaining an AFib condition. And those patients with heart disease, high blood pressure, and high cholesterol are on medications that cause more heart disease because those medications deplete magnesium and promote magnesium deficiency. That’s probably why doctors say that AFib is incurable. They don’t know that ADDING magnesium, potassium and other minerals to their treatment protocol may accelerate heart remineralization, stabilization and recovery allowing the patient to complete their drug therapy lickety-split.Tonight, we’ll talk with Dr. Carolyn Dean about Magnesium, Potassium and Cardiac Arrhythmia’s – along with a wide range of other health topics and clinically recommended nutritional assets to support your body. You will love hearing the beneficial interactions with our callers and hosts alike including the body/mind connection, identifying the ‘conflict’ in the ‘conflict basis’ of disease and much more!!Dr. Dean takes questions via email. Please write questions@drcarolyndeanlive.com We will be glad to respond to your emailLearn more about Dr. Carolyn here:  https://drcarolyndeanlive.com.

Part 1Magnesium, Potassium and Cardiac Rhythms – Carolyn Dean MD NDEvidence-based scientific research on the relationship between potassium, magnesium and cardiac arrhythmias date back to the early 1950’s – probably even before that but my Google wouldn’t take me that far!It’s said that most everybody’s heart will beat irregularly during the day at least once or twice.  But when the heart sustains an irregular rhythm it’s a sign that there is in imbalance in the electrical activity of the heart.Atrial fibrillation is the most commonly diagnosed heart arrhythmia, reaching epidemic proportions. In the United States, AFib hospitalizations increased by 23 percent be- tween 2000 and 2010.62 The number of people in 2010 with AFib was about 5.2 million, and this is predicted to increase to about 12.1 million cases in 2030. I believe the increase in AFib parallels the increase in magnesium deficiency in the population.The standard of care within the allopathic medical community has been developed to identify a-fib with an increased risk for heart failure, clots, and strokes. But that’s only if you already have heart disease. I believe that a significant portion of the population does not have a heart problem –they have a mineral deficiency problem!The heart has four chambers; the top two are atria and the bottom two are ventricles. What causes the atria to fibrillate? In a healthy heart, the electrical impulses in the atria are coordinated by the proper balance and interaction of several minerals that function as electrolytes: magnesium, calcium, sodium, and potassium. It seems logical that an imbalance of these minerals is the cause and balancing them to support the structure and function of the heart is an excellent strategy.But 2020 the medications that are used to treat AFib can themselves cause heart disease, which may just increase the likelihood of maintaining an AFib condition. And those patients with heart disease, high blood pressure, and high cholesterol are on medications that cause more heart disease because those medications deplete magnesium and promote magnesium deficiency. That’s probably why doctors say that AFib is incurable. They don’t know that ADDING magnesium, potassium and other minerals to their treatment protocol may accelerate heart remineralization, stabilization and recovery allowing the patient to complete their drug therapy lickety-split.Tonight, we’ll talk with Dr. Carolyn Dean about Magnesium, Potassium and Cardiac Arrhythmia’s – along with a wide range of other health topics and clinically recommended nutritional assets to support your body. You will love hearing the beneficial interactions with our callers and hosts alike including the body/mind connection, identifying the ‘conflict’ in the ‘conflict basis’ of disease and much more!!Dr. Dean takes questions via email. Please write questions@drcarolyndeanlive.com We will be glad to respond to your emailLearn more about Dr. Carolyn here:  https://drcarolyndeanlive.com.

Cardiac arrhythmia

Tonight, we'll talk with Dr. Carolyn Dean about Magnesium, Potassium and Cardiac Arrhythmia's - along with a wide range of other health topics and clinically recommended nutritional assets to support your body. You will love hearing the beneficial interactions with our callers and hosts alike including the body/mind connection, identifying the 'conflict' in the 'conflict basis' of disease and much more.

Tonight, we'll talk with Dr. Carolyn Dean about Magnesium, Potassium and Cardiac Arrhythmia's - along with a wide range of other health topics and clinically recommended nutritional assets to support your body. You will love hearing the beneficial interactions with our callers and hosts alike including the body/mind connection, identifying the 'conflict' in the 'conflict basis' of disease and much more.

Geraint Thomas is used to spending hours in the saddle but even he admits his latest challenge is a tough one. He's riding the turbo in his garage for three 12-hour shifts to raise money for the NHS. No team cars, no domestiques and no post-ride massages - but plenty of supporters joining him on Zwift. Ian Parkinson asks how he's coping and whether he's up for a delayed Tour De France in late August. We also hear from Danish journalist Emil Foget - who wrote Rouleur 20.2's story on cardiac arrhythmia in cyclists; Managing Editor Ian Cleverly appeals for subscribers to help the magazine survive the coming months and Stuart Clapp takes his top off and shares his Heinrich Haussler obsession. See acast.com/privacy for privacy and opt-out information.

Hallie Arnott interviews Dr Andrew Krahn from the University of British Columbia. Dr Krahn discusses the origin of cardiac arrhythmia and how the use of biobanks and registries can help physicians and patients to identify and treat inherited arrhythmias.

The inaugural episode of Casual Science! We speak with David Vidmar, a researcher at University of California: San Diego who works on the physics of "Cardiac Arrhythmia." Using a mathematical model of heart cells, David describes how spiral waves that wash over the heart can lead to the heart beating chaotically!

Dr. Vaughan and Larry Finney speak with Dr. Tsoi about heart arrhythmias. This was originally aired November 13, 2010. --- Send in a voice message: https://anchor.fm/medicallyspeakingradio/message

Integrating interactome and genetics data allows researchers to predict adverse drug effects.