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Cardionerds: A Cardiology Podcast

CardioNerds
Cardionerds: A Cardiology Podcast
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  • 428. Atrial Fibrillation: The Impact of Modifiable Risk Factors and Lifestyle Management on Atrial Fibrillation with Dr. Prash Sanders
    Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Sahi Allam discuss modifiable risk factors and lifestyle management of atrial fibrillation with Dr. Prash Sanders. Atrial fibrillation is becoming more prevalent across the world as people are living longer with cardiovascular disease. While much of our current focus lies on the pharmacological and procedural management of atrial fibrillation, several studies have shown that targeted reduction of risk factors, such as obesity, sleep apnea, hypertension, and alcohol use, can also significantly reduce atrial fibrillation burden and symptoms. Today, we discuss the data behind lifestyle management and why it is considered the “4th pillar” of atrial fibrillation treatment. We also explore ways to incorporate prevention strategies into our general cardiology and electrophysiology clinics to better serve the growing atrial fibrillation population. Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes.  CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls More people have atrial fibrillation because it is being detected earlier using wearable technology, and patients are living longer with subclinical or clinical cardiovascular disease  There are 3 components of atrial fibrillation: an electrical “trigger” + a susceptible substrate (due to age, sex, genetics) + “perpetuators” that cause the trigger to continue stimulating the substrate (lifestyle risk factors such as obesity, smoking, diabetes, etc.)  Obesity is the highest attributable risk factor for atrial fibrillation. Treating obesity often helps to treat other risk factors, such as hypertension and sleep apnea.  Counseling is patient-dependent. Most patients are unable to make major behavioral changes cold-turkey and will need to make small, incremental changes.  Dr. Sanders’ tip: He tells his own patients that “atrial fibrillation is the body’s response to stress.” The key to treating atrial fibrillation is to control your underlying stressors - procedures and medications are simply band-aids that do not fix the root of the problem.  Notes Notes drafted by Dr. Allam. 1. How common is atrial fibrillation?  Atrial fibrillation is the most common sustained arrhythmia. Currently, an estimated 50-60 million individuals worldwide are estimated to have atrial fibrillation, or roughly 1 in 4 individuals over the age of 45.1  The rising global prevalence of atrial fibrillation can be attributed to the aging of the population, increased rates of obesity, and greater accumulation of cardiovascular risk factors and survival with clinical cardiovascular disease.2 Atrial fibrillation is also being detected earlier through digital and wearable devices.2  Annually, we spend approximately $5,312 per adult on the management of atrial fibrillation in the United States.3  2. What is the underlying pathophysiology of atrial fibrillation? How do risk factors like sleep apnea or obesity “trigger” atrial fibrillation?  For atrial fibrillation to occur, there is an electrical “trigger”, a susceptible substrate (due to age, sex, genetics), and “perpetuators” that allow the trigger to continue stimulating the substrate.2  90% of electrical “triggers” come from the pulmonary veins  “Perpetuators” influence how the autonomic nervous system interacts with the triggers and substrate to perpetuate atrial fibrillation. Sleep apnea, obesity, and other risk factors are the “perpetuators”  Over time, as atrial fibrillation recurs, the substrate remodels to result in persistent atrial fibrillation.  3. What are some of the risk factors for atrial fibrillation and what are the possible benefits of controlling them?
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  • 427. The Approach to Asymptomatic Severe Aortic Stenosis with Dr. Parth Desai and Dr. Tony Bavry
    CardioNerds (Drs. Amit Goyal, Elizabeth Davis, and Keerthi Gondi) discuss the approach to asymptomatic severe aortic stenosis with expert faculty Drs. Parth Desai and Tony Bavry.   They review the natural history of aortic stenosis, current guidelines for treating severe aortic stenosis, multiparametric risk stratification, trial data on aortic valve replacement for patients with asymptomatic severe aortic stenosis, and a practical approach for our patients today.   This episode was supported by an educational grant from Edwards Lifesciences. All CardioNerds education is planned, produced, and reviewed solely by CardioNerds.  Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Aortic Stenosis SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!
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  • 426. Case Report: A Ruptured Saccular Aortic Aneurysm into the Right Ventricle – University of Tennessee, Nashville ​
    CardioNerds join Dr. Neel Patel, Dr. Victoria Odeleye, and Dr. Jay Ramsay from the University of Tennessee, Nashville, for a deep dive into cardiovascular medicine in the vibrant city of Nashville. They discuss the following case: A 57-year-old male with a history of prior cardiac surgery, hypertension, and polysubstance use presented with syncope and chest pain. Initial workup revealed a large saccular ascending aortic aneurysm. While under conservative management, he experienced acute hemodynamic collapse, leading to the discovery of an unprecedented aorto-right ventricular fistula. This episode examines the clinical presentation, diagnostic journey, and management challenges of this rare and complex aortic pathology, highlighting the role of multimodal imaging and the interplay of multifactorial risk factors. Expert commentary is provided by Dr. Andrew Zurick III. Episode audio was edited by CardioNerds Intern student Dr. Pacey Wetstein.   US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Saccular Aneurysm Risk: Saccular aortic aneurysms, though less common than fusiform, carry a higher inherent rupture risk due to concentrated wall shear stress, often exacerbated by prior cardiac surgery, chronic hypertension, and polysubstance use.     Unprecedented Rupture: The direct rupture of an aortic aneurysm into a cardiac chamber, specifically the right ventricle, is an exceedingly rare event, with no prior reported cases in the literature, highlighting the unpredictable nature of complex aortic pathology.     Hemodynamic Catastrophe: A large aorto-right ventricular fistula creates a massive left-to-right shunt, leading to acute right ventricular pressure and volume overload, culminating in rapid cardiogenic shock and refractory right ventricular failure.     Multimodal Imaging Imperative: Multimodal imaging (CT angiography for anatomy, TTE/TEE for real-time hemodynamics and fistula detection, CMR for tissue characterization) is indispensable for rapid diagnosis and comprehensive characterization of life-threatening cardiovascular emergencies.     High-Risk Intervention: Emergent surgical repair of a ruptured aortic aneurysm with an aorto-right ventricular fistula is a high-risk procedure associated with significant mortality, underscoring the need for prompt multidisciplinary care and realistic outcome expectations.     Notes - Notes (drafted by Dr Neel Patel):  What are the unique characteristics and rupture risk of saccular aortic aneurysms?  Saccular aortic aneurysms are less common than fusiform aneurysms.     They are generally considered more prone to rupture due to higher wall shear stress concentrated at the neck of the aneurysm, acting as a focal point of weakness.     Contributing Factors to Aneurysm Formation and Rupture in this Case:  Prior Cardiac Surgery: Aortic cannulation during the VSD/ASD repair decades ago likely created a localized structural weakness or predisposition.     Chronic, Poorly Controlled Hypertension: Imposed relentless systemic stress on the arterial walls, accelerating dilation and weakening.     Polysubstance Use: Particularly stimulants like cocaine and methamphetamines, which directly contribute to vascular damage by inducing severe, uncontrolled hypertension and direct arterial wall injury. This significantly increases the risk of aneurysm formation and rupture, especially with pre-existing conditions.     The direct rupture of an aortic aneurysm into a cardiac chamber, specifically the right ventricle, is an exceedingly rare event, with no prior reported cases in the literature,
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  • 425. Case Report: The Hidden Culprit – Unraveling the Cause of Malignant Ventricular Arrhythmias in a Young Adult – Trinity Health Livonia Hospital
    CardioNerds guest host Dr. Colin Blumenthal joins Dr. Juma Bin Firos and Dr. Aishwarya Verma from the Trinity Health Livonia Hospital to discuss a fascinating case involving malignant ventricular arrhythmias. Expert commentary is provided by Dr. Mohammad-Ali Jazayeri. Audio editing for this episode was performed by CardioNerds Intern,Julia Marques Fernandes.  This case explores the puzzling presentation of exercise-induced ventricular tachycardia in a young, otherwise healthy male who suffered recurrent out-of-hospital cardiac arrests. With no traditional risk factors and an unremarkable ischemic workup, the challenge lay in uncovering the underlying cause of his malignant arrhythmias. Electrophysiology studies and advanced imaging played a pivotal role in systematically narrowing the differentials, revealing an unexpected arrhythmogenic substrate. This episode delves into the diagnostic dilemma, the role of EP testing, and the critical decision-making surrounding ICD placement in a patient with a concealed but life-threatening condition.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Malignant Ventricular Arrhythmias This case highlights the challenges and importance of diagnosing and managing ventricular arrhythmias in young, seemingly healthy individuals. Here are five key takeaways from the episode:  Electrophysiology (EP) studies play a crucial role in identifying arrhythmogenic substrates in patients with exercise-induced ventricular tachycardia (VT) without obvious structural heart disease. In this case, substrate mapping revealed late abnormal ventricular afterdepolarizations in the basal inferior left ventricle, providing valuable insights into the underlying mechanism.  Cardiac MRI can be a powerful tool for detecting subtle myocardial abnormalities. The subepicardial late gadolinium enhancement (LGE) in the lateral and inferior LV walls suggested an underlying myocardial process, even when other imaging modalities appeared normal.  The VT morphology can provide clues about the underlying mechanism. In this case, the right bundle branch block pattern with a northwest axis and shifting exit sites pointed towards a scar-mediated mechanism rather than a channelopathy or idiopathic VT.  Implantable cardioverter-defibrillator (ICD) placement is crucial for secondary prevention of sudden cardiac death (SCD) in patients with malignant ventricular arrhythmias, even in young individuals. The patient's initial deferral of ICD implantation highlights the importance of shared decision-making and patient education in these complex cases.  "Scar-mediated VT introduces the risk of new arrhythmogenic substrates over time, reinforcing the need for ICD therapy even when catheter ablation is considered." This pearl emphasizes the dynamic nature of the arrhythmogenic substrate and the importance of long-term risk mitigation strategies.  Notes - Malignant Ventricular Arrhythmias Notes were drafted by Juma Bin Firos.  1. What underlying pathologies cause ventricular arrhythmias in young patients without overt structural heart disease? Myocardial fibrosis: Detected via late gadolinium enhancement (LGE) on cardiac MRI Present in 38% of nonischemic cardiomyopathy cases Increases sudden cardiac death (SCD) risk 5-fold Often localized to subepicardial regions, particularly in the inferolateral left ventricle (LV) May precede overt systolic dysfunction by years Subclinical cardiomyopathy: 67% of young VT patients show subtle cardiac dysfunction Suggests VT may be the first manifestation of cardiomyopathy
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  • 424. Treatment of Transthyretin Amyloid Cardiomyopathy (ATTR-CM) with Dr. Justin Grodin
    CardioNerds (Drs. Rick Ferraro and Georgia Vasilakis Tsatiris) discuss ATTR cardiac amyloidosis with expert Dr. Justin Grodin. This episode is a must-listen for all who want to know how to diagnose and treat ATTR with current available therapies, as well as management of concomitant diseases through a multidisciplinary approach. We take a deep dive into the importance of genetic testing, not only for patients and families, but also for gene-specific therapies on the horizon. Dr. Grodin draws us a roadmap, guiding us through new experimental therapies that may reverse the amyloidosis disease process once and for all.  Audio editing by CardioNerds academy intern, Christiana Dangas. This episode was developed in collaboration with the American Society of Preventive Cardiology and supported by an educational grant from BridgeBio.  Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: You must THINK about your patient having amyloid to recognize the pattern and make the diagnosis. Start with a routine ECG and TTE, and look for a disproportionately large heart muscle with relatively low voltages on the ECG.  Before you diagnose ATTR amyloidosis, AL amyloidosis must be ruled out (or ruled in) with serum light chains, serum/urine immunofixation, and/or tissue biopsy.  Genetic testing is standard of care for all patients and families with ATTR amyloidosis, and the future is promising for gene-specific treatments. Current FDA-approved treatments for TTR amyloidosis are TTR stabilizers and TTR silencers, but TTR fibril-depleting agents are on their way.  Early diagnosis of ATTR affords patients maximal benefit from current amyloidosis therapies.   TTR amyloidosis patients require a multidisciplinary approach for success, given the high number of concomitant diseases with cardiomyopathy.  Notes: Notes: Notes drafted by Dr. Georgia Vasilakis Tsatiris.  What makes you most suspicious of a diagnosis of cardiac amyloidosis from the typical heart failure patient?  You must have a strong index of suspicion, meaning you THINK that the patient could have cardiac amyloidosis, to consider it diagnostically. Some characteristics or “red flags” to not miss:   Disproportionately thick heart muscle with a relatively low voltages on EKG   Bilateral carpal tunnel syndrome – estimated that 1 in 10 people >65 years old will have amyloidosis   Previously tolerated antihypertensive medications  Atraumatic biceps tendon rupture   Bilateral carpal tunnel syndrome  Spinal stenosis   Concomitant with other diseases: HFpEF, low-flow low-gradient aortic stenosis  How would you work up a patient for cardiac amyloidosis?   Start with a routine ECG (looking for disproportionally low voltage) and routine TTE (looking for thick heart muscle)  CBC, serum chemistries, hepatic function panel, NT proBNP, and troponin levels  NOTE: It is critical to differentiate between amyloid light chain (AL amyloidosis) and transthyretin ATTR amyloidosis, as both make up 95-99% of amyloidosis cases.   Obtain serum free light chains, serum & urine electrophoresis, and serum & urine immunofixation to rule out AL amyloidosis. (See table below)  AL Amyloidosis ATTR Amyloidosis  → Positive serum free light chains and immunofixation (Abnormal M protein) → Tissue biopsy (endomyocardial, fat pad) to confirm diagnosis → Negative serum free light chains and immunofixation (ruled out AL amyloidosis) → Cardiac scintigraphy (Technetium pyrophosphate with SPECT imaging)  What treatment options do we have to offer now for ATTR CM, and how has this compared to prior years?   Before 2019, treatment options were limited outside of cardiac tr...
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