Cardionerds: A Cardiology Podcast

Latest Episodes:

184. CardioNerds Rounds: Challenging Cases of Cardiovascular Prevention with Dr. Martha Gulati Mar 14, 2022

Show notes

CardioNerds Rounds Co-Chairs, Dr. Karan Desai and Dr. Natalie Stokes and CardioNerds Academy Fellow, Dr. Najah Khan, join Dr. Martha Gulati – President-Elect of the American Society for Preventive Cardiology (ASPC) and prior Chief of Cardiology and Professor of Medicine at the University of Arizona – to discuss challenging cases in cardiac prevention. As an author on numerous papers regarding cardiac prevention and women’s health, Dr. Gulati provides many prevention pearls to help guide patient care. Come round with us today by listening to the episodes now and joining future sessions of #CardsRounds! This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - CardioNerds Rounds: Challenging Cases of Cardiovascular Prevention with Dr. Martha Gulati Case #1 Synopsis: A 55-year-old South Asian woman presents to prevention clinic for an evaluation of an elevated LDL-C. Her prior history includes hyperlipidemia, hypertension, obesity, and pre-eclampsia. She was told she had “high cholesterol” a few years prior and would need medication. She started exercising regularly and cut out sweets from her diet. Before clinic, labs showed: Total Cholesterol (mg/dL) of 320, HDL 45, Triglycerides 175, and (directly measured) LCL-C 180. Her Lipoprotein(a) is 90 mg/dL (ULN being ~ 30 mg/dL). Her HbA1C is 5.2% and her 10-year ASCVD Risk (by the Pooled Cohorts Equation) is 5.4%. Her recent CAC score was 110. She prefers not to be on medication and seeks a second opinion. Takeaways from Case #1 As Dr. Gulati notes, in the 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease, South Asian ethnicity is considered a “risk enhancing factor.” The pooled cohort equations (PCE) may underestimate risk in South Asians. Furthermore, risk varies within different South Asian populations, with the risk for cardiovascular events seemingly higher in those individuals of Bangladeshi versus Pakistani or Indian origin. There are multiple hypotheses for why this may be the case including cultural aspects, such as diet, physical activity, and tobacco use. A better understanding of these factors could inform targeted preventive measures.In the same 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease mentioned above, history of an adverse pregnancy outcome (APO) increases later ASCVD risk (e.g., preeclampsia) and is also included as a “risk-enhancing factor.” Studies have shown that preeclampsia is an independent risk factor for developing early onset coronary artery calcification. Recent data has shown that the risk for developing preeclampsia is not the same across race and ethnicity, with Black women more likely to develop preeclampsia. Black women also had the highest rates of peripartum cardiomyopathy, heart failure, and acute renal failure. After adjustment for socioeconomic factors and co-morbidities, preeclampsia was associated with increased risk of CVD events in all women, the risk was highest among Asian and Pacific Islander women. Listen to Episode #174. Black Maternal Health with Dr. Rachel Bond to learn more about race-based disparities in cardio-obstetric care and outcomes.Our patient thus has multiple risk-enhancing factors to help in shared decision making and personalize her decision for statin use. Another risk-enhancing factor for her is an elevated Lp(a), which is considered elevated when ≥ 50 mg/dL or ≥ 125 nmol/L. One other aspect that Dr. Gulati briefly covered was how CAC score may inform Aspirin use for primary prevention. There continues to be debate over when to prescribe aspirin when there is demonstrable calcium on imaging. In the MESA study, for individuals with CAC ≥ 100, the NNT (for 5 years to prevent an ASCVD event) was a 140 and NNH was 518. Case #2 Synopsis: A 58-year-old woman presents to establish care at a general cardiology clinic for shortness of breath. Her history includes hypertension, cutaneous lupus, and ongoing tobacco use. A year ago, she started having nausea, more common with stress or on exertion. She saw her PCP who obtained an EKG and GI evaluation. Endoscopy was unrevealing and EKG showed non-specific ST-T changes inferiorly. She was treated for GERD and then 6 months prior she developed dyspnea on exertion while exercising on her stationary bike after 10 minutes; she previously could go 30 minutes. She suffered a left knee meniscal tear shortly thereafter. She sees a cardiologist and obtains a cardiac PET-Stress which showed a small area of reversible ischemia in the basal to mid inferior wall and borderline reduced coronary flow reserve. Her symptoms continued and she was referred for LHC which showed non-obstructive CAD. No intracoronary physiologic testing was done. She is started on aspirin but still having symptoms. She seeks your opinion on how to prevent cardiovascular events. Takeaways Case #2 In the VIRGO study, investigators interviewed 2009 women and 976 men aged 18 to 55 years hospitalized for acute myocardial infarction (AMI) at 103 United States hospitals. Approximately 29.5% of women and 22.1% of men sought medical care for similar chest pain symptoms before their hospitalization; however, 53% of women reported that their provider did not think these symptoms were heart-related in comparison with 37% of men (p

183. Cardio-Obstetrics: The Fourth Trimester: Postpartum and Long-term Cardiovascular Care after Hypertensive Disorders of Pregnancy with Dr. Malamo Countouris and Dr. Alisse Hauspurg Mar 06, 2022

Show notes

CardioNerds (Amit Goyal), Dr. Natalie Stokes (Cardiology Fellow at UPMC and Co-Chair of the Cardionerds Cardio-Ob series), and episode lead Dr. Priya Freaney (Northwestern University cardiology fellow) discuss “The Fourth Trimester” with Dr. Malamo Countouris and Dr. Alisse Hauspurg, from the University of Pittsburgh Departments of Cardiology and Obstetrics and Gynecology, respectively. We discuss the cardiovascular considerations after adverse pregnancy outcomes in the postpartum and long-term follow-up periods. The discussion is focused mainly on hypertensive disorders of pregnancy (HDP), guided by a series of clinical vignettes. We cover a wide range of topics from cardiovascular complications and management considerations in the immediate postpartum period after a HDP, postpartum outpatient follow-up, long term cardiovascular morbidity related to HDP and related preventive strategies, contraceptive considerations for the cardiologist, and interdisciplinary care management pearls for cardiologists working in a cardio-obstetrics team. Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - The Fourth Trimester Blood pressures >160/110 should be treated like a true emergency during pregnancy and the postpartum period, as the cerebrovascular circulation is more sensitive to hypertension, due to hormonal changes related to pregnancy.Women with pre-eclampsia are at higher risk for peripartum cardiomyopathy. Have a low threshold to do a clinical heart failure evaluation (i.e., natriuretic peptides, echocardiogram), and administer diuretics as appropriate to improve volume status and blood pressure.Women with HDP should have their blood pressures monitored closely after discharge, ideally with a home BP monitoring program, as they can have exacerbations of their HTN for up to 2 weeks postpartum.The American Rescue Plan Act of 2021 included a landmark policy to extend postpartum Medicaid coverage up to a year postpartum (from 60 days).Remember to take a reproductive history for every woman you see in cardiology clinic! This can be done in one minute. At a minimum, include obstetric history [number of pregnancies, outcome of each pregnancy, gestational age and weight at delivery, pregnancy complications (HDP, GDM, etc), and delivery method] and menopausal history (age at menarche, age at menopause).The Pooled Cohort Equations may underestimate ASCVD risk for a woman who has had pregnancy complications or premature menopause – consider obtaining a CAC score to aid in risk-stratification in middle-aged women who may have underestimated risk.Low dose aspirin during pregnancy in women who have risk factors for pre-eclampsia reduces the risk of development of HDP by 15-20%. Quotables - The Fourth Trimester “Some of our traditional approaches to caring for women in the postpartum period just aren’t realistic…we need to think about how we can improve care from a policy standpoint to ensure women have access to care and think about how we deliver care.” – Dr. Alisse Hauspurg “Silos are never good. Cardio-obstetrics is a space where you really want to have open communications, be truly collaborative – taking into consideration the expertise of multiple disciplines…because it’s really hard to do it alone.” – Dr. Malamo Countouris Show notes - The Fourth Trimester For more on hypertensive disorders of pregnancy enjoy: Episode #128: Cardio-Obstetrics: Hypertensive Disorders of Pregnancy with Dr. Jennifer LeweyEpisode #66: Case Report: Severe Pre-eclampsia & Cardio-Obstetrics – UPMC Hypertensive Disorders of Pregnancy 1. What are some of the immediate postpartum cardiovascular risks and complications following a hypertensive disorder of pregnancy (HDP) and how do you manage these? Persistent hypertension: there can be a spike in BP in the days following delivery, and clinicians should remember that preeclampsia may develop de novo intra- or early postpartum. BPs >160/110 are considered severe HTN and should be treated urgently with an aggressive rapid-acting anti-HTN regimen to prevent stroke. BPs should be monitored at least every 4 to 6 hours for at least 3 days postpartum.1 A return visit for BP monitoring should be arranged at 1 week following discharge; alternatively, a home BP monitoring program may be consideredPulmonary edema: Women with preeclampsia should be delivered if they develop pulmonary edema. This is more likely to occur in women who have more severe preeclampsia features. Clinical practice guidelines suggest limiting intrapartum fluid intake/replacement to 60-80mL/h to avoid risks of pulmonary edema, with a goal euvolemic fluid balance.1Peripartum cardiomyopathy: Preeclampsia, gestational hypertension, and chronic hypertension all strongly predispose women to peripartum cardiomyopathy (PPCM). PPCM is defined as cardiomyopathy with reduced EF, usually EF 160/110) in the intra- and post-partum periods are associated with increased risk for stroke. BPs should be aggressively managed (see above) in the postpartum period to avoid this complication. 2. How should women who have had a HDP be followed in the postpartum period? What are the healthcare coverage considerations in the postpartum period? Blood pressures should be monitored closely in the postpartum period, especially in the 2 weeks following delivery – either via return in-person visits or a home BP monitoring program with remote visitsDepending on the location of care, specialized postpartum cardio-obstetrics clinics may or may not exist. Regardless, women with HDP history should be counseled (whether by OB, cardiology, PCP, etc.) regarding their long-term risk for cardiovascular diseaseThey should be counseled on the importance of optimizing their cardiovascular health (with maintenance of optimal weight and regular aerobic exercise).In addition to regular BP monitoring, these women should have periodic monitoring of their fasting lipids and blood sugars1Until recently, Medicaid coverage for pregnant women extended only 60 days postpartum, leaving many women uninsured just 2 months after delivery. In March 2021, the American Rescue Plan Act of 2021 was passed and calls for extension of Medicaid coverage from 60 days to 12-months postpartum. 3. What are the long-term cardiovascular complications related to HDPs? A history of HDP increases a woman’s risk of a diverse range of long-term cardiovascular risk factors and cardiovascular diseases (including HTN, CAD, Stroke, HF, and CV Mortality) (see figure below)6 Heart failure: A wide spectrum of changes in LV structure and function have been described in association with HDP. This includes increased LV wall thickness, adverse LV remodeling, and diastolic dysfunction (see below).7 Women with HDP also have been shown to have lower global longitudinal strain without overt systolic dysfunction8, PPCM (as described above) and later life cardiomyopathy.9 ASCVD: Women with pre-eclampsia are more likely to have atherosclerotic cardiovascular disease (CAD, CVA) than women without pre-eclampsia, independent of other traditional risk factors.6Despite significant independent association of HDP with long-term ASCVD, there was no incremental benefit in 10-year ASCVD risk prediction when added to the Pooled Cohort Equations (see below)10 4. How do you take a reproductive history in cardiology clinic? An optimal well-woman preventive cardiovascular visit should include a thorough reproductive history to identify adverse pregnancy outcomes and menstrual risk factors, amongst other sex-specific cardiovascular disease risk factors11Obstetric history: ask about pregnancies complicated by HDP (eclampsia, pre-eclampsia, gestational hypertension), low birth weight (

182. Case Report: Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics – Temple University Feb 27, 2022

Show notes

CardioNerds (Amit Goyal & Karan Desai) join Dr. Matthew Delfiner (Cardiology fellow, Temple University Hospital) and Dr. Katie Vanchiere (Internal medicine resident, Temple University Hospital) in the beautiful Fairmount Park in Philadelphia. They discuss a case of a 53-year-old man with an LVAD who presents with progressive dyspnea since LVAD implant due to right-to-left shunting due to a PFO. Dr. Val Rakita (Assistant professor of medicine and advanced heart failure and transplant specialist at Temple University Hospital) provides the E-CPR for this episode. Episode introduction by CardioNerds Clinical Trialist Dr. Anthony Peters (Duke Heart Center). This case has been published by Circulation: Heart failure. See Invasive Hemodynamic Study Unmasks Intracardiac Shunt With Ventricular Assist Device. Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Pearls - Notes - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Summary - Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics A 53-year-old man with an LVAD placed 3 months prior presents with progressive dyspnea since LVAD implant, though it has acutely worsened over the past 2 weeks. Two weeks ago, he had a hemodynamic and echocardiographic ramp study, where the LVAD speed was increased. By increasing the speed, his LV was more adequately decongested, and flow improved. In the Emergency Department, he was hypoxic on room air, and remained so with escalation ultimately with intubation. Even then he remained severely hypoxic requiring cannulation to veno-venous ECMO. Chest imaging was normal, and LVAD parameters were normal without any alarms. An astute clinician noticed that when the patient became hypertensive, his oxygen saturation improved. A subsequent echocardiogram revealed a patent foramen ovale, with right to left shunting. The patient then went to the cath lab, where simultaneous right atrial and left atrial pressures and oxygen pressures were measured, along with trans-esophageal echocardiography, while adjusting LVAD speed. It became evident that right-to-left shunting occurred only when there was high LVAD speed and low peripheral blood pressure. Essentially, faster LVAD speeds (sucking blood from the LV) and low systemic blood pressure (reducing LV afterload) increased right to left shunting by decreasing the left atrial pressure relative to the right atrial pressure. The PFO was closed at that time, drastically improving oxygenation. He was decannulated and extubated the following day. Invasive Hemodynamic Study Unmasks Intracardiac Shunt With Ventricular Assist Device | Circulation: Heart Failure (ahajournals.org) Episode Teaching -Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics Pearls PFOs are present in up to 25% of individuals, including those with LVADs.LV unloading, and therefore LA decompression, depends on both LVAD speed and systemic vascular resistance.Blood pressure dependent hypoxia may be suggestive of a right-to-left intracardiac shunt.Hypoxia refractory to mechanical ventilation should raise suspicion for intracardiac shunt.Patients with LVADs can suffer from the same diseases that anyone can. Notes - Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics 1. What factors influence LVAD flow? Factors that influence LVAD flow include pump speed, blood pressure, volume status, RV function, cardiac rhythm, and some other variables. The faster the pump is spinning, the more flow you should provide (to an extent). However, if your LV is underfilled, either from systemic hypovolemia or an RV not providing the needed LV preload, then you have no blood to flow! If you have high systemic vascular resistance, then you will have less forward flow, just as a native heart would. We must always think about the interaction between a patient and the LVAD, not just the machine settings. 2. What can cause dyspnea and hypoxia in LVAD patients? The same things that cause dyspnea in any other patient! But also… inadequate unloading of the LV due to the above factors in addition to possible suction events. Aortic regurgitation can cause an endless loop of flow from: LV > LVAD > aorta > AV > LV. Pump malfunction must always be considered, including inflow/outflow obstruction and pump thrombosis. Anemia may also contribute, as patients with LVAD are prone to both bleeding and hemolysis. 3. What are the ideal LVAD settings? There are no standard settings for LVADs, especially because there are different manufacturers. But most importantly, every patient is different, and therefore the patient-LVAD interaction is different. Overall, the ideal LVAD speed would decongest the heart while preserving RV function, maintaining the interventricular septum midline, and having intermittent aortic valve opening. 4. Explain how PFOs can result in hypoxemia. PFOs, or any septal defect, allow intra-cardiac flow from one side of the heart to the other. Flow will follow a pressure gradient. Usually, the left heart will have higher pressures than the right heart, but if the right heart pressure exceeds the left, then de-oxygenated venous blood can bypass the pulmonary circulation and enter the left heart and systemic circulation, causing hypoxemia. 5. List the methods that are used to diagnose and evaluate the severity of intra-cardiac shunts. Doppler color flow and bubble study with TTE or TEE. Blood gas measurement across various chambers can be used as well. For an in-depth review of LVADs, enjoy Ep #15. LVAD 101 with Dr. Steve Hsu. References Uriel, Nir, et al. "Clinical hemodynamic evaluation of patients implanted with a fully magnetically levitated left ventricular assist device (HeartMate 3)." The Journal of Heart and Lung Transplantation 36.1 (2017): 28-35. Adamson, R. M., et al. "Single center, 23 year experience with PFO management during HeartMate LVAD implants." The Journal of Heart and Lung Transplantation 34.4 (2015): S219. Bacich, Daniela, et al. "Patent foramen ovale-related complications in left ventricular assist device patients: A reappraisal for cardiovascular professionals." Journal of Artificial Organs 23.2 (2020): 98-104. Burkhoff, Daniel, et al. "Hemodynamics of mechanical circulatory support." Journal of the American College of Cardiology 66.23 (2015): 2663-2674. Jaski, Brian E., et al. "Assessment of recurrent heart failure associated with left ventricular assist device dysfunction." The Journal of heart and lung transplantation 24.12 (2005): 2060-2067. Stainback, Raymond F., et al. "Echocardiography in the management of patients with left ventricular assist devices: recommendations from the American Society of Echocardiography." Journal of the American Society of Echocardiography 28.8 (2015): 853-909. CardioNerds Case Report Production Team Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

181. Aortic Stenosis and the Story of TAVR – Historical Perspective & Future Directions with Dr. Jon Resar Feb 21, 2022

Show notes

CardioNerds, Daniel Ambinder and CardioNerds Academy Program Director, Dr. Tommy Das (Cardiology fellow, Cleveland Clinic), Dr. Jacqueline Latina (Structural heart fellow, Johns Hopkins) discuss aortic stenosis and the story of TAVR from both the historical perspective and in terms of future directions with Dr. Jon Resar, Professor of Medicine and Director of the Adult Catheterization Laboratory and Interventional Cardiology at the Johns Hopkins Hospital. This episode is brought to you for Heart Valve Disease Awareness Day. Audio editing by CardioNerds Academy Intern, Shivani Reddy. As many as 11 million Americans have heart valve disease (HVD)—a potentially disabling and deadly disease—yet 3 out of 4 Americans know little to nothing about heart valve disease. Learn more about valve disease. Pearls • Notes • References • Guest Profiles • Production Team 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! Pearls and Quotes - Aortic Stenosis and the Story of TAVR In the previous century, patients with severe aortic stenosis who were treated “medically” had 50% mortality over 2 years after developing symptoms. Balloon aortic valvuloplasty was initially touted as extremely “efficacious” for aortic stenosis but follow-up studies showed that the improvement in symptoms were not durable, and long-term prognosis was dismal. The PARTNER Trial started enrolling in 2007 in extreme risk patients – patients who were not surgical candidates. In 2010, the PARTNER trial was published and TAVR blew away the “standard of care” in inoperable patients at the time, cutting outcomes in half (composite of death and repeat hospitalization). The PARTNER trial studied balloon expandable intra-annular valve implantation. The CoreValve trial studied self-expanding supra-annular valve implantation and was published in 2014. The “Heart Team” approach entails collaborative decision making between cardiologists and cardiac surgeons to personalize management for patients. Both intra-annular and supra-annular valves show non-inferior outcomes to surgery in intermediate and low risk patients. Revascularization prior to TAVR is an evolving arena; the trend has been interventionalists performing fewer PCIs prior to TAVR given the benefit is not clear if angina is not a prominent symptom. Show notes - Aortic Stenosis and the Story of TAVR (TAVR/TAVI are using interchangeably) CardioNerds Aortic Stenosis, updated 1.20.21 1. In the 1990s, patients with severe aortic stenosis (AS) who were deemed to be at high surgical risk would weigh the risks of surgery and prolonged recovery. Balloon Aortic Valvuloplasty (BAV) was first performed by Dr. Alain Cribier in 1986. The technique was based on the foundation of pulmonary valvuloplasty performed initially in 1982 by Drs. Jean Kan and Bob White, and mitral valvuloplasty in 1984. BAV was initially touted as an efficacious cure for aortic stenosis, but unfortunately it had a high restenosis rate as well as high risks for stroke and vascular complications (no closure devices at that time) with an overall poor long-term prognosis. Balloon aortic valvuloplasty was primarily used for decompensated Class IV heart failure in non-surgical candidates. 2. Transcatheter aortic valve replacement (TAVR/TAVI) was developed and first performed in human in 2002.(1) This was performed by Dr. Alain Cribier in France in 2002, initially by trans-septal approach and then by retroaortic approach. Here is a representative diagram of the procedure. Figure: Transcatheter Aortic-Valve Replacement. The transcatheter valve is positioned at the level of the native aortic valve during the final step of valve replacement, when the balloon is inflated within the native valve during a brief period of rapid ventricular pacing. The delivery system is shown after it has traversed the aorta retrograde over a guidewire from its point of insertion in the femoral artery (transfemoral placement). Before balloon inflation, the valve and balloon are collapsed on the catheter (dark blue) and fit within the sheath (blue). After balloon inflation, the calcified native valve (upper panel) is replaced by the expanded transcatheter valve (lower panel, shown in short-axis view from the aortic side of the valve). Smith CR et al. N Engl J Med 2011;364:2187-2198. 3. The PARTNER trial was first published in a landmark NEJM article in extreme surgical risk patients comparing TAVR (with a balloon-expandable aortic valve implant) versus stndard “medical” therapy of aortic stenosis. TAVR markedly reduced the composite outcome of all-cause mortality and repeat hospitalization in these patients.(2) PARTNER then compared TAVR to aortic valve surgery in high risk patients, and TAVR performed quite well, though there were more strokes and vascular complications in the TAVR group compared to surgery.(3) Figure: PARTNER Trial Time-to-Event Curves for the Primary End Point and Other Selected End Points. Leon MB et al. N Engl J Med 2010;363:1597-1607. 4. CoreValve/Medtronic then published their results for their self-expanding valve, enrolling over 1400 participants.(4) The rate of death in the TAVR group was non-inferior to the SAVR group, and a subsequent test for superiority actually showed TAVR was superior to surgery in these high risk patients. Figure: Kaplan–Meier Cumulative Frequency of Death from Any Cause. The rate of death from any cause in the TAVR group was noninferior to that in the surgical group (P

180. Narratives in Cardiology: Raising Women Leaders in Academic Cardiology with Dr. Anu Lala Feb 17, 2022

Show notes

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Leticia Helms (Internal medicine resident at Columbia University), Dr. Silia DeFilippis (AHFT FIT at Columbia University), and Dr. Anu Lala (AHFT faculty and program director at Mount Sinai Hospital) to discuss diversity and inclusion in academic cardiology and more in this installment of the Narratives in Cardiology Series. The President of the New York ACC Chapter Dr. Hima Vidula discusses D&I initiatives at her chapter. Episode introduction and audio editing by CardioNerds Academy Intern, Shivani Reddy. Although women compose 50% of medical students in the United States, cardiology remains a male dominated field. Gender disparity is even more prominent when we look at leadership positions. In this episode we discuss why and how cardiology (and advanced heart failure) can be such a rewarding field for women. The episode reflects on the significant contributions women have made to the field in the past and how they continue to move the field with respect to clinical care and research. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Tweetorial - Raising Women Leaders in Academic Cardiology with Dr. Anu Lala https://twitter.com/Gurleen_Kaur96/status/1509286469051031556?s=20&t=9BFDUXbSnWLcAc5-daXK2A Video version - Raising Women Leaders in Academic Cardiology with Dr. Anu Lala https://youtu.be/vVuhUCbqwYk Quotables - Raising Women Leaders in Academic Cardiology with Dr. Anu Lala “We all have multiple roles – and those roles don’t always have to be completely distinct and separate from one another. You know, our ability in one role, maybe it makes us better at another.”“I felt like being there was like in medical Disneyland for research.” - Anu Lala“Heart failure is unique in that it truly requires that cross disciplinary collaboration at the precipice of what is often life and death.” - Anu Lala“It points to the importance of seeing people do things before you who look like you.” - Anu Lala“All human beings want to feel heard. They want to feel seen and they want to feel like their voice matters.” - Anu Lala“consciously deliberately disruptive”“I like the idea of calling it work-life harmony.” Show notes - Raising Women Leaders in Academic Cardiology with Dr. Anu Lala How do women compare to men in cardiology in 2022?Although nearly 50% of US medical graduates and more than 40% of internal medicine graduates are women, the field of cardiology remains male dominated.Approximately 20% of general cardiology fellows are women, which is comparable to women in surgical subspecialties like neurosurgery (17%), thoracic surgery (21%), and orthopedic surgery (15%) (Reza 2021).Additionally, women hold significantly fewer leadership positions and are less likely to be promoted to senior academic ranks.Out of LBCT presented at ACC 2021, zero had a female first author and zero were presented by women (Kaur 2021).What may make heart failure unique with respect to the recruitment of women?Heart failure is the only subspecialty of cardiology that was founded by a woman. Dr. Sharon Hunt is often described as the founder of the subspecialty.She posited a few reasons why heart failure may attract a higher proportion of women including presence of models and mentors for women, women have been included since the inception of the field, and one that requires collaboration (Hunt 2019).The number of women in HF training programs ranges between 26 to 36% which is much higher than that of women in other subspecialties like EP and interventional cardiology (Reza 2021).How can we increase diversity in clinical trial leadership?Women only represent 1 in 10 authors of cardiovascular trials in high impact journals (Van Spall 2021).Build diverse research team.Hold stakeholders accountable including academic institutions, professional societies, industry sponsors, funding agencies, and scientific journals (Van Spall 2021).Be deliberate about editorial authorship as well as equal representation of women on manuscripts.How can we increase the diversity of participants in clinical trials?We know that increasing the diversity of women investigators in clinical trials is associated with increased enrollment of women participants (Reza 2020).Increased enrollment of diverse populations is key to increasing the generalizability of findings (Van Spall 2021).Build partnerships with the community and community-level providers.Meet social and cultural needs such as family and child care responsibilities; socioeconomic and financial barriers; as well as absenteeism from work (Reza 2022).Provide sex-specific materials to encourage enrollment.For a related discussion, enjoy Ep #135. Underrepresentation in Clinical Trials & Guidelines with Dr. Clyde Yancy.How has the COVID-19 pandemic affected women in academic medicine?Women often bear disproportionate demands of personal life including schooling and caregiving duties and affected by school closures (Reza 2021).Data have suggested that female academic productivity has been affected as measured by decreased publication authorship which may translate into decreased research support (DeFilippis 2021).The decreased submission of manuscripts has been particularly pronounced among junior cohorts of women in academics (Squazzoni 2021). Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

179. Lipids: Polyunsaturated Fatty Acids, Omega-3 Fatty Acids, Eicosapentaenoic acid – Mechanisms of Action with Dr. Ty Gluckman Feb 16, 2022

Show notes

CardioNerds Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), Rick Ferraro (Director of CardioNerds Journal Club and cardiology fellow at the Johns Hopkins Hospital), and CardioNerds Healy Honor Roll Ambassador Dr. Justice Oranefo (UConn cardiology fellow) discuss omega-3 fatty acids acid with Dr. Ty Gluckman, preventive cardiologist and medical director of the Center for Cardiovascular Analytics, Research, and Data Science (CARDS) at the Providence St. Joseph Heart Institute in Portland, Oregon. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen. In the recent years, purified omega 3 fatty acids and its esters have emerged as a potential new tool in our arsenal for management of hypertriglyceridemia and atherosclerotic coronary artery disease. In this episode we review the sources and basic structure of these compounds, as well as their metabolic effects as it pertains to cardiovascular disease. Using hypothetical patient cases, we also discuss scenarios in which these therapies can be useful. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Omega 3 (n-3) fatty acids are a class of polyunsaturated fatty acids [PUFA]. The most studied n-3 fatty acids include eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA] and alpha linoleic acid [ALA]. ALA is found in certain vegetable oils while EPA and DHA are abundant in fish sources.Cardiovascular benefits of n-3 fatty acids include blood pressure reduction, enhanced diastolic function, triglyceride reduction, and immunomodulatory properties.Inflammation plays a major role in the atherogenic process and plaque rupture. Inflammatory marker hs-CRP is a risk enhancing factor for predicting future ASCVD risk. Ongoing trials are investigating therapy that target the inflammatory process in treatment of atherosclerotic heart disease.Prevention and management of ASCVD require aggressive lifestyle modifications and medical therapy addressing risk factors and underlying inflammatory conditions.Purified forms of n-3 fatty acids are approved for the treatment of severe hypertriglyceridemia and as an adjunct therapy to statins for reduction of coronary events in high-risk individuals. Show notes 1. What are omega 3 (n-3) fatty acids? What are the natural sources of n-3 fatty acids? n-3 fatty acids are class of polyunsaturated fatty acids [PUFA]. PUFA are types of unsaturated fats that have more than one double bond in their backbone. PUFAs are important constituents of the phospholipids of all cell membranes.The most studied n-3 fatty acids include eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA] and alpha linoleic acid [ALA].ALA is found in certain vegetable oils including walnuts, flaxseeds, chia seeds. EPA and DHA are abundant in cold water fish oils such as salmon, mackerel, tuna sardines. Interestingly, farm raised fish usually have higher levels of EPA and DHA than wild caught fish; however, this depends on what the fish are fed. Another important class of PUFAs are omega 6 (n-6) fatty acids, found in vegetable oils (1,2). 2. What are the metabolic effects of omega 3 fatty acids? Multiple early studies have demonstrated the anti-inflammatory properties of n-3 fatty acids.The typical Western diet with a high arachidonic acid (an n-6 fatty acid) content promotes atherogenesis leading to the high incidence of CAD in this population.Supplementation with diets rich in DHA and EPA has been associated with reduced arachidonic acid content as well as reduced markers of inflammation. The relative dietary ratios of n-6:n-3 fatty acids have major implications for cardiovascular health.Anti-inflammatory mechanism of n-3 fatty acids include cell membrane stabilization, anti-oxidant properties, reduced leukocyte chemotaxis. (1-3).Other studied cardiovascular benefits of n-3 fatty acids include triglyceride lowering properties (11, 12), blood pressure and heart rate reduction (13, 14), improved endothelial function and antithrombotic properties (15, 16).Importantly, EPA and DHA are distinct molecules (different hydrocarbon length and number of double bonds) with different biologic effects. EPA assumes an extended conformation in cellular membranes, allowing it to neutralize reactive oxygen species, facilitate membrane stabilization, and limit oxidation of LDL cholesterol more easily. In contrast, DHA has a longer carbon chain and has one additional double bond, resulting in less membrane stabilization. DHA also inhibits formation of Dihomo-γ-linolenic acid (DGLA), which is important for production of anti-inflammatory eicosanoids and thus can also increase levels of LDL cholesterol. 3. What role does inflammation play in coronary artery disease? The impact of inflammation in the pathogenesis of atherosclerosis and plaque rupture has been well studied. Inflammatory mediators such CRP, IL-6, and myeloperoxidase have been found to be associated with increased cardiovascular risk.The JUPITER trial demonstrated the benefit of statin therapy in patients with elevated hsCRP. Subsequent trials targeting inflammation in the management of CAD have shown promise. Examples include the LoDoCo which investigated colchicine therapy and the CANTOS trial with investigated the IL-1 beta inhibitor canakinumab.The pathogenic role of inflammation and potential therapeutic role of anti-inflammatory therapy remain key areas of interest and multiple pharmacologic agents are undergoing investigation. (6, 7, 8, 17, 18).Check out the #CardsJC on the LoDoCo 2 trial for more on Colchicine in the management of CAD. Table 1 below summarizes notable trials of anti-inflammatory therapies for ASCVD. 4. What is the role for n-3 fatty acids in management of coronary artery disease? While a diet rich in n-3 fatty acids is associated with a lower risk of cardiovascular events, supplementation with over-the-counter fish oil containing supplements have not demonstrated significant cardiovascular benefits.Purified forms of high dose n-3 fatty acid esters consisting of EPA and/or DHA have shown mixed results as therapies for ASCVD.In the JELIS trial, patients with hypercholesterolemia treated with high dose icosapent ethyl (an EPA ester) in addition to pravastatin 10mg/day or simvastatin 5mg/day experienced reduced incidence of cardiac events and reduced LDL with greater benefit seen in patients with impaired glucose metabolism.The REDUCE-IT trial showed similar results in patients with atherosclerotic disease and high risk patients with elevated fasting triglycerides.Interestingly, the STRENGTH trial, in which patients were treated with combination EPA+DHA, did not show a benefit in the treatment arm.Icosapent ethyl is currently indicated as an adjunct therapy in addition to maximally tolerated statin therapy in patients with triglyceride levels ≥150 mg/dL and either established cardiovascular disease or type 2 diabetes mellitus plus ≥2 risk factors for cardiovascular disease to reduce incidence of cardiac events. (19 – 21).Check out the #CardsJC on the STRENGTH trial for an overview of relevant trial data. Table 2 below summarizes notable trials of omega-3 fatty acids for ASCVD. 5. What is the role of n-3 fatty acids in management of hypertriglyceridemia? In the approach to hypertriglyceridemia, be sure to identify and treat secondary causes (alcoholism, hypothyroidism, uncontrolled diabetes, etc) before instituting pharmacotherapy. Enjoy the CardioNerds “Causes of Hypertriglyceridemia” infographic developed by Dr. Teodora Donisan.The 2021 ACC expert consensus decision pathway on the management of ASCVD in patients with hypertriglyceridemia provides guidelines and algorithmic strategies to management of hypertriglyceridemia in several patient populations (22).The triglyceride reducing properties of n-3 fatty acids have been demonstrated on several trials including the EVOLVE trial (11). One should note that while several therapies reduce triglycerides, the potential benefits from n-3 fatty acids likely extend beyond triglyceride reduction. Table 1. Previous randomized controlled trials investigating colchicine and other anti-inflammatory therapies in the treatment of atherosclerotic ischemic heart disease Table 2. Review of relevant randomized control trials on Omega-3 fatty acids. CAD, coronary artery disease; CV, cardiovascular; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; MACE, major adverse cardiovascular events. Infographic. Causes of Hypertriglyceridemia by Dr. Teodora Donisan. References - Triglycerides MOZAFFARIAN, D. & WU, J.H.Y., 2011. Omega-3 Fatty Acids and Cardiovascular Disease: Effects on Risk Factors, Molecular Pathways, and Clinical Events. Journal of the American College of Cardiology, 58(20), pp.2047–2067.Calder, Philip C, 2010. Omega-3 fatty acids and inflammatory processes. Nutrients, 2(3), pp.355–374.Raphael, William & Sordillo, Lorraine M, 2013. Dietary polyunsaturated fatty acids and inflammation: The role of phospholipid biosynthesis. International journal of molecular sciences, 14(10), pp.21167–21188.Schwalfenberg, G., 2006. Omega-3 fatty acids: their beneficial role in cardiovascular health. Canadian family physician, 52(6), pp.734–740.Hansson, Göran K, 2005. Mechanisms of disease: Inflammation, atherosclerosis, and coronary artery disease. The New England journal of medicine, 352(16), pp.1626–1695.Ridker, Paul M et al., 2008....

178. Case Report: Occam’s Razor or Hickam’s Dictum? Cardiogenic Shock With Severe Biventricular Heart Failure – Northwestern University Feb 10, 2022

Show notes

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Loie Farina (Northwestern University CardioNerds Ambassador), Dr. Josh Cheema, and Dr. Graham Peigh from Northwestern University for drinks along the shores of Lake Michigan at North Avenue Beach. They discuss a case of a 52-year-old woman with limited cutaneous systemic sclerosis who presents with progressive symptoms of heart failure and is found to have a severe, non-ischemic cardiomyopathy. The etiology of her cardiomyopathy is not clear until her untimely death. She is ultimately diagnosed with cardiac AL amyloidosis with isolated vascular involvement a real occam’s razor or hickam’s dictum conundrum. We discuss the work-up and management of her condition including a detailed discussion of the differential diagnosis, the underlying features of systemic sclerosis with cardiac involvement as well as cardiac amyloidosis, the role of a shock team in managing cardiogenic shock, and how to identify those with advanced or stage D heart failure. Advanced heart failure expert Dr. Yasmin Raza (Northwestern University) provides the ECPR segment. Episode introduction by CardioNerds Clinical Trialist Dr. Liane Arcinas. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen. Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Pearls - Notes - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Summary - Occam’s Razor or Hickam’s Dictum? This is a case of a 52-year-old woman with limited cutaneous systemic sclerosis who presented with progressive dyspnea on exertion and weight loss over the course of 1 year. Her initial work-up was notable for abnormal PFTs and finding of interstitial pneumonia on high-resolution CT, an ECG with frequent PVCs and normal voltage, a transthoracic echocardiogram with a mildly reduced ejection fraction of 40%, and a right/left heart catheterization with normal coronary arteries, filling pressures, and cardiac output. Scleroderma-related cardiac involvement is suspected. She is placed on GDMT, but her condition worsens over the next several months, and repeat echocardiogram shows severely reduced biventricular function, reduced LV global longitudinal strain (GLS) with apical preservation of strain, severely reduced mitral annular tissue Doppler velocities, and a normal left ventricular wall thickness. Scleroderma-related cardiac involvement remains highest on the differential, but because of some findings on the echo that are concerning for cardiac amyloidosis, an endomyocardial biopsy was obtained. It showed vascular amyloid deposition without interstitial involvement. The diagnosis of cardiac amyloid was discussed but deemed unlikely due to lack of interstitial involvement. However, a serologic work-up soon revealed a monoclonal serum lambda light chain and a follow-up bone marrow biopsy showed 20% plasma cells. She was discharged with very near-term follow-up in oncology clinic with a presumptive diagnosis of AL amyloidosis, but she unfortunately returned in shock and suffered a cardiac arrest. She initially survived and underwent emergent veno-arterial extracorporeal membrane oxygenation (VA ECMO) cannulation with subsequent left ventricular assist device placement (LVAD). However, she passed away due to post-operative hemorrhage. Autopsy was consistent with a final diagnosis of cardiac AL amyloidosis with isolated vascular involvement. Case Media - Occam’s Razor or Hickam’s Dictum? EKG CXR TTE Pathology CMR Episode Teaching -Occam’s Razor or Hickam’s Dictum? Pearls Scleroderma causes repeated focal ischemia-reperfusion injuries which result in patchy myocardial fibrosis. Cardiac involvement in scleroderma is frequent but often not clinically evident; when symptomatic, it is associated with a poor prognosis. Myocardial dysfunction in cardiac AL amyloidosis can result from myocardial infiltration, vascular deposition causing microvascular dysfunction and ischemia, and direct cardiotoxicity from circulating light chains. While isolated vascular amyloid is very rare, it can occur and can be seen without key characteristics of interstitial amyloid deposition, namely left ventricular hypertrophy and low voltage on an ECG. Cardiogenic shock outcomes are improved by multi-disciplinary discussions, commonly referred to as a “shock team call.” Heart failure is a progressive, morbid, and potentially fatal condition. LVADs and heart transplantation improve life expectancy and decrease morbidity among patients with stage D heart failure. Identification of patients with advanced heart failure can be challenging – a helpful mnemonic is “I NEED HELP Notes - Occam’s Razor or Hickam’s Dictum? 1. How does scleroderma affect the heart? Scleroderma is a connective tissue disorder characterized by extracellular matrix deposition, with widespread fibrosis of the skin and visceral organs, microvascular injury, and evidence of immune system activation. Cardiac involvement is common, although likely underestimated as it is often subclinical, and the estimated prevalence varies widely. Myocardial involvement is identified in up to 80% of patients in histological studies and clinical myocardial dysfunction is recognized in 15-25%. When clinically evident, cardiac involvement portends a poor prognosis, with up to a 70% mortality at 5 years. Approximately 25% of scleroderma-related deaths are due to cardiac causes. Primary involvement is thought to be mediated by repeated focal ischemic-reperfusion injury, impaired microcirculation, inflammation, and eventual focal irreversible fibrosis leading to heart failure and arrhythmias. Cardiac involvement can also occur secondary to lung or renal disease, pulmonary arterial hypertension, or other cardiovascular risk factors. Cardiac manifestations: Myocardial failure: diastolic dysfunction is frequently reported but less commonly associated with diastolic heart failure. Systolic dysfunction can also occur, but severe systolic dysfunction is rare. Electrical failure: arrhythmias and conduction disorders Pericardial failure: pericarditis and pericardial effusion Coronary failure: coronary microvascular dysfunction Valvular failure: valvular involvement (uncommon) 2. What is cardiac amyloidosis (CA) and what is the pathophysiology? For an in-depth review of Cardiac Amyloidosis, enjoy the CardioNerds Cardiac Amyloid Series! Amyloidosis is a process in which proteins misfold, aggregate, and form amyloid fibrils that deposit in various organs, thereby causing tissue injury and organ malfunction. The most common types of cardiac amyloidosis are AL (light chain) and TTR (transthyretin). AL amyloidosis is a hematologic disorder of clonal plasma cells that overproduce light chains, which may deposit in any organ sparing the central nervous system, and commonly deposit in the heart and kidneys. Delayed diagnoses are common, with an estimated one-third of patients visiting five or more physicians before receiving the diagnosis. Cardiac involvement with heart failure portends a particularly poor prognosis, with a median survival from onset of heart failure of less than six months without treatment. Stem cell transplantation has been shown to improve survival if performed prior to the diagnosis of advanced heart failure. Unfortunately, about 80% of patients are not candidates for aggressive therapy due to advanced stage of disease. In CA, amyloid deposits infiltrate and expand the extracellular space which results in increased ventricular wall thickness and classically manifests as a restrictive cardiomyopathy with relatively preserved EF; however, a subset of patients may present with reduced LVEF and minimal or no ventricular wall thickening. Patients with AL cardiac amyloidosis tend to have greater severity of heart failure than TTR despite less morphological involvement (in terms of LV wall thickness), felt due to the toxic effect of light chain amyloid fibrils on the tissue resulting in a toxic-infiltrative cardiomyopathy. Additional mechanisms thought to play a major contributing role in cardiac AL amyloidosis: Circulating light chains cause direct cardiotoxicity through cardiomyocyte oxidant stress and abnormal vascular reactivity, impairing vasodilation Vascular amyloid deposition in the small intramural coronary vessels results in microvascular dysfunction and global myocardial ischemia. Vascular involvement is common in AL cardiac amyloidosis (much more common than in TTR cardiac amyloid). A pathology study demonstrated obstructive intramural coronary amyloidosis in 63 of 96 patients (66%) and 86% of these patients had microscopic evidence of myocardial ischemia. Isolated vascular involvement, however, is rare - 97% of patients in this study had interstitial involvement. Coronary microvascular dysfunction occurs via 3 major mechanisms: Structural - with amyloid deposition in the vessel wall causing wall thickening and luminal stenosis Extravascular - through extrinsic compression of the microvasculature from perivascular and interstitial amyloid deposits and decreased diastolic perfusion Functional - through autonomic and endothelial dysfunction 3. What are common cardiac MRI (CMR) findings in scleroderma heart disease and cardiac amyloidosis? First, a review of a few key concepts in CMR (also, enjoy Episode #33. Cardiac MRI with Dr. Deborah Kwon): Native T1 signals are increased by edema (e.g. acute infarction) and an increase in interstitial space (e.g. fibrosis, amyloidosis). T1 signals are decreased by lipid and iron overload. Gadolinium contrast agents are distributed throughout the extracellular space and shorten the T1 relaxation times of myocardium

177. CCC: Cardiac Arrest, E-CPR, & Post-Arrest Care with Dr. Jason Bartos Feb 07, 2022

Show notes

Approximately 350,000 adults per year in the US experienced out-of-hospital cardiac arrest (OHCA). Only about 10% of such patients survive their initial hospitalization. The key drivers of successful resuscitation from OHCA are bystander cardiopulmonary resuscitation (CPR) and public use of an automated external defibrillator (AED). Survival rates from OHCA vary dramatically between US regions. For instance, the extracorporeal CPR (eCPR) program at the University of Minnesota has over a 40% survival rate in patients with OHCA and refractory ventricular fibrillation (VF) based on data published in the ARREST trial. In this episode, we are joined by experts from the University of Minnesota, including Dr. Jason Bartos (Interventional and Critical Care Faculty) and Dr. Julie Power (Chief Fellow at University of Minnesota and CardioNerds Academy Fellow), along with Dr. Yoav Karpenshif (Co-Chair Critical Care Series, University of Pennsylvania) and CardioNerds Co-Founders (Amit Goyal and Dan Ambinder) to discuss cardiac arrest, E-CPR, & post-arrest care. This includes targeted temperature management, coronary angiography and revascularization, as well as the growing field of eCPR and VA ECMO. Episode introduction by CardioNerds Clinical Trialist Dr. Jason Feinman. Audio editing by CardioNerds Academy Intern, Shivani Reddy. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Abbreviations - Cardiac Arrest, E-CPR, & Post-Arrest Care eCPR- extracorporeal cardiopulmonary resuscitation VA ECMO- veno-arterial extracorporeal membrane oxygenation VT/VF- ventricular tachycardia/ventricular fibrillation ACLS- advanced cardiovascular life support ROSC- return of spontaneous circulation- OHCA- out-of-hospital cardiac arrest IHCA- in-hospital cardiac arrest TTM- targeted temperature management Pearls and Quotes - Cardiac Arrest, E-CPR, & Post-Arrest Care The ARREST trial showed early VA ECMO-facilitated resuscitation for patients with OHCA and refractory VF significantly improved survival to hospital discharge when compared to standard ACLS treatment.Coronary artery disease is common in the setting of cardiac arrest, with up to 96% of patients with STEMI on post resuscitation EKG and up to 85% of refractory out-of-hospital VT/VF arrests.Guidelines recommend emergent coronary angiography for patients with ST-segment elevation on the post-ROSC ECG.The role of timing of revascularization after ROSC in patients without STEMI or shock is unknown.The role of coronary angiography in cardiac arrest with nonshockable rhythms is also unclear.The current AHA guidelines recommend initiation of targeted temperature management between 32°C and 36°C for at least 24 hours for all patients who do not follow commands after ROSC in both OHCA and IHCA. Show notes - Cardiac Arrest, E-CPR, & Post-Arrest Care 1. What are early post arrest management considerations? The key drivers of successful resuscitations from OHCA: CPR and public use of AEDs in the field. After initial stabilization, care of the critically ill post-arrest patient hinges on hemodynamic support, mechanical ventilation, temperature management, attending to adverse sequelae of arrest, and diagnosis and treatment of underlying causes of arrest. Coronary artery disease is common in the setting of VT/VF cardiac arrest, with up to 96% of patients with STEMI on post resuscitation EKG and up to 85% of refractory out-of-hospital VT/VF arrests.In the early post-arrest state, it is also important to diagnose and treat infections and any neurologic injury. Neurologic compromise is a common cause of mortality in patients who achieve ROSC. Over 50%, and in some cohorts around 75%, of patients with death after resuscitated OHCA die of neurologic injury. 2. What is the current evidence for targeted temperature management (TTM)? “[This is] the most hotly debated topic right now in the field of cardiac arrest.” - Dr. Jason BartosCurrent AHA guidelines recommend initiation of targeted temperature management between 32°C and 36°C for at least 24 hours for all patients who do not follow commands after ROSC in both OHCA and IHCA. TTM is a relatively safe and effective strategy that can improve neurological outcomes in patients who remain comatose after achieving ROSC from cardiac arrest. Current evidence supports a broad range of TTM from 33°C to 36°C and should be maintained for 24 hours. Although TTM should be initiated as early as possible, prehospital initiation of cooling has not been shown to improve survival outcomes.The TTM2 trial showed that in patient with coma following OHCA, targeted hypothermia versus normothermia (i.e., fever control) was not associated with improved survival or functional outcomes compared to normothermia. It should be noted that patients on VA ECMO were not included in this trial. 3. What are some possible complications from TTM? Arrhythmias: Hypothermia slows cardiac conduction leading to bradycardia and QT prolongation which can exacerbate underlying arrhythmias such as VT/VF. Consideration can be given to actively rewarming the patient in the setting of VT/VF.Clotting: Core temperatures below 35°C impede the clotting cascade and platelet function. Because of this, if a patient develops significant non-compressible bleeding while undergoing TTM, consideration should be given to actively rewarm the patient.Shivering is a natural response to hypothermia. Suppression of this is crucial for TTM. First line strategies include propofol, fentanyl, or midazolam. Dexmedetomidine is effective, but side effects of bradycardia can limit its use. Buspirone (a 5-HT agonist), when used in conjunction with opiate analgesia or dexmedetomidine, has been shown to lower the shivering threshold. Neuromuscular blocking agents are highly effective at preventing shivering but confound the neurologic examination and may mask seizures. Patients need to be deeply sedated (typically RASS –4 or lower) and be followed with train-of-four assessments.Diuresis increases with hypothermia potentially leading to electrolyte loss of potassium, magnesium and phosphorous. Therefore, electrolytes need to be frequently monitored. Interestingly, total body potassium may not actually be low due to cellular shifts; thus, conservative replacement is recommended.Insulin resistance can develop as well. 4. How do we select appropriate patients to pursue revascularization and consider the timing of revascularization in patients with recent cardiac arrest? Guidelines recommend emergent coronary angiography for patients with ST-segment elevation on the post-ROSC ECG.However, the role and timing of revascularization after ROSC in patients without STEMI or shock is unknown.The role of coronary angiography in cardiac arrest with non-shockable rhythms is also unknown. 5. What is the physiologic basis for eCPR? The biggest predictor of post-arrest outcome is time.In the ALPS trial (2016), patients who underwent zero to nine minutes of CPR with ROSC had a survival of 65%. Survival dropped by 17% for every extra 10 minutes of CPR, such that there were no survivors in the amiodarone arm of the trial after 40 minutes.The results of this study were replicated at the University of Minnesota: OHCA brought to University of Minnesota Cath lab within 30 minutes of their cardiac arrest had a >90% survival rate. Survival rate drops over elapsed time: for every additional 10 minutes of ACLS, there is 25% additional mortality. If VA ECMO is initiated >90 minutes after arrest, survival is poor (10-15%). The study showed eCPR was associated with improved neurologically favorable survival at all CPR durations 3 shocks or >15-20 min of ongoing CPR without recovery of a perfusing rhythm, VA ECMO should be considered. References - Cardiac Arrest, E-CPR, & Post-Arrest Care Bartos JA, Grunau B, Carlson C, et al. Improved Survival With Extracorporeal Cardiopulmonary Resuscitation Despite Progressive Metabolic Derangement Associated With Prolonged Resuscitation. Circulation....

176. Narratives in Cardiology: Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park – Florida Chapter Feb 04, 2022

Show notes

CardioNerd (Amit Goyal), Dr. Zarina Sharalaya (Interventional cardiology fellow at the Cleveland Clinic), Dr. Ashley Mohadjer (Interventional cardiology fellow, Vanderbuilt Heart and Vascular Institute), and Dr. Laurie Mbuntum (Cardiology fellow, UTSW) join Dr. Ki Park (Associate professor of medicine and an interventional cardiologist at the University of Florida and Malcom Randall VA Medical Center in Gainesville, FL.) for a a well-rounded discussion on all things ‘Women-in-Cardiology' #WIC . Dr. Ki Park discusses how she nurtured her interest in interventional cardiology, and further shares her thoughts and passion for cardio-obsetrics. She shares her advice for trainees thinking about interventional or cardioobetrics and anecdotes from her training as a successful woman in the field. We discuss the need for education on pregnancy outcomes and long-term cardiovascular risk, ideas to lower maternal mortality, how to start a women’s cardiovascular clinic, and her thoughts on how the field may look in the future. Special message by Florida ACC State Chapter Governor, Dr. David Perloff. Episode introduction and audio editing by CardioNerds Academy Intern, Shivani Reddy. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park https://youtu.be/_oYUc-_sdfU Tweetorial - Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park https://twitter.com/gurleen_kaur96/status/1495921275545563136?s=21 Quotables - Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park “I like the work life integration as opposed to work life balance. Balance just implies that you always have everything aligned perfectly at all times and that is just not doable.”Dr. Ki Park Show notes - Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park Why is screening for OB-GYN history for cardiovascular risk is important, and who should be responsible? Pregnancy is nature’s stress test and in some women can unmask someone’s predisposition to cardiac diseaseYearly screening for diabetes, hypertension, dyslipidemiaBig interdisciplinary effort in attempt to try to capture all women at risk, as many will not present with manifestation of disease initially How did you nurture your interest in cardioobsetrics? In interventional cardiology? Meetings and societiesConnect with those who work in the field, social mediaRegarding interventional cardiology – having interest in procedures, do as many cases “hands on” as possible, learning from mistakes What advise do you have to achieve work and life balance? It's important to understand the various occupational hazards of radiation exposure which include but are not limited to brain tumors, cataracts, thyroid disease, cardiovascular diseases, musculosketal problems and reproductive side effects. Have grace, one can’t be 100% at every single thing all the timeIts more work life integration as opposed to a balancePrioritize different things on different days, be honest with children and explain why you do what you do in age appropriate terms Maternal mortality is high in this country with cardiovascular disease as a leading cause. What are important factors to improve maternal mortality? EducationImproving access to care in the peripartum stage for mothers, particularly since the focus in that period is on babyLegislature to improve insurance coverage Where do you see cardioobsetrics field going in the next few years? Make the knowledge more mainstreamEducation of subspecialty fellows within cardiovascular educationCollaboration with ACOG and maternal fetal medicine societiesMore registries of patients to continue to learn more about these women What was involved to create the women’s heart clinic in your institution? Start small – there are plenty of women who want to seek specialized careHaving an MFM and congenital faculty at the same institution was helpfulSeek advice from those at expert centers What advise do you have for trainees looking to pursue a career in interventional cardiology who are worried about work-life integration? Understand what you’re getting into, particularly for that year Don’t be afraid to ask for help from friends or family at home to allow for more quality time with significant others, kids, friends, etc -- this isn’t a sign of weaknessYou don’t have to be perfect Physicians have been found to delay childbearing compared to peers in other professions. What are your thoughts on this? Progress has been made and overall there is increased awareness and supportLeave for trainees should be more flexible More societal and institutional support Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

175. ACHD: Single Ventricle Circulation and Fontan Palliation with Dr. Yuli Kim Jan 27, 2022

Show notes

CardioNerds (Amit Goyal and Daniel Ambinder), ACHD series co-chair Dr. Daniel Clark (Vanderbilt University), and ACHD FIT lead Dr. Danielle Massarella (Toronto University Health Network) join ACHD expert Dr. Yuli Kim (Associated Professor of Medicine & Pediatrics at the University of Pennsylvania), to discuss single ventricular heart disease and Fontan palliation. They cover the varied anatomical conditions that can require 3-step surgical palliation culminating in the Fontan circulation, which is characterized by passive pulmonary blood flow, high venous pressures, and low cardiac output. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship and CardioNerds Academy Fellow). The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls There are various forms of unpalliated ‘single ventricle’ congenital heart disease. The three main hemodynamic issues that need to be addressed in any form are unbalanced flow, pulmonary over-circulation, and blood mixing. The Fontan palliation is a series of operations for congenital heart disease patients in whom biventricular repair is not feasible. In the completed Fontan circulation, systemic venous blood is surgically routed directly to the lungs, effectively bypassing the heart, and creating passive pulmonary blood flow. The hallmarks of the Fontan circulation (and Fontan failure) are elevated central venous pressure and low cardiac output. Patients with Fontan circulation may experience significant morbidity in the long term from both cardiac and non-cardiac sequelae, and require lifelong specialist care. Show notes 1. Why do some patients require Fontan palliation? Many different types of anatomies may ultimately require single ventricular palliation via the Fontan procedure due to inadequate biventricular function to support both pulmonary and systemic circulations. Some examples include Tricuspid Atresia (hypoplastic RV), Double Inlet Left Ventricle (DILV; hypoplastic RV), Hypoplastic Left Heart Syndrome (HLHS; hypoplastic LV), and atrioventricular septal defects (AVSD; either RV or LV may be inadequate based on “commitment” of the common AV valve). The Fontan procedure was first described in 1971; at this time, mortality of single ventricular patients exceeded 90% in the first year of life. 2. What are the stages of Fontan palliation? Effective pulmonary blood flow/balancing flow to the pulmonary and systemic circulations: for many conditions, this involves retrograde pulmonary blood flow from a systemic -> PA shunt (i.e. Blalock-Taussig-Thomas “BTT” shunt in which the subclavian artery is turned down and anastomosed to the pulmonary artery). In infants, the pulmonary vascular resistance (PVR) is high perinatally and gradually lowers over the first 3 months of life to adult levels with exposure to the atmosphere’s natural pulmonary vasodilator: oxygen. Thus, in the first 3 months of life babies have an intrinsic PVR that is too high to directly connect the venous system to the lung arteries and thereby require staged surgeries. Protect the pulmonary vasculature from overcirculation: ultimately, the goal of single ventricular palliation is rerouting systemic venous drainage directly to the pulmonary vasculature passively, without a cardiac pumping chamber. This volume unloads the common ventricle and allows it a better chance to function over the lifespan by pumping only to a single circuit: the systemic vascular bed. Thus, steps 2 and 3 of Fontan palliation are passive head/neck venous connection to the pulmonary arteries (now typically accomplished with the modified bidirectional Glenn operation that anastomoses the SVC to the RPA typically) and finally total cavopulmonary connection by the Fontan conduit connecting the lower body’s venous return from the IVC to the Fontan tunnel and up to the RPA. 3. What is the ultimate “plumbing” of Fontan circulation? Venous blood from the head/neck is connected directly from the SVC to the right pulmonary artery (RPA; typically, via a Glenn operation).Venous blood from the legs, abdomen/pelvis and lower body is connected directly to the RPA via the Fontan tunnel.In sum, the pulmonary blood flow enters passively, without a pump to send venous blood to the lungs. http://pted.org/?id=fontan3 4. What are the types of Fontan? The classic Fontan operation involved a direct venous connection to the right atrium with an atriopulmonary connection to the RPA.Contemporary era Fontan operations typically involve the lateral tunnel (LT) or extracardiac conduit. The LT incorporates pericardium in the creation of the Fontan conduit along the surface of the heart, while the extracardiac conduit is entirely prosthetic material (typically GoreTex). https://www.ahajournals.org/doi/epub/10.1161/CIR.0000000000000696 5. What are the common complications of Fontan circulation? CardiacArrhythmias: both atrial and ventricular arrhythmias can be common, especially owing to surgical scar lines, residual valvular disease, and hemodynamic sequelae of the Fontan palliationVentricular dysfunction: this may take the form of both systolic and/or diastolic dysfunctionValvular disease: atrioventricular valvular insufficiency, etc.Thromboembolic complications: venous stasis, endothelial damage, and exposure of von Willebrand factor contribute to a risk of thrombosis and risk of paradoxical emboli into the systemic circulation for patients with residual venous-arterial system connections (such as Fontan fenestration/baffle leak) ExtracardiacNeurocognitive: mental health disorders (including PTSD, depression, and anxiety) are common, as are executive function limitations that can be identified as early as childhoodFontan-associated liver disease (FALD): including risk of developing hepatocellular carcinomaRenal disease: chronic kidney disease/renal venous hypertensionLymphatic: protein-losing enteropathy (PLE) and plastic bronchitis 6. When is it time to refer a patient with Fontan palliation for heart transplantation evaluation? This is a very challenging, multidisciplinary decision that must weigh operative risk, HT candidacy, allosensitization, need for multi-organ transplantation (heart-liver, heart-lung, etc.), and patient-centered discussion about their goals of care.The team must way high near-term per-transplantation risk with improved long-term outcomes. References 1. Cetta F, Dearani J, O'Leary P and Driscoll D.Tricuspid Valve Disorders: Atresia, Dysplasia and Ebstein Anomaly. In: H. Allen, R. Shaddy, D. Penny, T. Feltes and F. Cetta, eds. Moss and Adams' Heart Disease in Infants, Children and Adolescents Philadelphia: Wolters Kluwer; 2016. 2. Book WM, Gerardin J, Saraf A, Valente AM, Rodriquez III F. Clinical phenotypes of fontan failure: implications for management. Congenit Heart Dis. 2016;11:296–308. https://pubmed.ncbi.nlm.nih.gov/27226033/ 3. Rychlik J, Atz AM, Celermajer DS, Deal BJ, Gatzoulis MA, Gewillig MH et al. American Heart Association Council on Cardiovascular Disease in the Young and Council on Cardiovascular and Stroke Nursing. Evaluation and Management of the Child and Adult With Fontan Circulation: A Scientific Statement From the American Heart Association. Circulation. 2019 Jul 1. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000696 Meet Our Collaborators! Adult Congenital Heart AssociationFounded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers CHiP Network The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information. Heart UniversityHeart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease. It is a carefully curated open access library of educational material for all providers of care to children and adults with CHD or children with acquired heart disease, whether a trainee or a practicing provider. The site provides free content to a global audience in two broad domains: 1. A comprehensive curriculum of training modules and associated testing for trainees. 2....

Our TOPPODCAST Picks

Follow Us

Stay Connected

Cardionerds: A Cardiology Podcast

Related Podcasts

Links

Stay Connected