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    Health & Fitness

    Cardionerds: A Cardiology Podcast

    Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge, sharpen your skills, and become a true CardioNerd!

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    Latest Episodes:
    174. Cardio-Obstetrics: Black Maternal Health with Dr. Rachel Bond Jan 21, 2022
    Show notes

    CardioNerds (Amit Goyal), Dr. Natalie Stokes (Cardiology Fellow at UPMC and Co-Chair of the Cardionerds Cardio-Ob series), fellow lead Dr. Victoria Thomas (Cardionerds Ambassador, Vanderbilt University Medical Center), join Dr. Rachel Bond (Women's Heart Health Systems Director at Dignity Health, Arizona) for a cardio-obstetrics discussion about Black maternal health. Episode introduction by CardioNerds Clinical Trialist Dr. Chistabel Nyange. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen. This episode was developed in collaboration with the Association of Black Cardiologists. ABC is a 501(c)3 nonprofit organization whose mission is to promote the prevention and treatment of cardiovascular disease, including stroke, in Black persons and other minority populations, and to achieve health equity for all through the elimination of disparities. Learn more at https://abcardio.org/. 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! Show notes 1. Why does Black Maternal Health need to be deliberately highlighted episode on CardioNerds? Black women are three-four times more likely to die during their pregnancy. The deaths are primarily tied to cardiomyopathy and cardiovascular conditions such as coronary artery disease, pulmonary hypertension, chronic hypertension, preeclampsia, and eclampsia.63-68% of this cardiovascular mortality is preventable depending on one’s racial identity. As CardioNerds, we must educate ourselves on why this occurs and identifying diseases that may place patients at increased risk.Studies have shown the Black maternal mortality crisis exist irrespective of one’s education or socioeconomic status.We must recognize and admit that some patients are being treated differently because of their race and ethnicity alone. 2. When we consider or acknowledge a patient’s race, what should CardioNerds think about? Race is an important factor to think about, but we must remember that it is an imperfect variable. We should not focus on biology or genetic make-up. We should think about social determinants of health. 60% of the time social and personal aspects dictate one’s health.Unconscious biases and structural racism are likely playing a major role in race-based health inequities. 3. What are other vulnerable groups that have increased mortality rates related to cardioobstetric care? Native American women have similar maternal mortality rates to Black populations.Women who are veterans, live in rural communities, and/or are currently incarcerated have increased risk of mortality 4. What are some of the social determinants of health that should be considered for these patients? Food deserts or having poor access to nutrient rich/quality foods make these vulnerable patients have increased risk factors for high cholesterol, high blood pressure, obesity, and diabetes which increase the risk for pregnancy complications and infertility.The above vulnerable populations can have less access to higher levels of care for high-risk pregnancies. 5. What are some of the preventable causes of maternal mortality? Clinicians should actively listen to their patients' concerns. There have been several media stories in the news and on CardioNerds episodes where women’s concerns were not acknowledged or taken seriously.Preconception counseling is important to provide to all patients. 50% of women have one risk factor for cardiovascular disease when entering pregnancy. We should have discussions with patients regarding their lifestyles, with an emphasis on exercise and diet. 6. What are some of the psychosocial or health related differences we see in black mothers when compared to other races? The effect of stress is affecting not just black mothers but black women in general by predisposing them to increased cardiovascular disease and cognitive impairment. The stress effects on black women are being called superwoman schema.Superwoman schema is a combination/phenomenon of gender and racial oppression’s effect on the allostatic load (cumulative biological stress). Studies have shown that black women’s chronic stress levels affect their sympathetic nervous system with an inability to fight off or perhaps produce too much inflammatory response. This increases the risk of a variety worsening chronic morbidities in particular worsening cardiovascular health.One in eight women will struggle with infertility. Black women are two times more likely to suffer from infertility compared to their White counterparts. This is largely due to increased uterine fibroids. Black women are also less likely to be referred to a reproductive endocrinology specialist. 7. What pre-counseling assessments or work-up should be considered for women trying to conceive? Consider getting a baseline ECG as that would give a nice idea of structurally of what is going on within the heart. If there are several risk factors, there can be consideration for a baseline echocardiogram.There should be a specific focus on lifestyle. As cardiologists, we should try to have our patients monitor their weight and follow a well-balanced diet with exercise. They should monitor their blood pressure.Also try to have a birthing plan with OBGYN team as there is data to support that a birthing plan can lead to better outcomes for high-risk pregnancy. 8. What are some of the tools that have been recently used to help reduce black maternal mortality? Patients that are likely to have higher pregnancy complications should be considered to follow not only with a maternal fetal medicine doctor, but there should be consideration for extra help with a doula or a midwife if possible.We should promote home blood pressure monitoring during pregnancy and post-partum as there have been trials supporting the fact that blood pressure control was more successful using texting/ambulatory monitoring strategies vs office visits alone.Digital platforms such as MAHMEE are closing gaps in care to connect patients in their pregnancy and postpartum care to help with all patients but especially underserved populations. References 1. Bond RM, Gaither K, Nasser SA, et al. Working Agenda for Black Mothers: A Position Paper from the Association of Black Cardiologists on Solutions to Improving Black Maternal Health. Circ Cardiovasc Qual Outcomes. 2021;14(2):e007643. doi:10.1161/CIRCOUTCOMES.120.007643 2. Havranek EP, Mujahid MS, Barr DA, et al. Social Determinants of Risk and Outcomes for Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2015;132(9):873-898. doi:10.1161/CIR.0000000000000228 3. Chandra A, Copen CE, Stephen EH. Infertility and impaired fecundity in the United States, 1982-2010: data from the National Survey of Family Growth. Natl Health Stat Report. 2013;(67):1-19. 4. Woods-Giscombé CL. Superwoman schema: African American women's views on stress, strength, and health. Qual Health Res. 2010;20(5):668-683. doi:10.1177/1049732310361892 5. Allen AM, Wang Y, Chae DH, et al. Racial discrimination, the superwoman schema, and allostatic load: exploring an integrative stress-coping model among African American women. Ann N Y Acad Sci. 2019;1457(1):104-127. doi:10.1111/nyas.14188 6. Ofili EO, Schanberg LE, Hutchinson B, et al. The Association of Black Cardiologists (ABC) Cardiovascular Implementation Study (CVIS): A Research Registry Integrating Social Determinants to Support Care for Underserved Patients. Int J Environ Res Public Health. 2019;16(9):1631. Published 2019 May 10. doi:10.3390/ijerph16091631 7. Lantz PM, Low LK, Varkey S, Watson RL. Doulas as childbirth paraprofessionals: results from a national survey. Womens Health Issues. 2005;15(3):109-116. doi:10.1016/j.whi.2005.01.002 8. Pregnancy mortality surveillance system. Centers for Disease Control and Prevention. https://www.cdc.gov/reproductivehealth/maternal-mortality/pregnancy-mortality-surveillance-system.htm. Published November 25, 2020. Accessed December 18, 2021. 9. Cairns AE, Tucker KL, Leeson P, et al. Self-Management of Postnatal Hypertension: The SNAP-HT Trial. Hypertension. 2018;72(2):425-432. doi:10.1161/HYPERTENSIONAHA.118.10911 10. Hirshberg A, Sammel MD, Srinivas SK. Text message remote monitoring reduced racial disparities in postpartum blood pressure ascertainment. Am J Obstet Gynecol. 2019;221(3):283-285. doi:10.1016/j.ajog.2019.05.011 11. Vedam S, Stoll K, MacDorman M, et al. Mapping integration of midwives across the United States: Impact on access, equity, and outcomes. PLoS One. 2018;13(2):e0192523. Published 2018 Feb 21. doi:10.1371/journal.pone.0192523 Guest Profiles Dr. Rachel Bond Rachel M Bond, MD, FACC, Women's Heart Health & Prevention Specialist is devoted to expert diagnosis and treatment for improved patient outcomes. Her expertise is in cardiovascular disease with special interest in women's heart health, prevention, lipid disorders, pregnancy-related heart disease, cardio-oncology and autoimmune-related heart disease.Dr. Bond is a board-certified attending cardiologist and the System Director of the Women's Heart Health Program at Dignity Health in Arizona. She is affiliated with Chandler Regional Medical Center & Mercy Gilbert Medical Center. She is board certificated in cardiovascular disease, internal medicine, echocardiography and nuclear cardiology and is a registered physician in vascular interpretation. Dr. Bond is a well-known spokesperson for the American Heart Association, Go Red for Women Campaign. Dr. Victoria Thomas Dr. Victoria Thomas @Drvic_thomas is a cardiology fell


    173. Case Report: A Block and a Leak Lead to Shock – Weill Cornell Jan 17, 2022
    Show notes

    CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Jaya Kanduri, Dr. Dan Lu, and Dr. Joe Wang from Weill Cornell Cardiology for Levain cookies in Central Park. The ECPR is provided by Dr. Harsimran Singh (Cardiology Program Director and Interventional Cardiologist with expertise in ACHD). Episode introduction by CardioNerds Clinical Trialist Dr. Jeremy Brooksbank. We discuss a case of a 24-year-old female with a history of unicuspid aortic valve with associated aortopathy status post mechanical aortic valve replacement and Bentall procedure at age 16 presents with acute onset substernal chest pain and shortness of breath. She was found to have mechanical aortic valve obstruction and severe aortic regurgitation resulting in cardiogenic shock. Unfortunately, the shock quickly progressed to refractory cardiac arrest requiring mechanical support with VA-ECMO before valve debridement was performed in the operating room. The differential for mechanical prosthetic valve stenosis includes pannus, thrombus, or vegetation. She was eventually found to have thrombus obstructing the outflow tract and holding the mechanical leaflets open leading to torrential regurgitation. She underwent successful surgical debridement. We discuss unicuspid aortic valve and associated aortopathy, surgical considerations regarding AVR, diagnosis and management of prosthetic valve dysfunction, approach to cardiogenic shock and considerations around activating and managing VA-ECMO. With this episode, the CardioNerds family warmly welcomes Weill Cornell Cardiology to the CardioNerds Healy Honor Roll. The CardioNerds Healy Honor Roll programs support and foster the the CardioNerds spirit and mission of democratizing cardiovascular education. Healy Honor Roll programs nominate fellows from their program who are highly motivated and are passionate about medical education. The Weill Cornell fellowship program director, Dr. Harsimran Singh has nominated Dr. Jaya Kanduri for this position. 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 Media ECGCXREchoRHC PSL AP3 Color LHC - LCA LHC - LCA RCA Aortogram TEE TEE 2 Episode Teaching Pearls - Mechanical Valve Thrombosis (1) Unicuspid aortic valves present with aortic stenosis earlier in life. There can be concurrent aortic regurgitation and, like bicuspid aortic valves, unicuspids can be associated with aortopathy as well as other congenital anomalies. (2) Prosthetic valve stenosis is assessed with different echocardiographic parameters than what we use for native valves. The differential for mechanical valve stenosis includes pannus, thrombus, or vegetation. Patient prosthesis mismatch may also lead to elevated gradients. (3) VA-ECMO provides robust flow in the setting of cardiogenic shock as well as gas exchange. While this flow may improve end-organ perfusion, it also increases left ventricular afterload, thereby potentially worsening LV ischemia and impeding LV recovery. Elevated afterload may also decrease innate contractility and prevent aortic valve leaflets from opening. Therefore, if a patient with a mechanical valve is on VA-ECMO, ensuring valve opening to prevent valve (or ventricular) thrombosis is paramount. (4) Venting is sometimes necessary to decrease the left ventricular end diastolic pressure from the high afterload imposed by VA-ECMO. A microaxial temporary LVAD (example – Impella device) directly unloads the left ventricle, but cannot be used in the setting of a mechanical aortic valve. TandemHeart is also a consideration (inflow cannula placed across the interatrial septum in the left atrium) to unload the LV, but does not improve flow across the aortic valve so can lead to thrombus if a mechanical valve is present. Intra-aortic balloon counterpulsation using an IABP can be used to decrease afterload on the native heart and increase coronary perfusion, but does not directly unload the left ventricle. (5) Acute mechanical valve thrombosis can be managed with emergency surgery or with low dose fibrinolytic therapy. Surgery is preferable when operative risk is low and if there are contraindications to fibrinolytic therapy such as prior intracranial hemorrhage or active bleeding. (6) VA-ECMO can be weaned by slowly decreasing flow rates and assessing native cardiac function, hemodynamic response, and end-organ perfusion with assessments including echocardiography and pulmonary artery catheterization. Notes - Mechanical Valve Thrombosis 1. What is a unicuspid aortic valve? Unicuspid aortic valves (UAVs) are rare with an incidence of only 0.02%.There are two types of UAVs. Acommisural UAVs have a single cusp with a stenotic central orifice and rudimentary commissures that do not divide the valve (pin-hole shaped), and are usually complicated by severe stenosis in early childhood. Unicommisural UAVs are composed of a single cusp with a single commissural attachment to the aortic wall and an elongated orifice (slit-like orifice), which has a less aggressive course and is generally discovered in adulthood.Aortic stenosis is almost universal among UAVs, present with or without aortic regurgitation in 92% of cases. Some series have shown 14% of cases with concurrent aortopathy.UAVs may be associated with congenital abnormalities likes anomalous coronaries, PDA, VSD and coarctation. 2. How do we assess for aortic prosthetic valve stenosis? Assessment for mechanical valve stenosis involves different echocardiographic parameters than when evaluating a native valve. Doppler velocity index (DVI) is the dimensionless index with LVOT VTI/AV VTI, with severe stenosis suggested by a ratio of 100msec (it takes longer to gush through a more stenotic valve). Effective orifice area (EOA) 0.8cm2), presence of LA thrombus or concomitant CAD in need of revascularization, presence of other valve disease, and presence of possible pannus (which would not respond to fibrinolysis). 6. What is the approach to weaning VA-ECMO? Assessment of echocardiographic features, hemodynamics, and end-organ perfusion is essential for a successful VA-ECMO wean. First a turndown of the circuit is performed where the ECMO flow is decreased in a protocolized fashion. This should reduce afterload and therefore increase LV contractile reserve, as well as increase preload with return of flow through the ventricles. With these changes, successful hemodynamic parameters to look for are stable cardiac index, central venous pressure, pulmonary arterial pressures, and systemic blood pressures. Successful echocardiographic parameters include an increase in LVEF >20-25%, aortic VTI ≥10 cm, lateral mitral annulus peak systolic velocity ≥6 cm/s,...


    172. CCC: The Hemodynamic Evaluation of Cardiogenic Shock with Dr. Nosheen Reza Jan 11, 2022
    Show notes

    The hemodynamic evaluation of cardiogenic shock obtained via a Swan-Ganz catheter plays an essential role in the characterization of cardiogenic shock patients. Join Dr. Nosheen Reza, (Assistant Professor of Medicine and Advanced Heart Failure and Transplant cardiologist at the Hospital of the University of Pennsylvania), episode fellow lead Dr. Brian McCauley (Interventional and Critical Care Fellow at the Hospital of the University of Pennsylvania), Dr. Mark Belkin (Cardiac Critical Care Series Co-Chair and AHFT fellow at University of Chicago), and CardioNerds Co-Founders, Amit Goyal and Dan Ambinder, for this tour through the heart aboard the Swan-Ganz catheter. In this episode, we evaluate three separate admissions for a single patient to highlight pearls regarding waveform assessment, evaluating cardiac output, phenotyping hemodynamic profiles, targeted therapies based on hemodynamics and so much more. Episode introduction and audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship). 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! Pearls and Quotes - Hemodynamic Evaluation of Cardiogenic Shock Swan-Ganz catheters are not dead #ReviveTheSwan! They remain a useful tool to characterize cardiac patients & to help direct therapy, especially in Cardiogenic Shock.When looking at Swan-Ganz catheter data, it is important to always interpret your own tracings, to know what values are acquired directly, and which values are derived.It is important to understand the strengths and weakness of hemodynamic characterization by Swan-Ganz cathetersAdvanced metrics such as cardiac power output, pulmonary artery pulsatility index, and aortic pulsatility index are extremely useful in further phenotyping patients as well as guiding mechanical support platforms“The data will be wrong if the preparation is not right” Show notes - Hemodynamic Evaluation of Cardiogenic Shock 1. Swan-Ganz catheters are a useful tool to characterize cardiac patients and to direct therapy. With the ESCAPE trial in 2004, Swan-Ganz catheter utilization dropped drastically outside transplant centers across the United States (2). While the ESCAPE trial did demonstrate the possibility of harm when using a Swan-Ganz catheter, many of the truly ill cardiac patients we care for would have been excluded from the trial. For instance, patients on dobutamine at doses above 3 µg/kg/min or any dose of milrinone during the hospitalization were excluded from the trial.This is a classic example of “throwing the baby out with the bath water.”In a recent large, multicenter cardiogenic shock registry, complete hemodynamic assessment using pulmonary artery catheters prior to MCS is associated with lower in-hospital mortality compared with incomplete or no assessment (3). 2. When looking at Swan-Ganz catheter data, it is important to always interpret your own tracings, to know what values are acquired directly, and which values are derived. Incomplete or incorrect data can lead to mischaracterization of our patients. Therefore, it is essential to review all of the tracings, calculations, and data acquired for each individual patient before any clinical adjustments are made (1). An incomplete pulmonary capillary wedge tracing is an example from clinical practice (causing the PCWP, and therefore the left-sided filling pressures to be overestimated). It is equally important to know the limitations of cardiac output equations, and that no one measurement is perfect.Foibles of the Fick equation include assumed rather than measured oxygen consumption and variations in hemoglobin concentration. Traditionally, thermodilution has been thought to be likely less accurate in presence of tricuspid regurgitation, which could lead to blending of the cold dilutant, but recent data suggests even in these circumstances it remains the preferred method for estimating cardiac output over indirect Fick. 3. What are some tips of measuring a PCWP correctly? To ensure that we get the wedge pressure correctly, we must first make sure we understand the wedge pressure in relation to the respiratory cycle. For the majority of patients, the end expiratory intrathoracic pressure will be close to 0, and it will have the least influence on our readings. Thus, for most patients, that is why we measure the wedge pressure at end expiration.However, in patients with severe lung disease or significant obesity, the intrathoracic pressure may not be close to 0 at end expiration or there may be wide swings in intrathoracic pressure. For these patients, it is a reminder to look at the tracings yourself, and we may need to average the PCWP over the respiratory cycle.When we are measuring the PCWP, we have to remember that we are using it as a surrogate of the LV end-diastolic pressure. The point of the cardiac cycle when the pressure in the pulmonary veins, left atrium and LV are closest to equal is end-diastole. Thus, we typically want to measure the PCWP in end-diastole, which would specifically be measuring the mean of the A-wave.Now, for patients with severe mitral regurgitation and/or significant atrial myopathy leading to large V-waves, the wedge pressure estimated at end-diastole will not necessarily reflect the mean wedge (averaged throughout the cardiac cycle) that the pulmonary circulation “sees” throughout the cardiac cycle. As has been a theme in this episode, we have to make sure our inputs are accurate to appropriately help our patients. In this circumstance of large V-waves, if we were calculating the pulmonary vascular resistance (Mean PA Pressure – PCWP / CO), but used the end-diastolic PCWP instead of the PCWP averaged through the cardiac cycle we may end up with an inaccurate estimation of PVR. 4.Advanced metrics such as cardiac power output, pulmonary artery pulsatility index, and aortic pulsatility index are extremely useful in further characterizing hemodynamics. Over the past several years individual indices of ventricular performance have been developed and studied, these include CPO, PAPi, API, and LVSWI (4,5,10-12). These values can further flesh out our hemodynamic profiles, and help guide decision-making for choosing the proper mechanical circulatory support platform (7,8,9).See the infographic developed by CardioNerds Academy Fellow Ahmed Ghoneem for more information on different thresholds for these parameters.The API is a novel hemodynamic parameter that was recently applied to ESCAPE trial patients by series Co-Chair, Mark Belkin. 5. “The data will be wrong if the preparation is not right.” Dr. Reza’s point on the episode is apt and high-yield.Incorrect data acquisition and/or interpretation will not benefit our patients. We need to know what values are measured directly (chamber pressures, SvO2) and which are derived (cardiac output/index, SVR/PVR, CPO/PAPi/API, and so forth). As cardiologists and intensivists, we need to be critical of the tracings themselves, avoid anchoring to a single value, and be observant of the overall hemodynamic trajectory our patient is taking. Only through thoughtful intervention in coordination with careful and consistent monitoring will we bring to bear the benefits bestowed by Swan-Ganz catheter supplemented-care (1). Schematics and Graphics - Hemodynamic Evaluation of Cardiogenic Shock RHC Tracings Discussed in the Episode References - Hemodynamic Evaluation of Cardiogenic Shock 1.Ragosta M. Textbook of Clinical Hemodynamics. Elsevier; 2017. 2.Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA. 2005;294(13):1625-33. https://jamanetwork.com/journals/jama/fullarticle/201634 3. Garan AR, Kanwar M, Thayer KL, et al. Complete hemodynamic profiling with pulmonary artery catheters in cardiogenic shock is associated with lower in-hospital mortality. JACC Heart Fail. 2020;8(11):903-913. https://pubmed.ncbi.nlm.nih.gov/33121702/ 4.Korabathina R., Heffernan K.S., Paruchuri V., Patel A.R., Mudd J.O., Prutkin J.M., et al: The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv 2012; 80: pp. 593-600. https://pubmed.ncbi.nlm.nih.gov/21954053/ 5.Fincke R, Hochman JS, Lowe AM, et al. Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. J Am Coll Cardiol. 2004;44(2):340-8. https://pubmed.ncbi.nlm.nih.gov/15261929/ 6.Kochav SM, Flores RJ, Truby LK, Topkara VK. Prognostic impact of pulmonary artery pulsatility index (Papi) in patients with advanced heart failure: insights from the escape trial. J Card Fail. 2018;24(7):453-459. https://pubmed.ncbi.nlm.nih.gov/29597051/ 7.Feldman D, Naidu SS. Percutaneous Mechanical Circulatory Support Devices. Cardiac Interventions Today. 2016; 10 (1): 26-33. https://citoday.com/articles/2016-jan-feb/cover-stories 8.Briceno N, Kapur NK, Perera D. Percutaneous mechanical circulatory support: current concepts and future directions. Heart. 2016;102(18):1494-507. https://pubmed.ncbi.nlm.nih.gov/27503999/ 9.Baran DA, Grines CL, Bailey S, et al. Scai clinical expert consensus statement on the classification of cardiogenic shock: this document was endorsed by the american college of cardiology (Acc), the american heart association (Aha), the society of critical care medicine (Sccm), and the society of thoracic surgeons (Sts) in april 2019. Catheter Cardiovasc Interv. Published online May 19, 2019:ccd.28329. https://pubmed.ncbi....


    171. Narratives in Cardiology: Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia – Ohio Chapter Jan 07, 2022
    Show notes

    CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Zarina Sharalaya (Interventional Cardiology Fellow at the Cleveland Clinic), and Dr. Simrat Kaur (General Cardiology Fellow at the Cleveland Clinic) join Dr. Samir Kapadia, the Chair of the Robert and Suzanne Tomsich Department of Cardiovascular Medicine, Sydell and Arnold Miller Family Heart, Vascular & Thoracic Institute at Cleveland Clinic. They discuss future advancements in the field of structural interventional cardiology. Dr. Kapadia sheds light on his journey starting as an international medical graduate from India and speaks about his mentors that helped shape his career and his life. We later delve into several advancements in the field of structural and interventional cardiology, along with the amalgamation of different sub-specialities with intervention such as heart failure and critical care cardiology. We also discuss the measures being taken to reduce the occupational hazards associated with interventional cardiology and how to make this field more appealing to women in cardiology. Special message by Ohio ACC State Chapter Governor, Dr. Kanny Grewal. 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 • References • 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 on Innovation, Excellence and Leadership in Interventional Cardiology with by Dr. Gurleen Kaur https://twitter.com/gurleen_kaur96/status/1484205728663576590?s=21 Video version - Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia https://youtu.be/BfqnRkaVGkk Quotables - Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia “A very important thing for all international medical graduates and for everybody, for that matter - it is important to recognize that the opportunities are what you perceive and not what others perceive.”Dr. Samir Kapadia Show notes - Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia How do international medical graduates contribute to the work force in medicine across the United States of America? International medical graduates account for 25% of the physician work force, with over 85% being involved in direct patient care.IMGs are usually accomplished, consummate and highly motivated physicians who often have to overcome challenges such as language proficiency, acculturation and difficulties with obtaining a visa status in the United States.IMGs also help fill gaps in health care by working in geographical areas that are otherwise not desirable by US or Canadian medical graduates.IMGs contribute to diversity of the field which provides a richer training environment, improved access to health care for underrepresented minorities, as well as better patient outcomes. What are key qualities of a good mentor? A good mentor is responsible for enhancing the education of his or her mentees along with motivating them to challenge their limits.Qualities of a good mentor extend beyond mere mentorship to sponsorship, where the mentor opens up his or her network for the mentee allowing them to pursue a path of success.A mentor serves as an advisor and a counselor, helping his or her mentees navigate difficult paths teaching them to become resilient physicians.A mentor also serves as a confidante for the trainee with whom mentees can share their dreams, aspirations and vulnerabilities knowing not only will this be kept in confidence but will also provide a catalyst for their growth. What are the recent advancements in minimizing radiation exposures for structural cardiologists? 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.When dealing with possible occupational radiation exposure, we should strive for the ALARA (as low as reasonably achievable) principle of radioprotection.The RADPAD (RADPAD 5100A-O; Worldwide Innovations & Technologies, Inc, Lenexa, KS) is a new development that is a lead field shield that is placed between the patient and the operator to reduce scatter radiation and significantly reduce operator radiation exposure.The use of Zero gravity lead is a novel suspension shield which has also been shown to significantly reduce the operator radiation exposure and potentially decrease orthopedic injuries particularly spinal injuries secondary to the protective lead garments. What are the future directions for structural interventions and how is the field of structural cardiology going to evolve in the next few years? The future of structural cardiology provides great promise. After the success of transcatheter aortic valve replacement (TAVR) and transcatheter mitral valve edge to edge repair (TEER), there has been increasing development in tricuspid interventions as well as interventions for severe mitral stenosis due to mitral annular calcification.The amalgamation of structural interventional cardiology and heart failure as well as with critical care are also exciting fields that is still developing. Advancements in left ventricular restoration devices such as the Revivant TC system may help several patients with end stage congestive heart failure due to ischemic heart disease. References Steward DE. The internal medicine workforce, international medical graduates, and medical school departments of medicine. Am J Med 2003;115(1):80–4. Doi: 10.1016/s0002-9343(03)00307-3.Kostis JB., Ahmad B. International medical graduates and the cardiology workforce. J Am Coll Cardiol 2004;44(6):1172–4. Doi: 10.1016/j.jacc.2004.05.081.Al Hussein Al Awamlh B. Alien J-1 Physicians in a Pandemic. JAMA Intern Med 2021;181(6):743–4. Doi: 10.1001/jamainternmed.2021.0730.David YN., Issaka RB. Advancing diversity: the role of international medical graduates. Lancet Gastroenterol Hepatol 2021;6(12):980–1. Doi: 10.1016/S2468-1253(21)00376-9.Shikhar A. Mentorship During Fellowship. J Am Coll Cardiol 2014;64(15):1637–8. Doi: 10.1016/j.jacc.2014.08.017.Tobin MJ. Mentoring: seven roles and some specifics. Am J Respir Crit Care Med 2004;170(2):114–7. Doi: 10.1164/rccm.2405004.Picano E., Vano E. The Radiation Issue in Cardiology: the time for action is now. Cardiovasc Ultrasound 2011;9(1):35. Doi: 10.1186/1476-7120-9-35.Vlastra W., Delewi R., Sjauw KD., et al. Efficacy of the RADPAD Protection Drape in Reducing Operators’ Radiation Exposure in the Catheterization Laboratory: A Sham-Controlled Randomized Trial. Circ Cardiovasc Interv 2017;10(11). Doi: 10.1161/CIRCINTERVENTIONS.117.006058.Zanca F., Dabin J., Collard C., et al. Evaluation of a suspended radiation protection system to reduce operator exposure in cardiology interventional procedures. Catheter Cardiovasc Interv Off J Soc Card Angiogr Interv 2021;98(5):E687–94. Doi: 10.1002/ccd.29894.GP., Y.S. C. Continuing Advances and Challenges of Structural Heart Imaging. JACC Cardiovasc Imaging 2021;14(1):128–30. Doi: 10.1016/j.jcmg.2020.12.002.Klein P., Anker SD., Wechsler A., et al. Less invasive ventricular reconstruction for ischaemic heart failure. Eur J Heart Fail 2019;21(12):1638–50. Doi: 10.1002/ejhf.1669. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD


    170. ACHD: Transposition of the Great Arteries with Dr. Maan Jokhadar Jan 03, 2022
    Show notes

    In this episode, CardioNerds (Amit Goyal), ACHD series co-chair, Dr. Josh Saef (ACHD fellow at University of Pennsylvania) and episode lead fellow, Dr. Brynn Connor (Pediatric Cardiology fellow at Lucile Packard Children's Hospital at Stanford) are joined by Dr. Maan Jokhadar (Advanced heart failure and adult congenital heart disease specialist at Emory University) to discuss transposition of the great arteries. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. For a brief review of the basic anatomy and physiology of D-TGA, check-out this great video by Dr. Maan Jokhadar! 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! https://www.youtube.com/watch?v=Ifu8nVtXT_c Pearls (1) In D-TGA following an atrial switch operation, the right ventricle IS the systemic ventricle! (2) Evaluation of systemic right ventricular function often requires use of both transthoracic echocardiography and cardiac MRI. (3) Use of medical heart failure therapies should be individualized, without any proven long-term mortality benefit and potential unique complications in this patient population (i.e. SA node dysfunction). Show notes D-transposition of the great arteries (D-TGA) is one of the most common forms of cyanotic congenital heart disease presenting in the newborn period. Anatomically, d-transposition of the great arteries is characterized by atrioventricular concordance and ventriculoarterial discordance, such that the aorta arises from the morphologic right ventricle and pulmonary artery arises from the morphologic left ventricle. The resultant physiology is that of a parallel circulation, with deoxygenated blood recirculating in the systemic circulation (via the RA-RV) and oxygenated blood recirculating in the pulmonary circulation (via the LA-LV). At birth, this invariably results in cyanosis, with survival dependent upon adequate mixing of the two circulations via an atrial or ventricular level defect. Prior to surgical advances in the late 1950s, this lesion was uniformly fatal, with most infants dying before their first birthday. The subsequent development of the Senning and Mustard atrial-level repairs led to good immediate outcomes and improved long-term survival. However, following these “physiologic” types of repair, patients are far from cured, with several long-term established complications, including (1) dysfunction of the systemic right ventricle, (2) tricuspid regurgitation (the systemic atrioventricular valve), (3) atrial and ventricular arrhythmias, and (4) systemic and pulmonary venous baffles leaks and obstruction. These complications ultimately lead to substantial morbidity and premature mortality, with ACHD providers facing unique challenges in the medical and surgical management of this heterogenous patient population. 1. What are the basic anatomic features of d-transposition of the great arteries (d-TGA)? D-transposition of the great arteries is defined by the origin of the arterial trunks from the morphologically inappropriate ventricle, specifically with the aorta arising from the morphologic right ventricle (now the systemic ventricle) and the pulmonary trunk arising from the morphologic left ventricle.This is termed “ventriculoarterial discordance”, and importantly, does not define the spatial relationship of the great arteries. Rather, the “d” terminology refers to the looping of the ventricles and distinguishes d-TGA from l-TGA (or congenitally corrected transposition), where there is additional atrioventricular discordance. The resultant physiology is that of a parallel circulation, with deoxygenated blood recirculating in the systemic circulation and oxygenated blood recirculating in the pulmonary circulation. At birth, this invariably results in cyanosis, with survival dependent upon adequate mixing of the two circulations via an atrial or ventricular level defect.There are three major anatomic variations in dTGA, including dTGA with an intact ventricular septum (most common), dTGA with a ventricular septal defect, and dTGA with LVOT obstruction. These anatomic subtypes can lead to variable presentations in the neonatal period, as well as pose unique challenges to surgical repair, and are therefore important diagnostic considerations.The arrangement of the coronary arteries and their spatial course can additionally be highly variable, posing added complications when performing the arterial switch operation (which requires reimplantation of the coronary arteries into the neo-aortic root). The most common, “usual,” arrangement is the left coronary artery originating off the anterior facing sinus, and the right coronary artery originating off the posterior facing sinus. 2. What surgical approaches have been utilized in the management of D-TGA?What are the key features of aortic coarctation anatomy? Prior to surgical advances in the late 1950s, this lesion was uniformly fatal, with most infants dying before the age of 1 year.Infants were initially palliated with an atrial septostomy, which allowed for mixing at the atrial level and improved survival in the immediate newborn period. However, these infants were still left with profound cyanosis, with inevitable mortality in the first year of life.In the mid-1950s, the Senning (1958) and Mustard (1964) atrial-level repairs were first performed, with good short-term outcomes and improved long-term survival.In the Senning procedure, a baffle is created within the atria that redirects the deoxygenated caval blood to the mitral valve and the oxygenated pulmonary venous blood to the tricuspid valve with use of native atrial tissue.Mustard subsequently described a simpler technique with creation of an atrial baffle using synthetic patch material. By the late 1980s, late complications of these repairs became well recognized, with the ultimate adoption of the neonatal arterial switch operation, which remains the gold standard for surgical management of transposition. 3. What are the long-term complications of the Mustard and Senning procedures? Systemic Right Ventricular Dysfunction:Clinical Features - Systemic RV dysfunction is an evitable consequence of the atrial switch operation, with 50% of patients developing right ventricular systolic dysfunction by 30 years of age.While right ventricular dysfunction is often mild and clinically asymptomatic for several years, patients ultimately develop related symptomatology over the subsequent 10-20 years.Most commonly, patients present to care with diminished exercise tolerance, with symptomatic arrhythmias being an additional common reason for patients to seek care. DiagnosisAccurate assessment of RV size and function in this population is critical for adequate surveillance and management planning. However, quantitative right ventricular assessment remains challenging, with no model for comparison and no clear criteria for abnormalities.Volumetric assessments are the gold standard, although made difficult by the complex geometry of the right ventricle.Cardiac MRI is most commonly utilized to assess RV size and systolic function, and additionally permits simultaneous evaluation of the systemic and pulmonary venous baffles and quantitative assessment of the degree of tricuspid regurgitation (the systemic AV valve).Transthoracic echocardiography is still routinely employed for serial evaluation of systemic right ventricular function. However, providers should have a low threshold to obtain further advanced imaging with any significant change in symptomatology or qualitative decrement in right ventricular systolic function on serial echocardiographic assessment.ManagementMedical Therapy: In contrast to ischemic cardiomyopathy, there are no long-term, randomized, placebo-controlled drug trials evaluating the efficacy of ACEI/ARB/ARNI or beta-blockers on systemic RV function. Small studies performed to date have not shown any appreciable benefit of ACEI/ARB on improving right ventricular ejection fraction or exercise capacity, which may reflect minimal baseline activation of the renin-angiotensin-aldosterone system in this form of heart failure. Use of beta-blocker therapy pathophysiologically makes sense, specifically reducing myocardial oxygen demand and allowing for improved ventricular filling; however, prior studies have produced mixed results, with evidence of improved right ventricular remodelingalthough no appreciable improvement in right ventricular ejection fraction, functional class, or long-term survival. Use of beta-blockers should also be cautioned in patients with established SA node dysfunction.Left Ventricular Re-Training: Conversion to an arterial switch operation often requires a staged approach to ensure that the left ventricle is adequately “trained” to handle systemic pressures. The left ventricle becomes rapidly deconditioned with time when continually exposed to the low-resistant pulmonary c


    169. Case Report: Chest pain in a Young Man – “A Gray (Gy) Area” – UC San Diego Dec 26, 2021
    Show notes

    CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Patrick Azcarate and Dr. Antoinette Birs from the University of California San Diego along with a guest host Dr. Christine Shen from Scripps Health for a hike along Torrey Pines. They discuss a case of a 30-year-old man with a history of malignant thymoma status post two partial lung resections and radiation for pleural/pulmonary metastasis, as well as a history of myasthenia gravis on rituximab, and Ig deficiency on IVIG presents with progressive exertional chest pain. We focus on the differential diagnosis of patients with a history of chest radiation exposure and dive into the complex management and surveillance for patients with radiation associated cardiac disease (RACD). The E-CPR is provided by Dr. Milind Desai (multimodality cardiovascular imaging expert, Director of Clinical Operations, Director of Center for HCM, Medical Director for Center for Aortic Diseases, and Medical Director for Center for Radiation Heart Disease at the Cleveland Clinic). 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 Media TTE TTE TTE TTE AP Cranial Pre PCI LAO Caudal Pre PCI RAO Caudal Pre PCI RAO Cranial Pre PCI AP cranial Post PCI Episode Teaching Pearls - radiation associated cardiac disease Radiation-associated cardiac disease (RACD) is a heterogeneous disease that can manifest several years, or decades following radiation exposure to the chest and is associated with high morbidity and mortality. Given the non-specific or vague symptoms, one of the greatest challenges for this patient population may be diagnosing RACD which requires high clinical suspicion. In patients with a history of chest radiation, we should remember to ask three important questions: 1. What was the total dose of radiation given? 2. How long ago was radiation therapy administered? 3. Was the heart exposed?A cumulative dose of >30 Gray (Gy) chest radiation significantly increases the risk of RACD long-term, but cardiac damage can occur at even lower doses. Effects from chest radiation can take years to become clinically detectable. Screening for radiation induced coronary artery disease with stress testing should start 5 years following XRT and in low-risk patients (without risk factors for typical coronary artery disease) and continue at 5-year intervals, and 2-year intervals in high-risk patients. Valvular heart disease surveillance should begin 10 years post XRT and can be accomplished with echocardiogram. Regarding revascularization planning, a Heart Team approach is recommended. However, percutaneous intervention is preferred over bypass surgery in most cases. Notes - radiation associated cardiac disease 1. What is Radiation-Associated Cardiac disease (RACD)? A spectrum of disease that can affect any part of the heart and typically develops anywhere from 5 to 20 years after radiation. It may present with non-specific or vague symptoms. Manifestations include myocarditis, pericarditis (typically early in the course) and well as long term sequela such as myocardial fibrosis, valvular heart disease (regurgitation or stenosis), pericardial disease, vasculopathy (CAD), conduction system disease. Radiation may impact any tissue of the heart: Vascular: microvascular, coronary artery disease, macrovascular (ascending aorta) Valvular: has a longer latency ~10-20 years with the left sided valves being more commonly affected; Aorto-mitral curtain thickening/calcification is a hallmark of previous heart radiation and associated with higher mortality Conduction: Sick sinus syndrome, AV nodal block, atrial fibrillaiton; infra-nodal conduction disease and RBBB are common. Myocardial: fibrosis in the myocardium leading to HFpEF, or HFrEF; XRT + anthracycline is thought to be synergistic. Pericardial: chronic pericardial inflammation, scarring, calcification, restrictive physiology. Constrictive pericarditis from radiation has a particularly poor prognosis given often concurrent myocardial involvement. 2. What is the Pathophysiology of RACD? The severity of disease is related to total radiation dose, fraction size and volume of the heart in the radiotherapy field. The resulting cell damage leads to activation of the acute inflammatory cascade and pro-fibrotic milieu. 3. What are the additional risk factors for RACD? Therapy-related risk factors:Net dosage (dependent on cancer type and tumor site) > 30Gy received by the heart.Proximity to heart to the radiation field.Concomitant chemotherapy – anthracyclines may particularly have a radiation sensitizing effect, thereby increasing the risk of RACD.Patient-related risk factors:Life expectancy – younger age at the time of radiation and a good cancer prognosis, as these patients may have more time to manifest the longer-term sequelae of RACD.Presence of traditional cardiovascular risk factors 4. How common is RACD? RACD is most often seen in those receiving chest radiation for breast cancer (particularly left sided), Hodgkin Lymphoma, lung cancer and esophageal cancers.There is a distinct population presenting with latent symptoms from treatment with wide-field radiation of Hodgkin lymphoma that was more commonly practiced 20-40 years ago.Prevalence of radiation associated cardiomyopathy is ~10% based on population studies although difficult to determine given the heterogeneity of presentation and under-recognition. Valvular abnormalities in 7-39% at 10 years, 12-60% at 20 years Mitral and aortic valves are most affected; symptoms arise 1-2 decades after radiation and later than CAD; AR in 60% vs 4% at 20 years vs 10 years post treatment. Aorto-mitral curtain thickening/calcification is a hallmark of previous heart irradiation, and its extent is strongly associated with mortality in subjects undergoing cardiac surgery. Radiation induced coronary vasculopathy has a prevalence of 85%. 5. What is Radiation induced coronary artery disease (RICAD)? Pathophysiology: inflammatory plaque, with accumulation of myofibroblasts, resulting in intimal proliferation with aggregation of lipid-rich macrophages; high collagen and fibrin content like accelerated atherosclerosis; doses of > 0.50 Gy can initiate atherosclerosis and affects micro and macro vasculature.Angiographically: Ostial or proximal epicardial coronary lesions of the anterior and central vessels are most common (left main trunk, proximal LAD, mid diagonal, or RCA) given the location of the heart in the chest.Lesions are often severe, proximal, and diffuse. They are typically long, smooth, concentric, and tubular and may require intravascular ultrasound (IVUS) for diagnosis as they can appear normal on coronary angiography (lumenography). 6. What are different types of radiation? 3D vs Intensity modulated radiation therapy (IMRT): both are x-ray-based radiationProton therapy: Unlike x-rays which go all the way through the body, protons are charged and can go to a specified depth causing less scatter radiation 7. What techniques may be used to reduce cardiac exposure to the radiotherapy field? ABC device, breathing techniques such as deep inspiratory breath hold (DIBH) which pulls the heart more inferiorly in the chest and allows treatment of the upper mediastinum with less cardiac exposure, shielding 8. What are the surveillance recommendations? The risk of RACD is 7.5% per Grey Unit (Gy) and is constant, beginning several years after exposure and persists for at least 2-3 decades (>50% of excess ischemic events occurring >10 years after RT). Those who will receive >30 Gy may warrant cardiology consultation prior to treatmentScreening for CAD: 5 years after radiation exposureScreening for valvular disease: 10 years after exposure with 5-year surveillance intervals 9. What is the recommended approach for revascularization for RICAD? PCI is generally preferred if feasible over bypass given chest radiation as this patient group has increased risk of complications from bypass surgery related to severely calcified aorta, possible radiation injury to the IMAs, restrictive lung disease, difficulty weaning patient from a ventilator, and lack of intra-thoracic lymphatics References Desai MY, Jellis CL, Kotecha R, Johnston DR, Griffin BP. Radiation-Associated Cardiac Disease: A Practical Approach to Diagnosis and Management. JACC Cardiovasc Imaging. 2018 Aug;11(8):1132-1149. doi: 10.1016/j.jcmg.2018.04.028. PMID: 30092970. https://www.jacc.org/doi/abs/10.1016/j.jcmg.2018.04.028 Desai MY, Windecker S, Lancellotti P, Bax JJ, Griffin BP, Cahlon O, Johnston DR. Prevention, Diagnosis, and Management of Radiation-Associated Cardiac Disease: JACC Scientific Expert Panel. J Am Coll Cardiol. 2019 Aug 20;74(7):905-927. doi: 10.1016/j.jacc.2019.07.006. https://www.jacc.org/doi/full/10.1016/j.jacc.2019.07.006 Cuomo JR, Javaheri SP, Sharma GK, Kapoor D, Berman AE, Weintraub NL. How to prevent and manage radiation-induced coronary artery disease. Heart. 2018 Oct;104(20):1647-1653. doi: 10.1136/heartjnl-2017-312123. Epub 2018 May 15. PMID: 29764968; PMCID: PMC6381836. https://heart.bmj.com/content/104/20/1647.long Wu W., Masri A., Popovic Z.B.et al. : "Long-term survival of patients with radiation heart disease undergoing cardiac surgery: a cohort study". Circulation 2013; 127: 1476. https://www.ahajournals.org/doi/epub/10.1161/CIRCULATIONAHA.113.001435 CardioNerds Case Report Production Team Karan Desai, MDAmit Goyal, MDDaniel Ambinder, MD


    168. CCC: Cardiogenic Shock – Initial Assessment and The Shock Team Call with Dr. Anu Lala Dec 21, 2021
    Show notes

    Cardiogenic shock is a state of cardiac dysfunction leading to hemodynamic instability and end-organ hypoperfusion. At the bedside, clinicians take various data points – from history to physical exam to labs/imaging and invasive hemodynamics – to make an assessment of the etiology, severity and management of cardiogenic shock. Health systems have developed “Shock Teams” to collectively interpret this data to deliver the optimal care for each patient. In this episode, Dr. Mark Dela Cruz (Advanced Heart Failure and Transplant Fellow at University of Chicago), CardioNerds Critical Care Series Co-Chairs Dr. Mark Belkin (Advanced Heart Failure and Transplant Fellow at University of Chicago) and Dr. Karan Desai (General Cardiology Fellow at University of Maryland), and CardioNerds Co-Founder Dr. Daniel Ambinder (Structural Fellow at Johns Hopkins Hospital) join Dr. Anu Lala (Director of the AHFT Fellowship, Associate Professor of Medicine and Cardiology at Mount Sinai Hospital and Deputy Editor of the Journal of Cardiac Failure) on a Shock Team Call! Dr. Lala leads us in a discussion of the systematic bedside evaluation of cardiogenic shock, from understanding a patient’s physiology and their humanity, to manage their illness and make a rapid but thorough evaluation when on the Shock Call. Audio editing and episode introduction by CardioNerds Academy Intern, Hirsh Elhence. 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! Pearls and Quotes - Shock Team Call The classic definition of cardiogenic shock was derived from studies of left ventricular dysfunction in the setting of acute myocardial infarction. With the advent of early primary percutaneous coronary intervention (PCI) and trends in cardiovascular disease risk factors, the prevalence of non-ischemic etiologies of cardiogenic shock (e.g., progression/exacerbation of chronic heart failure) has increased significantly. The diagnosis of cardiogenic shock should be made by integrating key clinical features such as physical exam findings and objective laboratory and imaging data in an iterative fashion. Focused transthoracic echocardiography and invasive hemodynamics are helpful in further characterizing the type of shock and the etiology of cardiogenic shock. Early evaluation of right ventricular function is an important aspect of cardiogenic shock evaluation. Significant RV dysfunction portends poor prognosis, can necessitate more aggressive interventions, and defines the types of mechanical circulatory support necessary. Classification systems for cardiogenic shock help to further characterize a patient’s illness severity. The INTERMACS and SCAI classification systems are particularly designed to allow for early identification of patients who would most benefit from more advanced interventions such as vasoactive medications or mechanical circulatory support. Shock Team Calls improve mortality for patients in cardiogenic shock. By rapidly bringing together heart failure specialists, interventional cardiologists, cardiothoracic surgeons, and critical care physicians, appropriate interventions and contingencies can be discussed and quickly implemented without adding delays to patient care. Importantly, these calls should attempt to integrate patient goals of care in order to best serve our patients. Show notes - Shock Team Call 1. What is the classic definition of cardiogenic shock? The classic definition of cardiogenic shock was initially derived from the Shock Trial published in 1999 (1). In this trial, cardiogenic shock was defined as shock due to left ventricular dysfunction occurring in the setting of acute myocardial infarction in the setting of acute MI as confirmed by specific criteria: Clinical criteria: SBP 90mmHgEnd-organ hypoperfusion as defined by cool extremities, UOP 60bpmHemodynamic criteria: CI ≤ 2.2 L/min/m2 BSAPCWP ≥ 15mmHgWith the advent of primary percutaneous coronary intervention, non-ischemic etiologies have become more prevalent as the etiology of cardiogenic shock such as decompensation of chronic heart failure, valvular heart disease, etc.As discussed on the episode, cardiogenic shock occurs on a spectrum from a “pre-shock” state to “extremis.” To facilitate early recognition of cardiogenic shock, appropriate phenotyping (e.g., LV-predominant, RV-predominant, biventricular, pericardial, valvular, pulmonary vascular, etc), timely interventions, and allocation of advanced therapies (e.g., mechanical circulatory support), a more granular approach to the classification is needed (see below regarding SCAI classification). 2. What are some of the clinical features of cardiogenic shock? Physical Exam Findings - A careful head-to-toe assessment should be conducted during the initial patient encounter. Important markers include (but are not limited to):Signs of hypervolemiaPatient positioning as a sign of orthopneaElevated JVPTachypneaPresence of pulmonary ralesLower extremity edemaHepatomegalyAscitesSigns of poor organ perfusionCool extremitiesPoor hourly urine output.Confusion or Altered Mental StatusSigns of poor cardiac outputPulse quality – is it fast, slow, thready?Pulsus alternans – alternation between strong and weak beats in sinus rhythm without change in cadence or cycle length (a marker of low output and ejection from the LV) (2).Narrow pulse pressureClues to help determine the etiology of the shockPoint of maximal impulse displacementRight ventricular heaveAuscultation of murmurs may indicate a valvular and/or congenital anomaliesAn accentuated P2 may indicate pulmonary hypertensionGallops may indicate filling pressures and/or underlying cardiomyopathyA pericardial knock may indicate constrictive pericarditisAn irregular pulse may indicate an arrhythmia causing or contributing to shockLaboratory studiesLaboratory markers of end organ hypoperfusion include markers of renal function such as creatinine and of hepatic injury (AST, ALT) and function (INR).Lactate has also been shown to display prognostic significance though clear correlations between objective thresholds to clinical outcomes have yet to be fully established.More important than individual values themselves are their temporal trends and the integration of multiple data points across numerous variables. Early Imaging studies EKG should be obtained and reviewed early after presentation to evaluate for acute coronary syndrome and need for urgent coronary angiography.Chest x-ray findings of pulmonary edema or effusions, assessment of heart size, and presence of cardiovascular hardware (sternal wires, implantable electrical devices, valvular interventions, etc). Focused transthoracic echocardiography, if available in the acute setting, can be helpful.Focused TTE should assess left and right ventricular morphology and function, the presence of a left ventricular thrombus, stenotic or regurgitant valvular lesions, or dynamic outflow tract obstructions.Echo surrogates of filling pressures may be supportive though may be limited by technique and image quality. Evaluation of RV function and illness severitySignificant RV dysfunction is a marker of illness severity and leads to worse clinical outcomes.RV dysfunction limits total cardiac output, worsens systemic venous congestion, and worsens end organ dysfunction.RV assessment is critical when evaluating for the need for mechanical circulatory support, and severe RV dysfunction may increase the likelihood that MCS will be necessary.Severe RV dysfunction may necessitate the use of specific MCS devices (e.g., RV assist devices). It may also impact decision-making regarding what types of temporary or, even more importantly, durable MCS devices the patient may qualify for. Enjoy the upcoming RV-Predominant Shock Episode with Dr. Ryan Tedford for a more in-depth discussion!Invasive hemodynamic assessment Invasive hemodynamic evaluation with a pulmonary arterial catheter (PAC) is particularly useful for confirming and profiling cardiogenic shock as well as tailoring initial and subsequent management.An accurate assessment of filling pressures, cardiac output (by Thermodilution or Indirect Fick), right ventricular function, systemic vascular resistance, and specific calculated indices (e.g., CPO, PAPi, RA/PCWP) provide a more nuanced evaluation of a patient’s shock.Specifically, a PAC can assist in early identification of an under-recognized form of cardiogenic shock, under the classic Stevenson paradigm, a “wet and warm” picture. These patients have a systemic inflammatory response in addition to or as a result of their cardiac pathology, with a reduced cardiac index, low to normal SVR, and elevated pulmonary capillary pressures.Enjoy the upcoming Invasive Hemodynamics episode with Dr. Nosheen Reza and the following infographic from CardioNerds Academy Fellow, Dr. Ahmed Ghoneem, for more details! 3. How is cardiogenic shock classified and how are these classifications useful in the management of cardiogenic shock? Differentiating cardiogenic shock from other types of shock and the severity of shock can often be challenging. Constructs such as Dr. Lynne Warner Stevenson’s physical exam-based shock classifications are helpful in broadly phenotyping cardiogenic shock at the bedside (3). However, these classification systems may have their limitations. Determining the underlying etiology relies heavily on integrating various pieces of clinical information ranging from the physical exam as well as laboratory and imaging information. In clinical practice,...


    167. Cardio-Obstetrics: Cardiac Interventions During Pregnancy with Dr. Michael Luna Dec 16, 2021
    Show notes

    In this episode, CardioNerds (Amit Goyal), Cardio-OB series co-chair and UT Southwestern cardiology fellow, Dr. Sonia Shah, and episode lead fellow, Dr. Laurie Femnou (UT Southwestern) are joined by Dr. Michael Luna (UT Southwestern) to discuss cardiovascular interventions during pregnancy. We discuss practical considerations for performing coronary angiography and valvular interventions in the pregnant patient, the timing and indication of procedures, and ways to minimize radiation exposure to both mom and baby. Audio editing by CardioNerds Academy Intern, Hirsh Elhence. This episode is made possible with support from Panacea Financial. Panacea Financial is a national digital bank built for doctors by doctors. Visit panaceafinancial.com today to open your free account and join the growing community of physicians nationwide who expect more from their bank. Panacea Financial is a division of Primis, member FDIC. Pearls • 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- Cardiac Interventions during Pregnancy Attempt should be made to manage pregnant patients with valvular disease with medical therapy, and cardiac interventions during pregnancy should be considered a last resort.Ideally, procedures in the gravid patient should be performed after 20 weeks gestation to minimize fetal risk. Specific ways to minimize radiation to the pregnant patient and fetus in the catheterization lab include: using an abdominal shield, radial access for coronary procedures, proper positioning of the C-arm to avoid extreme angulation, using collimation, and minimizing fluoroscopic time, frame rate, and use of cine-acquisition. When appropriate, intracoronary imaging modalities (ie. IVUS or OCT) should also be considered.Fetal monitoring should be performed during any cardiac intervention in the pregnant patientMultidisciplinary involvement and contingency planning are critical for the success of any high-risk cardiac intervention in the pregnant patient. Quatables - Cardiac Interventions during Pregnancy “Meetings including all providers— our cardiac surgical colleagues, cardiac anesthesiologists, and our obstetrics team—in the care of [pregnant] patients has to be had well ahead of a cardiac procedure to plan every detail.” Show notes - Cardiac Interventions during Pregnancy 1. What are special considerations for performing a balloon valvuloplasty in a pregnant patient with mitral stenosis? In pregnant patients with severe mitral stenosis who cannot be adequately managed with medical therapy, percutaneous balloon mitral valvuloplasty (PMBV) is the treatment of choice given the high risk of morbidity and fetal loss with cardiac surgery.Ideally, procedures in the gravid patient should be performed after 20 weeks gestation to minimize risk to the fetus. Assessment of valve anatomy and consideration of the Wilkin’s score are especially important in pregnant patients to minimize the risk of peri-procedural complications.PBMV should performed at experienced centers with cardiac surgery and MFM available.Complications of PBMV are rare but include atrial perforation, cardiac tamponade, arrhythmias, emboli, mitral regurgitation, hypotension and maternal death. Mechanical support should be readily available and a delivery strategy in place in case there is sudden maternal or fetal deterioration. 2. What are ways to minimize radiation exposure in the catheterization lab to the pregnant patient and fetus? The general principle for imaging during pregnancy is similar to imaging for the general population, with the goal of radiation exposure being as low as reasonably achievable (ALARA). The mean radiation exposure to the unshielded abdomen is 1.5 mGy, and


    166. CardioNerds Rounds: Challenging Cases of Hypertrophic Cardiomyopathy with Dr. Michelle Kittleson Dec 09, 2021
    Show notes

    CardioNerds Rounds Co-Chair, Dr. Karan Desai, joins Dr. Michelle Kittleson (Director of Postgraduate Education in Heart Failure and Transplantation, Director of Heart Failure Research, and Professor of Medicine at the Smidt Heart Institute at Cedars-Sinai) to discuss challenging cases of hypertrophic cardiomyopathy. As a guideline author on the 2020 ACC/AHA Hypertrophic Cardiomyopathy Guidelines, Dr. Kittleson shows us how the latest evidence informs our management of HCM patients, while sharing many #Kittlesonrules and pearls on clinical 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 - Hypertrophic Cardiomyopaty Cases Case #1 Synopsis: Two non-white brothers in their early 20s come to clinic to establish care. They have no cardiopulmonary symptoms, normal EKGs and normal echos, but there was a possible family history of HCM. Their mother had LV hypertrophy and underwent septal myectomy, but she could not afford genetic testing and was no longer in the patients’ lives. The path report suggested “myocyte hypertrophy without disarray or bundles of myocytes.” How would you advise these patients regarding screening and surveillance? Listen to #CardsRounds for the full details! Quotes from Case #1: “Let’s take a walk down memory lane and let’s get to our evolution of understanding hypertrophic cardiomyopathy… [our understanding] follows the parable of the six blind men and the elephant. Each of the six blind man approached it from different angles, its tusk, its ear, its tail, and they all try to convince each other what an elephant is … because none of them can see the big picture.” Dr. Kittleson on the history of HCM and coming to a unifying diagnosis “The next time you are sitting there mashing your teeth because you have to memorize what the HCM murmur does squat to stand, Valsalva, or handgrip … remember you are standing on the shoulder of Giants. They [Drs. Braunwald and Morrow] pioneered surgical myectomy based on physical exam and cath lab findings” Dr. Kittleson on the physical exam guiding HCM management Takeaways from Case #1 Before we round, we think it is important to get on the same page regarding the nomenclature around HCM. Since the original characterization of hypertrophic cardiomyopathy (HCM) more than 60 years ago (see the Braunwald Chronicles for the origin stories!), different terms have been used to describe the disease. These include idiopathic hypertrophic subaortic stenosis, hypertrophic obstructive cardiomyopathy (HoCM), and “burnt out HCM” when heart failure develops.The 2020 guideline committee recommended a common language to avoid confusion: since left ventricular (LV) outflow tract obstruction (LVOTO) occurs in >60% of patients over time, but one-third remain non-obstructive, the recommendation is t0 call the disease state HCM with or without outflow tract obstruction.Dr. Kittleson added that when heart failure develops we should characterize the pathology as HCM with heart failure rather than “burnt out HCM.” Do we use HCM to describe any LV that has thick walls? Some clinicians will use HCM to describe all disease states that can lead to increased LV wall thickness, including those associated with systemic disorders such as RASopathies, mitochondrial myopathies, glycogen/lysosomal storage diseases, Fabry’s disease, hemochromatosis, Danon disease, and amyloidosis (especially in adults).However, the pathophysiologic mechanisms, genetic underpinnings, and treatment of these diseases are different. Secondary causes of left ventricular hypertrophy (LVH) – such as athlete’s heart and hypertensive disorders – can also cause confusion with identifying the correct terminology and diagnosis.As Dr. Kittleson (and the guidelines) made clear, the clinical definition of HCM is a disease state in which (1) the morphologic expression is restricted to the heart, characterized primarily by LVH in the absence of another systemic; (2) a metabolic or cardiac cause; (3) and for which a disease-causing sarcomere (or sarcomere-related) variant is identified or genetic etiology remains undetermined.See some of our original CardioNerds episodes to review the clinical manifestations, diagnosis and treatment of HCM! Ok. We are with you on the terminology! But as you mentioned there are many disease states that can look like HCM. What are phenocopies? As alluded to above, there are multiple genes that can lead to the phenotypic appearance of HCM, but rather these are “phenocopies” masquerading as HCM.Dr. Kittleson noted that many of these phenocopies are diagnosed in childhood (e.g., glycogen storage diseases, Friedrich ataxia, Danon disease); however, for adult cardiologists, particular attention should be given to recognizing amyloidosis (see our Amyloidosis page).We should remain alert for “LVH+” states: when we see left ventricular hypertrophy but also systemic signs including peripheral neuropathy, renal dysfunction, and skin changes, which could clue us into a systemic pathology like Amyloidosis. After all, Imitation is the sincerest form of flattery!The classic pathologic findings of HCM include myocyte disarray (where individual cardiomyocytes vary in size, shape and form), abnormal intercellular connections, expansion of the interstitial compartment and areas of replacement fibrosis, and small vessel disease (in which intramural vessels are narrowed by medial hypertrophy). So back to this case. It is possible the patients’ mother had a HCM phenocopy. And the pathology was not classic for HCM. What do the guidelines say regarding genetic screening in general? It was not until the 1990s when DNA sequencing of HCM pedigrees led to the discovery of variants in genes coding for sarcomere proteins were co-inherited in patients with LVH. Thus, HCM since has been regarded as a monogenic cardiac disease.The two most common genes with damaging variants are beta myosin heavy chain (MYH7) and myosin-binding protein C3 (MYBPC3).70% of variant-positive patients have gene variants in these genes; however, it is important to recognize that many patients with HCM are currently without any identifiable pathogenic genetic etiology to their disease (40 to 60% of patients depending on the study).Thus, genetic testing is crucial to the diagnosis and management of HCM, especially to inform cascade testing in family member and preconception and prenatal genetic counseling. As has been discussed previously on the CardioNerds podcast, appropriate pre- and post-test genetic counseling is necessary to ensure patients and their families understand the medical, social, psychological, ethical and professional implications of having a genetic disease, underscoring the value of multidisciplinary HCM centers. How do we apply the guidelines regarding genetic screening to our patients? As was done in this case, a detailed family history of at least three generations regarding HCM and SCD events should be taken. Typically, genetic testing for HCM is first done in the family member with clear phenotypic evidence of HCM – the index case. The 2020 ACC/AHA HCM guidelines nicely outline subsequent testing based on whether a variant is pathologic (Figure 1) Please remember to review the Guidelines yourself as it is a comprehensive text that provides key details not covered here!However, the index case could not afford genetic testing and the pathology available to us was not definitive for HCM. Postmortem testing for HCM-associated variants using blood or tissue samples collected at autopsy is possible, but access to a molecular autopsy and insurance coverage can vary significantly based on jurisdiction.Our patients (the brothers in their 20s) were arriving without genetics to inform their screening. In this circumstance we utilize Figure 2 (below) from the guidelines and would consider the index patient (the mother) phenotype negative. And since no variant was identified in the index patient, we would likely offer screening ECG/Echo (or cardiac MRI) to the brothers and follow up with clinical surveillance with imaging/ECG every 3-5 years. How do we decide if a variant is pathogenic? The pathogenicity of variants is based on American College of Medical Genetics and Genomics criteria and can actually change over time. As Dr. Kittleson noted, there are fewer quality genetic data in non-white HCM populations.The five highest frequency variants for HCM in the Human Gene Mutation Database of the NHLBI Exome sequencing Project were more frequent in Black Americans vs. White Americans which could lead to false positive diagnoses of HCM in Blacks. Furthermore, a lack of diverse racial/ethnic control populations could lead to a misclassification of benign variantsAs Dr. Kittleson noted on #CardsRounds, this again highlights the importance of multidisciplinary HCM clinics that have the expertise to periodically re-evaluate the pathogenicity of variants. If they a particular variant has been reclassified (either upgraded or downgraded), it would affect cascade testing and clinical surveillance in families. Case #2 Synopsis: ...


    165. Narratives in Cardiology: Diversity & Inclusion Via Allyship & Leadership with Dr. Bob Harrington – California Chapter Dec 02, 2021
    Show notes

    CardioNerds (Amit Goyal and Daniel Ambinder) join CardioNerds Ambassadors Dr. Pablo Sanchez (FIT, Stanford University) and Dr. Christine Shen (FIT, Scripps Clinic) for a discussion with Dr. Bob Harrington (Interventional Cardiologist, Professor of Medicine, and Chair of the Department of Medicine at Stanford University) about diversity and inclusion in the field of cardiology. This episode discusses Dr. Harrington’s broader approach to mentorship, sponsorship, and allyship; and particularly how (and why) he used his position as the president of the American Heart Association to advocate against all-male panels, or “manels.” Listen to the episode to learn the background and motivations behind his evidence-based efforts to make Cardiology a more inclusive field. Special message by California ACC State Chapter President, Dr. Jamal Rana. 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 • References • 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 - Diversity and Inclusion https://youtu.be/SnUadVRhH70 Quotables - Diversity and Inclusion “If senior men don’t change the field, it’s not going to change. We have the senior positions. We have to change it.”“You’re missing talent. You’re missing talent of the women who have decided not to go into Cardiology. I say to a lot of my male colleagues...don’t you care about the health of our specialty? Don’t you want the very best people going into it?”“How great is that--to open up an artery in the middle of the night?... What could be better than that?...Why would you not want to be a cardiologist? Frankly, maybe the field is not so friendly to women...And that bothers me greatly because I love the specialty.”“To those who have been given much, much is expected. That’s what people like me should do.”Dr. Bob Harrington Show notes - Diversity and Inclusion What are the gender disparities in the field of Cardiology? 45.8% of residents and fellows in ACGME-accredited programs are women. 14.9% of cardiologists are women. 8% of interventional cardiologists are women [1]. 30.6% of male faculty were full professors, while 15.9% of female faculty are full professors [2].Men are more likely to be influenced by positive attributes of a field, while women are more likely to be influenced by negative attributes [3].3% of percutaneous coronary interventions in the United States are performed by female operators [4]. What is mentorship, sponsorship, and allyship? A mentor provides advice and helps someone develop a skill.A sponsor is an advocate who helps someone secure career advancement opportunities.An ally partners with people, utilizing their power and influence to champion the rights of others [5].According to some studies, women report less sponsorship experiences than men. Additionally, in women it seems to translate less frequently into experiences that further their career (speaking engagements, serving on editorial boards, etc) [6].“I’m a mentor to a few people, I'm a sponsor to many, and I’m an ally to all.” - Dr. Bob Harrington Why is a diverse cardiovascular workforce so important? Teams that are diverse pursue innovative and creative solutions.Medicine requires meaningful connections and having a physician with a common background enhances the patient-doctor interaction by a spectrum of constructive effects.Minority groups are less likely to be treated with effective cardiac medications [7].There continue to be barriers in clinical trials to include diverse and underrepresented patients [8].A diverse workforce of clinical scientists is crucial to promoting diversity in clinical trials, including understanding the problem, asking the right questions, and proposing solutions [9]. References AAMC 2019. Physician Specialty Data Report. Accessed November 18, 2021.Blumenthal DM, Olenski AR, Yeh RW, et al. Sex Differences in Faculty Rank Among Academic Cardiologists in the United States. Circulation. 2017;135(6):506-517. doi:10.1161/CIRCULATIONAHA.116.023520Yong CM, Abnousi F, Rzeszut AK, et al. Sex Differences in the Pursuit of Interventional Cardiology as a Subspecialty Among Cardiovascular Fellows-in-Training [published correction appears in JACC Cardiovasc Interv. 2019 Apr 8;12(7):695]. JACC Cardiovasc Interv. 2019;12(3):219-228. doi:10.1016/j.jcin.2018.09.036Wang TY, Grines C, Ortega R, et al. Women in interventional cardiology: Update in percutaneous coronary intervention practice patterns and outcomes of female operators from the National Cardiovascular Data Registry®. Catheter Cardiovasc Interv. 2016;87(4):663-668. doi:10.1002/ccd.26118Sharma G, Narula N, Ansari-Ramandi MM, Mouyis K. The Importance of Mentorship and Sponsorship: Tips for Fellows-in-Training and Early Career Cardiologists. JACC Case Rep. 2019;1(2):232-234. Published 2019 Aug 21. doi:10.1016/j.jaccas.2019.06.007Patton EW, Griffith KA, Jones RD, Stewart A, Ubel PA, Jagsi R. Differences in Mentor-Mentee Sponsorship in Male vs Female Recipients of National Institutes of Health Grants. JAMA Intern Med. 2017;177(4):580-582. doi:10.1001/jamainternmed.2016.9391Tran HV, Waring ME, McManus DD, et al. Underuse of Effective Cardiac Medications Among Women, Middle-Aged Adults, and Racial/Ethnic Minorities With Coronary Artery Disease (from the National Health and Nutrition Examination Survey 2005 to 2014). Am J Cardiol. 2017;120(8):1223-1229. doi:10.1016/j.amjcard.2017.07.004Clark LT, Watkins L, Piña IL, et al. Increasing Diversity in Clinical Trials: Overcoming Critical Barriers [published correction appears in Curr Probl Cardiol. 2021 Mar;46(3):100647]. Curr Probl Cardiol. 2019;44(5):148-172. doi:10.1016/j.cpcardiol.2018.11.002Poppas A, Albert MA, Douglas PS, Capers Q 4th. Diversity and Inclusion: Central to ACC's Mission, Vision, and Values. J Am Coll Cardiol. 2020;76(12):1494-1497. doi:10.1016/j.jacc.2020.08.019 Production Team Dr. Gurleen KaurAmit Goyal, MDDaniel Ambinder, MD


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