Cardionerds: A Cardiology Podcast

CardioNerd (Daniel Ambinder) and series co-chairs Mark Belkin (AHFT Fellow, University of Chicago) and Karan Desai (Cardiologist, Johns Hopkins), join fellow lead, Dr. Pablo Sanchez (FIT, Stanford) for a discussion with Dr. Ryan Tedford (Professor of Medicine at the Medical University of South Carolina) about Right Ventricular (RV) predominant cardiogenic shock. In this episode we explore risk factors, pathophysiology, hemodynamics, and treatment strategies in this common and complex problem. We dissect three cases that epitomize the range of diagnostic dilemmas and management decisions in RV predominant shock, as Dr. Tedford expertly weaves us through the pathophysiology and decision-making involved in managing the “people’s ventricle.” Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds internship program, CardioNerds academy fellow, and IM resident at Brigham and Women’s Hospital). 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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References • 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 – RV Predominant Cardiogenic Shock The degree of RV dysfunction and failure are modulated by stretching its capacity to tolerate insults from deranged afterload, preload, and contractility. Afterload insults are MUCH LESS tolerated than other insults and broadly comprise the most common pathophysiologic cause of both acute and chronic RV failure. RV and left ventricular (LV) function are anatomically and physiologically connected.  Progressive derangements in RV function can lead to the deadly “RV spiral,” in which poor RV function causes lower LV preload, leading to hypotension, and thus worsening RV perfusion and function. In RV failure/shock, some basic tenets including treating reversible causes, optimizing preload and afterload, and using inotropes and/or temporary MCS for as limited time as possible. Many acute RV failure patients can recover, but multiorgan injury plays an important role. Therefore, thoughtful and expeditious use of mechanical circulatory support is important. Show notes – RV Predominant Cardiogenic Shock Notes drafted by Dr. Pablo Sanchez. What is the basic difference between RV dysfunction and failure? Dysfunction: Abnormalities in systolic/diastolic function of the RV, but not necessarily to the point of leading to end-organ perfusion defects. RV dysfunction leads to poor outcomes regardless of mechanism.1 Failure: Clinical syndrome of inability of RV to maintain adequate output despite adequate preload. 1 How is the RV different from the LV and what impact does it have on pathophysiology and hemodynamics? The LV and RV originate from different embryologic “heart fields.”1,2 The RV wall is thinner and more compliant and has only two layers (instead of 3 like the LV).3 Furthermore, unlike the LV which has a significant proportion of endocardial and epicardial transverse myocardial fibers, the RV myocardial fibers are aligned in a longitudinal plane for the most part. Thus, a more significant proportion of RV systolic contraction is longitudinal – base of the ventricle moving towards the apex. The RV is crescent-shaped and has a large surface-to-volume ratio meaning smaller inward motion ejects the same stroke volume. 1 Hemodynamically, the RV takes blood from a low-pressure venous system and gives it to a distensible system with low impedance (the normal pulmonary circuit at baseline typically has a resistance one-tenth of the systemic resistance). Therefore, volume loads (preload) are much better handled than pressure (afterload).1 What is RV-PA coupling? As Dr. Tedford noted, RV-PA coupling describes “the interaction of RV contractility and afterload (resistive and pulsatile components). It is the most comprehensive description of RV function and therefore the Gold Standard.” Whether we are referring to the LV or RV, the basic concept of coupling describes the energy transfer between ventricular contractility and arterial afterload. RV-PA coupling has typically been assessed by pressure-volume loops, with ventricular contractility assessed by end-systolic elastance (a load-independent measure of systolic function) and arterial afterload by effective arterial elastance. MODUS OPERANDI: RV dysfunction and eventual failure is modulated by stretching its capacity to tolerate insults from afterload, preload, and contractility. What leads to ACUTE right heart failure? Most commonly results from:1 Abrupt increases in afterload (e.g., think PE, hypoxia, and acidemia). Decreased contractility (e.g., think ischemia such as RV infarction, myocarditis, and post-cardiotomy). Volume overload can sometimes lead to acute right heart failure, particularly in the setting of another categorical insult such as septic cardiomyopathy or LVAD support. What leads to CHRONIC right heart failure? This is different than acute right heart failure. Most commonly chronic right heart failure results from:1 Gradual increases in afterload (e.g., think pulmonary arterial hypertension). Chronic volume overload (e.g., longstanding tricuspid regurgitation, atrial septal defect, and other congenital lesions like double outlet RV). Contractility (e.g., including the isolated RV cardiomyopathies like arrhythmogenic right ventricular cardiomyopathy or ischemic cardiomyopathy). Other pathologies certainly affect multiple categories (e.g., Ebstein’s anomaly which is a function of contractility and volume overload or single ventricle physiology like post-Fontan patients – for more on these and other ACHD lesions, enjoy the CardioNerds ACHD Series!) MODUS OPERANDI: The cardiovascular system is wholly connected, and acute decompensation leads to progressive derangements in the above levers (including LV function). This phenomenon is called the RV spiral. How do we manage RV failure? The most important and first step is the treatment of reversible causes. For instance, acute coronary syndrome involving the RV requires percutaneous intervention (PCI) or pulmonary embolism requires anticoagulation and/or thrombolytic/device/surgical therapy. PRELOAD OPTIMIZATION Ensuring that there is adequate preload is a key tenet of diagnosing and treating RV failure. This may require diuresis or judicious volume resuscitation to maintain cardiac output. While guiding fluid management in the setting of RV failure, one should STRONGLY consider invasive hemodynamic monitoring (e.g., over-resuscitation can lead to decreased LV output through septal shift and ventricular interdependence from pericardial constraint).1 General target: We could consider a CVP 10-15 mmHg; however, this will be individualized. Another general rule would also be if that a bolus of 500 cc of crystalloid does not result in hemodynamic improvement, further loading should not be continued, especially without invasive hemodynamic guidance. AFTERLOAD OPTIMIZATION  The goal should be to correct reversible causes of elevated pulmonary vascular resistance (e.g., acidosis, hypercapnia, hypoxia, and generally in ventilated patients avoid elevated inspiratory pressures > 30mmHg).1 With specialized expert guidance, we can consider selective pulmonary vasodilators (acutely and short-term): One example includes inhaled NO, and in observational studies, short-term use lowered PVR and increased RV ejection.4 We also have to remember the consequences of reducing RV afterload. Acutely increasing LV preload in a baseline abnormal LV may lead to distention, lowered cardiac output, and pulmonary edema.1 Pulmonary vasodilators can act on specific pathways (e.g., nitric oxide, prostacyclin, endothelin-1, and soluble guanylate cyclase stimulators) and come in various forms (oral, inhaled, and intravenous). CONTRACTILITY AUGMENTATION (INOTROPES) We typically utilize inotropes in concert with the prior two but optimize loading so the time we need inotropes is minimal.1 Short-term use can improve hemodynamics. Longer-term use will typically increase myocardial O2 consumption and is associated with increased mortality.  The RV has coronary perfusion in systole and diastole, so peripheral vasopressors are helpful to maintain perfusion, especially if systolic blood pressure is less than RV systolic pressure.1 GOAL: Increase contractility without increasing RV afterload. For those failing to respond to these above measures to optimize preload, afterload, and contractility, there may be a role for temporary mechanical circulatory support (see #10 below). How do we decide between dobutamine and milrinone? BOTH inotropes can lead to hypotension, have similar clinical outcomes, hemodynamic efficacy and arrhythmogenic potential1 (despite the adage that attributes more arrhythmias to dobutamine, studies show the risk is typically the same in both5). Milrinone is a more potent vasodilator (systemic and pulmonary) typically leading to greater decreases in end-diastolic pressures in the ventricles.1 It is renally cleared, has a longer half-life, and acts through a separate mechanism pathway compared to beta-blockade, thus patients can be on milrinone and beta blockers at the same time on a case-by-case basis.1 Dobutamine has a shorter half-life, with rapid onset/offset and so may be more ideal in unstable/hypotensive patients.1 What if the patient is hypotensive? In this circumstance, we would need an ino-constrictor or peripheral vasoconstrictor. Vasopressin has almost no impact on PVR, so unlike catecholamines, it does not directly worsen RV afterload.1 What are some important invasive hemodynamic parameters to be aware of? RAP/PCWP ratio: Disproportionate RV dysfunction can be portrayed by an RAP/PCWP ratio > 0.5-0.8 (depending on the clinical situation). In other words, the closer that RAP and PCWP are, the more likely you have disproportionate RV dysfunction. The predictive power of this ratio is different depending on the situation. Pre-operatively, a ratio > 0.63 is associated with RHF post-LVAD.6 In acute inferior MI, a ratio of > 0.86 is associated with RHF.7 PAPi: The PA pulse pressure gives us an idea of the ability of the RV to generate SV. Dividing this by the RAP, gives us an index that takes into account right-sided filling pressures. As above, the context is important. In acute inferior MI a PAPi of < 1.0 is predictive of mortality or MCS need,8 while a pre-operative PAPi < 1.8 was predictive of RHF after LVAD.9 Caveats: As Dr. Tedford mentioned, the PAPi is related to RV function, but not a direct measure of it. Manipulation of each component (e.g., pulse pressure or RA pressure) can ultimately lead to a similar absolute value of PAPi under very different loading conditions. PA pulse pressure is a function not only of SV but also of PA capacitance. In other words, a narrow pulse pressure can be due to a failing RV or a low pulmonary capacitance (from fluid overload for example). This isn’t clearly gleaned from the PAPi alone and requires us to keep in mind the context of the equation. Note: The gold standard assessments of RV contractility are derived from Pressure-Volume loops which require both simultaneous assessment of pressure and volume as well as alteration of preload over multiple beats. This limits applicability because it is technically challenging to do.10  What are important concepts to remember for Mechanical Support of the RV? One of the first things to consider is the end-game: are we using MCS as a bridge to recovery, bridge to decision, bridge to transplant, or bridge to durable MCS? Many acute RHF patients can recover with adequate support and a significant prognostic factor is preventing multiorgan failure.11,12 If MCS is needed, early use is better than later. Another important question is if we need oxygenation? Many of the MCS options, except the Impella RP, can have an oxygenator spliced into the system.11 A key question will be if we need RV-only support or biventricular support?11 RV-targeted support will increase LV preload, and the LV has to be able to accommodate the increased volume. If the LV is unable to tolerate the increased return, systemic cardiac output can become inadequate, LV filling pressures will rise, which can lead to pulmonary edema and increase mean PA pressures further (which can also lead to acute lung injury and worse outcomes). In these circumstances, biventricular support with either VA-ECMO or permutations of isolated RV + LV support may be needed. We also have to ask ourselves, if pulmonary arterial HTN primarily responsible for RV shock?11 If so, then VA-ECMO may be the most appropriate option. Increased flow from an RVAD, combined with a pre-existing elevated PVR can lead to elevated pulmonary artery pressures, which can precipitate pulmonary hemorrhage.1 References – RV Predominant Cardiogenic Shock Konstam MA, Kiernan MS, Bernstein D, et al. Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation. 2018;137(20). doi:10.1161/CIR.0000000000000560 Haddad F, Hunt SA, Rosenthal DN, Murphy DJ. Right ventricular function in cardiovascular disease, part I: Anatomy, physiology, aging, and functional assessment of the right ventricle. Circulation. 2008;117(11). doi:10.1161/CIRCULATIONAHA.107.653576 Sheehan F, Redington A. The right ventricle: Anatomy, physiology and clinical imaging. Heart. 2008;94(11). doi:10.1136/hrt.2007.132779 Wasson S, Govindarajan G, Reddy HK, Flaker G. The Role of Nitric Oxide and Vasopressin in Refractory Right Heart Failure. J Cardiovasc Pharmacol Ther. 2004;9(1). doi:10.1177/107424840400900i102 Mathew R, Di Santo P, Jung RG, et al. Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock. N Engl J Med. 2021;385(6). doi:10.1056/nejmoa2026845 Kormos RL, Teuteberg JJ, Pagani FD, et al. Right ventricular failure in patients with the HeartMate II continuous-flow left ventricular assist device: Incidence, risk factors, and effect on outcomes. J Thorac Cardiovasc Surg. 2010;139(5). doi:10.1016/j.jt Lopez-Sendon J, Coma-Canella I, Gamallo C. Sensitivity and specificity of hemodynamic criteria in the diagnosis of acute right ventricular infarction. Circulation. 1981;64(3 I). doi:10.1161/01.CIR.64.3.515 Korabathina R, Heffernan KS, Paruchuri V, et al. The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv. 2012;80(4). doi:10.1002/ccd.23309 Morine KJ, Kiernan MS, Pham DT, Paruchuri V, Denofrio D, Kapur NK. Pulmonary Artery Pulsatility Index is Associated with Right Ventricular Failure after Left Ventricular Assist Device Surgery. J Card Fail. 2016;22(2). doi:10.1016/j.cardfail.2015.10.019 El Hajj MC, Viray MC, Tedford RJ. Right Heart Failure: A Hemodynamic Review. Cardiol Clin. 2020;38(2). doi:10.1016/j.ccl.2020.01.001 Esposito ML, Bader Y, Morine KJ, Kiernan MS, Pham DT, Burkhoff D. Navin K. Kapur, MD Mechanical Circulatory Support Devices for Acute Right Ventricular Failure. Circulation. 2017;136. Cheung AW, White CW, Davis MK, Freed DH. Short-term mechanical circulatory support for recovery from acute right ventricular failure: Clinical outcomes. J Hear Lung Transplant. 2014;33(8). doi:10.1016/j.healun.2014.02.028 CardioNerds Cardiac Critical Care Production Team Karan Desai, MD Dr. Mark Belkin Dr. Yoav Karpenshif Amit Goyal, MD Daniel Ambinder, MD

CardioNerds (Dr. Patrick Azcarate, Dr. Teodora Donisan, and Amit Goyal) discuss Radiation-Associated Cardiovascular Disease (RACD) with Dr. Eric Yang, cardio-oncologist, assistant professor of medicine, and associate fellowship program director at UCLA. RACD is a consequence of radiation treatment for various mediastinal tumors (breast, lung, lymphoma). It is the second most common cause of morbidity and mortality in patients treated with mediastinal radiation for cancer. While novel techniques decrease radiation exposure during cancer treatment, the incidence is expected to increase because of historical practices and delayed onset of symptoms. The prevalence of RACD is difficult to estimate given under-recognition. Additionally, most of the data comes from patients treated with radiation techniques from decades ago. In this discussion we review every nook and cranny of RACD to help guide you the next time you see a patient with a history of chest radiation. Review this CardioNerds Case Report of radiation associated cardiovascular disease for more: Episode #169. Chest pain in a Young Man – “A Gray (Gy) Area” – UC San Diego. Audio editing by CardioNerds Academy Intern, student doctor Yousif Arif. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology 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. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology 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 – Radiation-Associated cardiovascular disease Due to the legacy effect, the incidence of RACD will continue to increase in the next few years. When treating patients with a history of mediastinal radiation, we should remember to ask: How much radiation was given? Could the heart have been exposed? Radiation can affect every part of the heart by causing coronary artery disease (CAD), valvulopathy, myocardial disease, conduction disease, and pericardial disease. Exposure to ~25-30 Gy or more significantly increases the risk but RACD can occur at lower doses. Try to delay surgery as much as possible and do all you can in one operation to avoid re-operation in the future. For revascularization, percutaneous coronary intervention (PCI) is typically preferred over coronary artery bypass grafting (CABG) but the choice should be individualized in consultation with a multidisciplinary heart team experienced in the management of RACD. In general, for aortic valve disease, transcatheter replacement is recommended over surgical aortic valve replacement. For mitral valve disease, surgical replacement is recommended over repair. Every decision should be made with a heart team approach and made unique to that specific patient. Show notes – Radiation-Associated cardiovascular disease Notes were drafted by Dr. Patrick Azkarate. 1. Understand the pathophysiology of RACD Ionizing radiation has the potential to damage DNA. Both normal cells and cancer cells get damaged, but cancer has less effective DNA repair mechanisms and therefore malignant cells are more vulnerable to radiation therapy. After radiation causes acute damage, this sets off an inflammatory cascade leading to myofibroblast activation, fibrosis and collagen deposition, and subsequent stiffening of the myocardium and vessels. 2. What may increase one’s risk of developing RACD? Young age (<50 years-old) at the time of radiation High cumulative dose (>30 Gy) or high dose of radiation fractions (>2 Gy/day) Anterior or left chest radiation (breast cancer, lung cancer, lymphoma) Pre-existing cardiovascular disease Tumor in or next to the heart Concomitant chemotherapy (e.g. anthracyclines) 3. What are some techniques being used to reduce radiation exposure? Shielding Respiratory gating techniques (e.g. deep inspiratory breath-hold, activated breathing control) Smaller repeated fractions Narrow tangential beams Proton therapy 4. What are prevention and screening strategies for RACD? Annual history and physical examinationTreat pre-existing conditionsScreen for RACD (myocardial, valvular, pericardial, CAD, or conduction system disease)5 years post-exposure, screen for CAD and consider stress test every 2 years10 years post-exposure, screen for valvular heart disease with an echocardiogram every 2 years1 5. Discuss diagnosis and management of specific complications of RACD CAD The risk of radiation induced CAD (RICAD) is 7.5% per Grey Unit (Gy). The risk is roughly constant, begins several years after exposure, and persists for at least 2-3 decades (>50% of excess ischemic events occurring >10 years after RT).2 Radiation causes inflammatory plaque with high collagen and fibrin content, similar to accelerated atherosclerosis. Angiographic characteristics: Ostial or proximal Anterior and central (predominantly affecting the left anterior descending and the right coronary arteries) Severe, diffuse Long, smooth, concentric, and tubular Treatment: CABG vs PCI While there are no head-to-head trials comparing CABG vs PCI in patients with RICAD, it is known that compared to the general population, following CABG they have worse outcomes (increased risk of wound dehiscence, infection, graft failure, and death).3 The data for PCI is mixed but most recently have shown that patients with RICAD undergoing PCI have similar outcomes compared to patients without radiation exposure.4 Unless there is an additional indication for surgery, PCI for chronic CAD usually preferred. If multi-vessel CAD or higher Syntax score (≥ 22) consider CABG. Other considerations might guide percutaneous vs surgical revascularization Porcelain aorta Fibrotic bypass grafts (internal mammary artery) in the radiation field Multi-valvular disease Valvular disease Radiation causes progressive valve thickening and calcification leading to valve leaflet retraction, followed by regurgitation and then stenosis. Patients usually become symptomatic 1-2 decades after radiation exposure (later than CAD). Prevalence of aortic regurgitation (AR) at 10 years is 4% and at 20 years is 60%. The prevalence of aortic stenosis (AS) at 10 years 0% but at 20 years: 16% Mitral regurgitation (MR) and AR are the most common and occur due to leaflet retraction. These ultimately progress to stenosis. MR is the most common reason for surgery. Echocardiogram is done to evaluate the valves. Surrounding structures may show calcification, such as the annulus, subvalvular apparatus, or aorta-mitral curtain (a hallmark of previous heart irradiation which is associated with mortality in patients undergoing cardiac surgery). Management decisions are complex, depends on the valvular lesion(s) involved, and should be guided by a heart team approach. For aortic valve disease, TAVR is preferred over SAVR (unless there is another indication for surgery or there is excess risk for coronary obstruction or annular rupture). If SAVR is pursued, usually try to replace all valves (even if one is just mild to moderate) to avoid re-operation. For the mitral valve, data is mixed between surgical vs transcatheter approaches. In general, if surgery is indicated then the valve is replaced and not repaired (irradiated valve tissue is fibrotic and calcified) Given increased risk of reoperation, mechanical prostheses may be appealing, especially for younger patients. If there are contraindications to anticoagulation, then a bioprosthesis should be used. General cardiothoracic surgery principles in patients with RACD Worse long-term outcomes compared to age and sex-matched controls undergoing similar procedures Reoperation portends significantly higher risk compared to non-RACD patients Delay surgical intervention as long as possible Address all issues with a complete operation the first time Surgical planning may involve cardiac magnetic resonance imaging (CMR) to look for fibrosis, computer tomography (CT) to identify calcified structures (intra- and extra-cardiac), transthoracic echocardiogram (TTE), right and left heart catheterization to evaluate for restriction vs constriction, coronary angiogram. Myocardial disease In terms of pathophysiology, radiation causes an acute inflammatory cascade, then a pro-fibrotic milieu which leads to myocardial fibrosis and reduced microvascular proliferation and density. RACD-related myocardial dysfunction is defined as >10% decrease in LVEF to a value <50% confirmed by repeated imaging 2-3 weeks after the first diagnostic study or heart failure with preserved ejection fraction (HFpEF) HFpEF is more common than heart failure with reduced ejection fraction (HFrEF). Risk of myocardial disease increases with total radiation dose, fraction size, and volume of heart in the radiotherapy field. Benefit of heart failure pharmacotherapy in subclinical myocardial dysfunction remains unknown, however guideline directed medical therapy is recommended. While transplant is not broadly recommended due to poor outcomes and high risk of recurrent malignancy, this remains a consideration.  Conduction system disease The conduction system can sustain direct damage from radiation or can be affected by ischemia or fibrosis. 75% of long-term survivors who received mediastinal radiation have conduction defects on electrocardiogram (ECG). Acutely, we can see transient, nonspecific repolarization abnormalities. Long-term, patients may develop right bundle branch block (anteriorly located). High risk for ectopy, supraventricular ventricular tachycardia, ventricular tachycardia, and non-specific T-wave and ST-segment ECG changes. Inappropriate sinus tachycardia is a sign of extensive RACD. There are no specific treatments in RACD patients and providers should treat according to guidelines. Radiation and Devices Radiation can impair healing after device implantation Devices can malfunction Manufacturers advise that the lifetime dose a device can take is 5 Gray (this is when circuit board can start to malfunction) It is recommended to interrogate device before and after radiation therapy Pericardial disease Radiation causes pericardial thickening, calcification, and fibrosis with subsequent constriction and effusion. It can be hard to diagnose constriction since many patients may have concomitant restrictive physiology. Patients may present with pericarditis, pericardial effusion, chronic pericardial disease, or cardiac tamponade. TTE, CT, and CMR are helpful to identify pericardial thickening, enhancement and septal shift. When in doubt, simultaneous right and left heart catheterization can help with the diagnosis. To treat constriction, we can try anti-inflammatory therapy first (in case of reversibility), then standard of care. References – Radiation-Associated cardiovascular disease Desai MY, Windecker S, Lancellotti P, et al. Prevention, Diagnosis, and Management of Radiation-Associated Cardiac Disease: JACC Scientific Expert Panel. J Am Coll Cardiol. 2019;74(7):905-927. doi:10.1016/j.jacc.2019.07.006 Darby SC, Ewertz M, McGale P, et al. Risk of ischemic heart disease in women after radiotherapy for breast cancer. N Engl J Med. 2013;368(11):987-998. doi:10.1056/NEJMoa1209825 Wu W, Masri A, Popovic ZB, et al. Long-term survival of patients with radiation heart disease undergoing cardiac surgery: a cohort study. Circulation 2013;127:1476–85. Liang JJ, Sio TT, Slusser JP, et al. Outcomes after percutaneous coronary intervention with stents in patients treated with thoracic external beam radiation for cancer. J Am Coll Cardiol Intv 2014;7:1412–20. Heidenreich PA, Hancock SL, Lee BK, et al. Asymptomatic cardiac disease following mediastinal irradiation. J Am Coll Cardiol 2003;42:743–9. Meet Our Collaborators International Cardio-Oncology Society ( IC-OS). IC-OS exits to advance cardiovascular care of cancer patients and survivors by promoting collaboration among researchers, educators and clinicians around the world. Learn more at https://ic-os.org/.

Cardiogenic shock (CS) remains a complex, multifactorial syndrome associated with significant morbidity and mortality. The CardioNerds Critical Care Cardiology Series tackles this important syndrome in a series of several episodes including: LV-predominant Shock, RV-predominant Shock, and Bi-ventricular Shock. In this episode, we review the definitions, pathophysiology, evaluation, and contemporary management, including use of inotropes and mechanical circulatory support, of left ventricular (LV) predominant CS. Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai along with CardioNerds Co-founders Dr. Amit Goyal and Dr. Daniel Ambinder were joined by FIT lead, Dr. Vanessa Blumer, the recipient of the AHA 2021 Laennec Fellow in Training Clinician Award and currently pursuing Advanced Heart Failure and Transplant fellowship at the Cleveland Clinic. Our episode expert is Dr. Shashank Sinha, an Advanced Heart Failure, Mechanical Circulatory Support, and Cardiac Transplant cardiologist, Medical Director of the Cardiac Intensive Care Unit, and Director of the Cardiovascular Critical Care Research Program at INOVA Fairfax Hospital. His illustrious career accomplishments include being a Steering Committee member and site Principal Investigator for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network. Audio editing by CardioNerds academy intern, Anusha Gandhi. 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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Pearls • Notes • References • 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 – LV Predominant Cardiogenic Shock LV-CS is complex! It is important to recognize that the pathophysiology of heart failure-related cardiogenic shock (HF-CS) is distinct from that of acute myocardial infarction (AMI-CS), and also crucial to differentiate between LV-dominant, right ventricular (RV)-dominant and biventricular (BiV)-shock. The SCAI SHOCK Stage Classification provides a unified and standardized vocabulary when assessing severity of CS, and facilitates communication about the diagnosis, presentation, and evolving nature of CS. Norepinephrine is considered the initial vasopressor of choice in most CS patients; the initial inotrope choice is a bit more nuanced! When considering mechanical circulatory support (MCS) for LV shock, high-quality data to guide therapy is lacking but one must always consider “the right patient, for the right device, at the right time” and remember that “pumps pump blood, decisions save lives”. Multidisciplinary, team-based care is paramount to improving survival of the critically ill patient with CS. Show notes – LV Predominant Cardiogenic Shock Notes drafted by Dr. Vanessa Blumer. 1. What tools do you use to define LV CS? CS is a hemodynamically complex and multifactorial syndrome, one of the most common indications for admission to a cardiac intensive care unit, with short-term mortality ranging from 35-50%. It is defined by systemic hypoperfusion and tissue hypoxia due to a primary cardiac insult or dysfunction. Clinical criteria used to define CS typically include evidence of hypotension (classically defined as SBP < 90 mmHg for 30 minutes and/or use of vasopressors, inotropes, or MCS to maintain systolic blood pressure > 90 mmHg) AND evidence of end-organ hypoperfusion (for example, serum lactic acid > 2 mmol/L, acute kidney injury, acute liver injury, altered mental status) in the setting of acute coronary syndrome or acute decompensated heart failure. Laboratory markers, including serum lactic acid, liver function tests, kidney function, and biomarkers including troponin and natriuretic peptides may be helpful. An echocardiogram is an excellent point of care tool to help demonstrate and confirm evidence of LV systolic dysfunction and/or valvular abnormalities.  Finally, a right heart catheterization (demonstrating an abnormally low cardiac output and index with elevated filling pressures) may be useful in facilitating the diagnosis and subsequent management. 2. How do HF-CS and AMI-CS lead to different phenotypes? It is important to recognize that HF-CS is now the predominant cause of CS, accounting for more than half of all CS. AMI-CS is characterized by an abrupt presentation due to a primary myocardial ischemic insult leading to necrosis (occurring in 5-10% of AMI patients) and can occur after STEMI or NSTEMI. The canonical clinical course is hypotension due to primary myocardial dysfunction leading to hypoperfusion with congestion as a later clinical or hemodynamic finding. Conversely, a patient with heart failure related shock commonly presents with acutely decompensated heart failure and congestion, leading to hypoperfusion, and culminating in hypotension. 3. How do you distinguish LV-dominant, RV-dominant and BiV shock? LV predominant CS is characterized by high pulmonary capillary wedge pressure (PCWP) and normal or reduced central venous pressure (CVP) in the setting of reduced cardiac output (CO). RV dominant CS is characterized by elevated CVP, normal to low PCWP, and normal to reduced CO. BiV shock is characterized by hypotension, elevated CVP, normal or elevated PCWP, and reduced CO. 4. What is the current role for inotropes, vasodilators, and vasopressors in the management of LV CS? The Acute Cardiovascular Care Association of the European Society of Cardiology published a position statement for the diagnosis and treatment of patients with AMI complicated by CS in 2020. According to this, vasopressors (norepinephrine preferable over dopamine) in the presence of persistent hypotension received a Level of IIb/B recommendation. Intravenous inotropes to increase cardiac output received a IIb/C recommendation. Based on the available evidence and its accompanying limitations, norepinephrine is considered the initial vasopressor of choice in most CS patients. 5. When should we consider management with temporary mechanical circulatory support (t-MCS) devices and how should one strategize device selection? Initiation or escalation of t-MCS largely depends on matching the right device to the right patient at the right time. Because the risk and number of complications increases with duration and type of MCS, these decisions are complex, nuanced, and must consider operator and institutional expertise. When considering type of device (IABP, Impella, ECMO), SCAI Staging and phenotyping (AMI vs HF CS) are absolutely critical. 6. What are treatment goals when following patients with LV CS? Optimize preload, afterload, and contractility Perform serial reassessment (≤ q 6hr) of hemodynamics & end-organ perfusion Aim for timely and tailored treatment escalation/de-escalation    Assess for LV and RV recovery (wean t-MCS, vasopressors and inotropes as able Early identification of worsening shock:  Rising Lactate  Increasing pressor requirement  Worsening end-organ function  CPO < 0.6 and/or PAPi < 1  RA > 15 and/or PCWP > 15 References – LV Predominant Cardiogenic Shock Abraham J, Blumer V, Burkhoff D, Pahuja M, Sinha SS, Rosner C, Vorovich E, Grafton G, Bagnola A, Hernandez-Montfort JA, Kapur NK. Heart Failure-Related Cardiogenic Shock: Pathophysiology, Evaluation and Management Considerations: Review of Heart Failure-Related Cardiogenic Shock. J Card Fail. 2021 Oct;27(10):1126-1140. doi: 10.1016/j.cardfail.2021.08.010. PMID: 34625131. Kapur NK, Kanwar M, Sinha SS, Thayer KL, Garan AR, Hernandez-Montfort J, Zhang Y, Li B, Baca P, Dieng F, Harwani NM, Abraham J, Hickey G, Nathan S, Wencker D, Hall S, Schwartzman A, Khalife W, Li S, Mahr C, Kim JH, Vorovich E, Whitehead EH, Blumer V, Burkhoff D. Criteria for Defining Stages of Cardiogenic Shock Severity. J Am Coll Cardiol. 2022 Jul 19;80(3):185-198. doi: 10.1016/j.jacc.2022.04.049. PMID: 35835491. CardioNerds Cardiac Critical Care Production Team Karan Desai, MD Dr. Mark Belkin Dr. Yoav Karpenshif Amit Goyal, MD Daniel Ambinder, MD

Dr. Rick Nishimura, a professor of medicine at Mayo Clinic, discusses managing mitral regurgitation in challenging cases. The podcast covers topics such as guidelines, real patient cases, treatment challenges, microclip usage, atrial fibrillation impact, and postoperative complications. The conversation delves into the nuances of mitral regurgitation management and the importance of echocardiograms in therapy decisions.

In this episode, Dr. Carly Fabrizio (Advanced Heart Failure and Transplant Cardiology Physician at Christiana Care Hospital), CardioNerds Critical Care Series Co-Chair Dr. Mark Belkin (Advanced Heart Failure and Transplant Fellow at University of Chicago) and CardioNerds Co-Founder Dr. Amit Goyal (Cleveland Clinic) join Dr. Gavin Hickey (Director of the AHFTC Fellowship and medical director of the left ventricular assist device program at UPMC) and Dr. David Kaczorowski (Surgical Director for the Advanced Heart Failure center, Department of Cardiothoracic Surgery at UPMC) for a discussion on post-cardiotomy shock. Audio editing by CardioNerds Academy Intern, student doctor, Shivani Reddy. Post-cardiotomy shock is characterized by heart failure that results in the inability to wean from cardiopulmonary bypass or develops post cardiac surgery. Patients who develop post-cardiotomy shock typically require inotropic support and may ultimately require temporary mechanical circulatory support. Post-cardiotomy shock carries a high mortality rate. However, early recognition and prevention strategies can help mitigate the risk for developing post-cardiotomy shock. 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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. This episode is supported by the 5th Annual Going Back to the Heart of Cardiology (A MedscapeLIVE Conference). Join co-chairs Dr. Robert Harrington and Dr. Fatima Rodriguez January 24-26, 2025 at the Fontainebleau Hotel in Miami Beach, Florida. The agenda will explore the latest advancements in cardiology including cardiovascular prevention, atherosclerosis and thrombosis, cardiovascular dysfunction, arrhythmias, and valvular heart disease. Network, attend engaging presentations by renowned cardiologists, visit the exhibit and poster hall, participate in an exclusive immersive experience, and earn up to 13 CME/CE credits. Register today with code CARDIONERDS for 30% OFF your registration. Click here for more information. Pearls • Notes • References • 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 – Post-cardiotomy Shock Weaning from cardiopulmonary bypass is an intricate process that includes: rewarming the patient, de-airing the cardiac chambers, ensuring a perfusing heart rhythm, confirming adequate ventilation and oxygenation, removing the intracardiac catheters and cannulas and slowly reducing the blood diverted to the cardiopulmonary circuit and returning it small aliquots to the patient. Much to monitor during the process! Assessing the risk for post-cardiotomy shock prior to going to the OR is important. Consider left ventricular, right ventricular, and valvular function, and don’t forget about the value of hemodynamic assessments (pulmonary artery catheter evaluations) to ensure patients are adequately compensated. Close peri-operative monitoring of hemodynamics, hemo-metabolic derangements, and acid/base status can help identify patients who are failing therapy and may require upgrade to temporary MCS. RV assessment is challenging. Utilizing both imaging and hemodynamic evaluations can help understand which RV’s will require more support. Multi-disciplinary discussions with a heart team approach prior to cardiac surgery are valuable in identifying high risk patients for post cardiotomy shock and discussing contingency plans if issues arise. Show notes – Post-cardiotomy Shock (drafted by Dr. Carly Fabrizio) How can we diagnose post cardiotomy shock? We can diagnose post cardiotomy shock as patients who are undergoing cardiac surgery that develop hypotension and or tachycardia with hypoperfusion and end organ dysfunction. How can assess the risk of developing postcardiotomy shock prior to going to the OR? LV systolic function is not the only evaluation of cardiac function Don’t ignore the RV! Valvular function must be evaluated in conjunction with LV/RV function Hemodynamics can be helpful prior to going to the OR Filling pressures and CO/CI evaluation –> the more normal range – the less risk of post cardiotomy shock If going in more deranged –> more complications are likely to occur Think about what options are available post operatively if issues arise Include a multi-disciplinary discussions and planning prior to going to the OR Are there any specific pre-operative or intra-operative risk factors that may predispose someone to developing post cardiotomy shock? Many factors can lead to postcardiotomy shock. Some pre-op factors include: Poor pre-operative cardiac function (RV and /or LV function) Entering the OR in cardiogenic shock (inotropes, temporary MCS) Well compensated patients with chronic ventricular dysfunction Intra-operative factors: Prolonged cross-clamp time Prolonged cardiopulmonary bypass (CPB) times (often seen in complex operations) Inadequate myocardial protection Ventricular distention Technical factors What is actually occurring in the OR when weaning from CPB? After the aorta cross clamp is removed- the heart is allowed to re-perfuse Remember that the heart has been ischemic for a considerable amount of time Lungs are re-inflated Temporary atrial and ventricular pacing wires are placed Stable rhythm is achieved and the heart is paced if necessary Acid / base status and electrolytes (potassium) are optimized Once the heart is de-aired, CPB is gradually weaned The flow of the CPB circuit is gradually reduced and more of the patient’s blood volume is gradually allowed to pass through the heart and lungs TEE is performed while weaning bypass Once bypass is completely weaned, the cannulas used to establish CPB are removed Anticoagulation is reversed Assess for hemostasis Chest tubes are placed, and closure occurs What are the clinical and laboratory parameters which help determine whether vasoactive support alone will be enough vs. when temporary MCS may be needed? Assess perfusion first BP Urine output Lactic acid PA catheter data /  hemodynamic data Cardiac output/index (CO/CI) Pulmonary artery pressures (PAP) Central venous pressures (CVP) Mixed venous oxygen saturation Cardiac power output (CPO) and cardiac power index (CPI) CPO < 0.6 or CPI < 0.32 are considered low Serial blood gas Focus on pH and bicarbonate (acid/base status) Optimize inotropic support accordingly Favor epinephrine in safe dosing limits and minimizing drugs that increase afterload whenever possible Consider Milrinone if the blood pressure is adequate If pulmonary hypertension Inhaled nitric oxide or inhaled prostacyclin If worsening despite these measures –> consider escalation to temporary MCS Left ventricular assist devices (LVAD) do not support the right ventricle. How can we identify RV failure in these patients and when should you upgrade to RV mechanical circulatory support? Most patient that require left-sided support by nature often have underlying right-sided dysfunction as well Pre-operative – assessment of the RV is important: CVP PAPi (PA systolic pressure- PA diastolic pressure / CVP) CVP: PCWP ratio RV failure can occur in any patient No great, reliable, and reproducible data on when or how to support the RV following LVAD implantation, or cardiogenic shock in general. More studies are needed. What’s different about how you assess the RV dysfunction in the OR compared to someone who is in the ICU? When do you consider using RV mechanical support upfront in the OR? Intra-operative TEE and direct visualization are both used in the OR to assess RV function Try to avoid upfront RV mechanical support in the OR Optimize with invasive hemodynamic monitoring prior to OR Temporary MCS can be used to optimize patient and help with diuresis pre-operatively Continue to optimize the RV while in the OR Remove volume through hemoconcentration while on CPB circuit to optimize volume status Consider temporary MCS for the RV when medical therapy is maximized, and the patient still remains marginal as measured by: LVAD flows, cardiac output/index, mixed venous gases and metabolic parameters Are there any surgical consideration to influence the type of temporary MCS for postcardiotomy shock? Strategize first by asking: What is failing? LV, RV, lungs, or a combination What access is available? Ex: Bi-ventricular failure with hypoxemia and peripheral arterial disease: consider central VA ECMO Ex: Pure LV failure but RV and lungs OK –> temporary LV assist device How can we prevent, or decrease the risk, of post-cardiotomy shock ? Optimized hemodynamics going into the OR using a PA catheter Multi-disciplinary discussion with cardiac anesthesia, critical care team, etc. for high-risk cases Ensure adequate end-organ perfusion Avoid pre-operative medications that worsen peri-operative vasoplegia ACE-i/ARB/ARNI, milrinone etc. What is role of advanced therapy evaluations when assessing high risk patients going to the OR? Important to think about options pre-operatively Selection committee discussions to weigh-in on candidacy for LVAD or cardiac transplant and if that may be more beneficial than other cardiac surgical interventions How does team-based care help with decision making? Optimize patients pre procedure and support them peri-procedure Involving palliative care team and establishing patient goals prior to surgery References – Post-cardiotomy Shock Lorusso, Raffa, Alenizy, et al. “Structured review of post-cardiotomy extracorporeal membrane oxygenation: part 1—Adult patients.” JHLT. 38(11): 1125-1143. 2019.https://www.sciencedirect.com/science/article/pii/S1053249819316328 Fukuhara, Takea, Garan, et al. “Contemporary mechanical circulatory support therapy for postcardiotomy shock.” Curr Topics Review Article. 64:183-191. 2016. https://link.springer.com/content/pdf/10.1007/s11748-016-0625-4.pdf CardioNerds Cardiac Critical Care Production Team Karan Desai, MD Dr. Mark Belkin Dr. Yoav Karpenshif Amit Goyal, MD Daniel Ambinder, MD

In this episode, Daniel Ambinder and Amit Goyal (CardioNerds co-founders), Dr. Gurleen Kaur (medicine resident at Brigham and Women’s Hospital and Director of CardioNerds Internship), student doctor Adriana Mares (medical student at the University of Texas El Paso/Texas Tech University Health Sciences Center El Paso, CardioNerds Academy Intern), and Dr. Teodora Donisan (general cardiology fellow at the Mayo Clinic and CardioNerds Academy Chief) discuss with Dr. Mayra Guerrero (Interventional Cardiologist and Professor of Medicine at the Mayo Clinic) about challenges with diagnosing and treating valve disease in women, as well as ideas on how to increase recruitment for women in cardiology including interventional and structural cardiology. Dr. Guerrero shares her inspiring personal journey and advice for how to navigate becoming a structural cardiologist as an international medical graduate, woman, and mother. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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 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 – Structural Heart Disease and LatinX Representation in Cardiology with Dr. Mayra Guerrero https://youtu.be/KvKADqUwUHQ Quoatables – Structural Heart Disease and LatinX Representation in Cardiology with Dr. Mayra Guerrero “Work hard, give it your best, and your work will speak for itself. Don’t be afraid to work hard and you’ll be able to achieve anything you want.” “I’m very fortunate to have had the opportunities that I’ve had, but now it’s my responsibility and the responsibility of many to make sure that we create those opportunities and that we provide mentorship for others who may want to follow the same steps into this field.” “I get angry, it’s normal to have emotions, but what I’ve learned is to transform my anger into something good – think of a project, find a paper, do something good for your career…channel that energy to do something good.” “It’s important that even at young ages you start thinking about how to pay it forward.” “Don’t wait too long to have kids. There’s never a perfect time to be a parent. Once you decide to have a family don’t put a pause on your personal life for your career.” Notes – Structural Heart Disease and LatinX Representation in Cardiology with Dr. Mayra Guerrero Notes (by Dr. Teodora Donisan) Structural valve disease in women and valve care in the global setting Heart disease is the leading cause of death for women. However, the awareness regarding this major public health concern has been declining over the past decade. Valve disease awareness is one of the lowest, at less than 3%. Women have higher mortality than men when they undergo surgical aortic or mitral interventions, mainly because of a higher risk profile. For example, women with severe aortic stenosis usually present at older ages and have many associated comorbidities, however the outcomes are good when they are treated with transcatheter aortic valve replacement (TAVR). Despite this, women are less likely to be referred for aortic valve replacement (AVR) than men. Once women are referred for therapy, they are more likely to be treated with TAVR than surgical aortic valve replacement (SAVR). There is a deficiency in trial enrollment for women which we need to address in order to generate the knowledge we require with regards to treatment. We also need to identify whether there are referral biases when it comes to AVR. Another hypothesis for the disparities in valve disease treatment for women when compared with men might be the decreased number of women in cardiology, especially in interventional cardiology (<10% of interventional cardiologists are women). Of note, <3% of TAVR operators are women (1.5% are surgeons and 1.5% are interventional cardiologists). Diversity and inclusion in interventional cardiology About 8% of interventional cardiologists are women and only 4.2% of cardiologists are Latinx. In order to increase recruitment for WIC, the problem needs to be addressed on multiple levels. Mentorship should be provided to cardiology fellows, and they should be supported in their choice for interventional cardiology. This should be equally offered and tailored to women and underrepresented minorities. Support should be given even earlier in their careers and lives, at school and even with the education they receive at home. Career goals can be achieved with hard work and determination, and this should be an integral part of the education and upbringing from an early age. There is an institutional responsibility to help address this problem. It can start with training to decrease unconscious bias, improvements in workplace conditions (e.g., schedule flexibility, provide maternity/paternity leave, lactation rooms), opening leadership opportunities for women and URiMs, establishing diversity and inclusion committees. The FDA, industry, and societies should have DE&I committees to ensure inclusive representation in clinical trial leadership and to ensure recruitment of women and minorities. Work life harmony as an interventional cardiologist You must choose your life partner well, caring for your family is teamwork. You might miss moments, but if you work together with your partner and children, it works out. It’s important to provide a strong role model for your family. References Vogel B, Acevedo M, Appelman Y, et al. The Lancet women and cardiovascular disease Commission: reducing the global burden by 2030. Lancet. 2021;397(10292):2385-2438. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

CardioNerds (Amit Goyal and Dan Ambinder), Series Co-Chair Dr. Dinu Balanescu (Academy House Faculty and Chief Resident at Beaumont Hospital), and Episode Lead Dr. Manu Mysore (Former CardioNerds Ambassador and Cardiologist at the University of Maryland) discuss The Need for Cardio-Oncology with Expert Faculty Dr. Bonnie Ky, Director of Penn Cardio-Oncology Translation Center of Excellence and Editor-in-Chief of JACC CardioOncology. Audio editing by CardioNerds Academy Intern, student doctor Yousif Arif. This episode is supported by a grant from Pfizer Inc. Cardio-Oncology is a burgeoning field. There is a need for cardiologists and oncologists to work together in a multidisciplinary fashion using multi-modality imaging and personalized medicine. Cardiologists in particular need to understand basic oncology, anti-cancer therapies, and address risk factors which play an important role in oncologic progression and/or adverse cardiovascular events. The field can only be furthered by research with a focus on specificity of endpoints and multidisciplinary collaboration. The future of the field is in the hands of investigators and clinicians alike. This CardioNerds Cardio-Oncology 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. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. This episode is supported by the 5th Annual Going Back to the Heart of Cardiology (A MedscapeLIVE Conference). Join co-chairs Dr. Robert Harrington and Dr. Fatima Rodriguez January 24-26, 2025 at the Fontainebleau Hotel in Miami Beach, Florida. The agenda will explore the latest advancements in cardiology including cardiovascular prevention, atherosclerosis and thrombosis, cardiovascular dysfunction, arrhythmias, and valvular heart disease. Network, attend engaging presentations by renowned cardiologists, visit the exhibit and poster hall, participate in an exclusive immersive experience, and earn up to 13 CME/CE credits. Register today with code CARDIONERDS for 30% OFF your registration. Click here for more information. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology 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 – The Need for Cardio-Oncology with Dr. Bonnie Ky Over 20 million new cancer cases are expected to be added annually to the global burden as novel therapies have improved cancer survivorship. These therapies may be directly associated with cardiotoxicity or may prolong life to allow time for cardiovascular disease to develop in cancer survivors. Hypertension, hyperlipidemia, and obesity are modifiable risk factors that portend a poor prognosis from both an oncologic and cardiovascular perspective. Multi-modality imaging is useful in risk assessment within oncology, with echocardiography (including strain imaging) having a class I indication prior to treatment with many chemotherapeutics. Diverse trial enrollment is essential for furthering the science within Cardio-Oncology to translate clinically into personalized management. There is a need to strengthen a pipeline of young physicians and scientists to further the field of Cardio-Oncology. Show notes – The Need for Cardio-Oncology with Dr. Bonnie Ky Why should cardiologists have familiarity with cancer therapies? By 2030, 23.6 million new cancer cases are expected to be added annually to the global burden.1 Novel therapies and/or combination therapies have improved cancer survivorship but are associated with cardiovascular complications, especially in the elderly and those with pre-existing cardiovascular comorbidities.2 Cardiologists currently lack an understanding of oncologic treatments, with poor knowledge of dosing protocols and cardiotoxicities. This can lead to less aggressive protocols administered, as well as early discontinuation of important treatments for both oncologic and cardiovascular conditions.3 A multidisciplinary collaboration between pharmacists, cardiologists, oncologists, and nurse navigators is needed to improve treatment decision-making for the benefit of cancer patients. Cardiologists should have basic knowledge and understanding of some of the commonly used chemotherapeutic drugs and any adverse events during treatment courses based on clinical trials, FDA reporting, and epidemiological data. JACC Cardio-Oncology seeks to disseminate knowledge through live courses such as Advancing the Care of the Oncology Patient and journal-associated podcasts, with plans to develop a “how-to” series to educate both cardiologists and oncologists. What is the impact of cardiovascular risk factors and morbidity in oncology? In the age of personalized cancer therapies, patients with metastatic disease are living longer and are instead dying from cardiovascular events. Hypertension, obesity, and dyslipidemia are a growing epidemic within the oncologic population. Retrospective analysis by Dr. Sun from the University of Pennsylvania VA suggests that only 68% of men receiving treatment for prostate cancer had a comprehensive cardiovascular risk factor assessment and of those, 54.1% had uncontrolled risk factors!4 Of these, 29.6% were not receiving corresponding cardiac risk-reducing medications.4 Treat the modifiable risk factors aggressively! What type of conditions do cardio-oncologists manage? Cardio-oncologists manage a variety of treatment-associated cardiovascular conditions and adverse events. Common oncologic therapeutics with known cardiotoxicity include anthracyclines, HER-2 receptor antibodies, radiation, tyrosine kinase inhibitors, VEGF-associated tyrosine kinase inhibitors (TKIs), aromatase inhibitors, and even modern treatments including stem cell transplantation and CAR-T therapies. Patients follow-up with the cardio-oncologist before, during, and after treatment sessions. Common cardiovascular events addressed include hypertension, dyslipidemia, arrhythmias, heart failure, coronary artery disease, and obesity. More on these in future episodes! After cancer therapy completion, focus is on addressing cardiovascular and cancer-related risk factors and lifestyle modification. What are strategies for risk assessment of cancer patients in terms of cardiovascular toxicity? Advanced imaging plays a vital role within the field of Cardio-Oncology. The European Society of Medical Oncology gives echocardiography a 1A recommendation that all patients who receive anti-cancer therapy associated with left ventricular dysfunction should have a baseline ejection fraction (EF) assessment. Those who have a reduced EF at baseline are at a higher risk of cardiotoxicity. This can be limited however by body habitus or recent mediastinal surgery.5 Cardiac MRI is a gold standard for measuring left and right ventricular volume and function and is used when there is suboptimal image acquisition. It is particularly useful in the assessment of cardiac masses and inflammatory conditions such as myocarditis.5 Stress echocardiography plays a vital role in the risk stratification of patients undergoing cancer therapies associated with myocardial ischemia, including VEGF inhibitors and TKIs. There is a potential role for assessing diastolic dysfunction as well. Calcium scoring can be determined on non-gated non-contrast CT scans performed for staging of malignancy. Hundley et al. have done remarkable work in understanding if exercise programs will help prevent heart disease with strict cardio-metabolic testing in patients undergoing cancer treatment.6 Large efforts are underway to identify risk calculators to predict cardiotoxicity in a personalized approach. What are monitoring strategies for cardiotoxicity? Consensus statements and expert opinions continue to grow and more of this will be addressed in future episodes. In particular, guidelines are in place for anthracycline use and HER-2 targeted therapy. In August 2022, the European Society of Cardiology released Cardio-Oncology Guidelines, addressing the cardiotoxicity of numerous other classes of anti-cancer therapies and further highlighting the importance of echocardiography and multi-modality imaging for the monitoring of cardiotoxicity in cancer patients.7 What are challenges in designing clinical trials in cardio-oncology? Patients feel vulnerable during the early treatment course with chances of lower trial enrollment. Multi-disciplinary collaboration with a patient-centric focus is needed. Partnership with key stakeholders, including NIH/AHA, is needed. Defining the optimal timing for the initiation of cardio-protective therapy and the duration of such therapy is another challenge. Where do we go from here in Cardio-Oncology? Scientifically, we need to advance personalized medicine to improve patient outcomes. We need to understand the mechanistic overlap between cardiovascular and oncologic disease. We need to leverage technology to assist in the treatment of cancer therapy-related adverse cardiovascular events and oncologic progression. We need to work together to overcome healthcare disparities which play a vital role in Cardio-Oncology. We need to strengthen the pipeline of young investigators and clinicians. References – The Need for Cardio-Oncology with Dr. Bonnie Ky Cancer Statistics (National Institute of Cancer website). https://www.cancer.gov/about-cancer/understanding/statistics. Published 2018. Accessed August 4, 2022. Cardinale D, Biasillo G, Cipolla CM. Curing Cancer, Saving the Heart: A Challenge That Cardioncology Should Not Miss. Curr Cardiol Rep. 2016;18(6):51. Okwuosa TM, Prabhu N, Patel H, et al. The Cardiologist and the Cancer Patient: Challenges to Cardio-Oncology (or Onco-Cardiology) and Call to Action. J Am Coll Cardiol. 2018;72(2):228-232. Sun L, Parikh RB, Hubbard RA, et al. Assessment and Management of Cardiovascular Risk Factors Among US Veterans With Prostate Cancer. JAMA Netw Open. 2021;4(2):e210070. Yu C, Pathan F, Tan TC, Negishi K. The Utility of Advanced Cardiovascular Imaging in Cancer Patients-When, Why, How, and the Latest Developments. Front Cardiovasc Med. 2021;8:728215. Bellissimo MP, Canada JM, Jordan JH, et al. Changes in Physical Activity, Functional Capacity, and Cardiac Function during Breast Cancer Therapy. Cancer Epidemiol Biomarkers Prev. 2022;31(7):1509. Lyon AR, López-Fernández T, Couch LS, et al. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS). Eur Heart J. 2022. Meet Our Collaborators International Cardio-Oncology Society ( IC-OS). IC-OS exits to advance cardiovascular care of cancer patients and survivors by promoting collaboration among researchers, educators and clinicians around the world. Learn more at https://ic-os.org/.

CardioNerds (Daniel Ambinder and Amit Goyal) join Dr. Arielle Schwartz (Emory University cardiology fellow), Dr. Joshua Zuniga (former Emory vascular medicine fellow and now USC cardiology fellow), and Dr. Patrick Zakka (UCLA cardiology fellow) from the Emory University School of Medicine. They discuss a case of a young woman with new onset hypertension refractory to 3 antihypertensive agents who is ultimately diagnosed renovascular hypertension due to fibromuscular dysplasia complicated by saccular aneurysm. Dr. Bryan Wells (Director of Vascular Medicine at Emory University) provides the ECPR for this episode. Audio editing by CardioNerds Academy intern, Dr. Christian Faaborg-Andersen. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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 References Gornik HL, Persu A, Adlam D, Aparicio LS, Azizi M, Boulanger M, Bruno RM, de Leeuw P, Fendrikova-Mahlay N, Froehlich J, Ganesh SK, Gray BH, Jamison C, Januszewicz A, Jeunemaitre X, Kadian-Dodov D, Kim ES, Kovacic JC, Mace P, Morganti A, Sharma A, Southerland AM, Touzé E, van der Niepen P, Wang J, Weinberg I, Wilson S, Olin JW, Plouin PF. First International Consensus on the diagnosis and management of fibromuscular dysplasia. Vasc Med. 2019 Apr;24(2):164-189. doi: 10.1177/1358863X18821816. Epub 2019 Jan 16. Erratum in: Vasc Med. 2019 Oct;24(5):475. Erratum in: Vasc Med. 2021 Aug;26(4):NP1. PMID: 30648921. Olin, Circulation. 2014;129:1048-1078. Fibromuscular Dysplasia: State of the Science and Critical Unanswered Questions A Scientific Statement From the American Heart Association S.H.KimMD, MPH†Jeffrey W.OlinDO‡James B.FroehlichMD, MPH§XiaokuiGuMA§J. MichaelBacharachMD‖Bruce H.GrayDO¶Michael R.JaffDO#Barry T.KatzenMD∗∗EvaKline-RogersMS, RN, NP§Pamela D.MaceRN††Alan H.MatsumotoMD‡‡Robert D.McBaneMD§§Christopher J.WhiteMD‖‖Heather L.GornikMD, MHS†. Clinical Manifestations of Fibromuscular Dysplasia Vary by Patient Sex: A Report of the United States Registry for Fibromuscular Dysplasia. JACC. Volume 62, Issue 21, 19–26 November 2013, Pages 2026-2028

CardioNerds Dr. Josh Saef, Dan Ambinder, join Dr. Jim Kimber and interview experts Dr. Adrienne Kovacs, and Dr. Lauren Lastinger and discuss behavioral health needs and psychosocial wellbeing in the congenital heart disease population. In this episode, our experts tackle issues surrounding mental and behavioral health including anxiety/depression, ADHD, neurodevelopmental disabilities, psychosocial challenges, stressors unique to patients with ACHD and their families, and how the healthcare system can better optimize mental health care for the CHD patient population. Audio editing by CardioNerds Academy Intern, Pace Wetstein. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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 Disclosures: None This episode is supported by the 5th Annual Going Back to the Heart of Cardiology (A MedscapeLIVE Conference). Join co-chairs Dr. Robert Harrington and Dr. Fatima Rodriguez January 24-26, 2025 at the Fontainebleau Hotel in Miami Beach, Florida. The agenda will explore the latest advancements in cardiology including cardiovascular prevention, atherosclerosis and thrombosis, cardiovascular dysfunction, arrhythmias, and valvular heart disease. Network, attend engaging presentations by renowned cardiologists, visit the exhibit and poster hall, participate in an exclusive immersive experience, and earn up to 13 CME/CE credits. Register today with code CARDIONERDS for 30% OFF your registration. Click here for more information. 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 – Congenital Heart Disease and Psychosocial Wellbeing Among patients with congenital heart disease, symptoms of anxiety are more common than symptoms of depression. “Heart-focused anxiety” relates to symptoms attributable to a heart condition including fear of appointments, surgery, or health-uncertainty. It is important to differentiate this from generalized anxiety. Predictors of depression and anxiety include patient-reported physical health status. Defect severity (mild, moderate, great complexity) and physician-diagnosed NYHA class were NOT associated with rates of depression/anxiety [2]. Despite CHD, patient self-reported Quality of Life (QoL) is relatively high. Predictors of decreased QoL include older age, lack of employment, never having married, and worse self-reported NYHA functional class Important treatment strategies include: education for patients and caregivers, early identification and referral to mental health providers, incorporation of providers into CHD teams, and encouraging physical activity and peer-interaction. Show notes – Congenital Heart Disease and Psychosocial Wellbeing Notes (developed by Dr. Jim Kimber) Mental Health Terminology: Adults with CHD face the same mental health challenges as people who don’t have a heart condition. Symptoms of depression and anxiety are the most common: Approximately 1/4 – 1/3 of CHD patients will struggle with clinically significant depression or anxiety at any one point. Up to ½ will meet lifetime diagnostic criteria for these conditions Mood and anxiety disorders differ in that they have separate diagnostic criteria. Importantly, research often uses self-reported symptoms, rather than patients who have formally met diagnostic criteria. Historically, the focus has been on depression.  However, elevated symptoms of anxiety are much more common than elevated symptoms of depression. It is important to make the distinction between “Generalized Anxiety,” and “Heart-Focused Anxiety.” Heart-Focused Anxiety: symptoms of anxiety directly related to having a heart condition, such as fear of appointments / worry about a decline in health status, getting an ICD, preparing for surgery, transplants, or having a shortened life expectancy, etc. This may also include a significant component of health uncertainty – the idea that patients are aware of need for a likely intervention but without ability to prognosticate timelines (e.g. need for valve replacement). This component differentiates CHD patients from those with acquired heart disease who have not been surrounded by such uncertainty for significant components of their life. Generalized Anxiety: excessive worry about a lot of factors beyond their control and accompanied by other symptoms like: muscle tension, sleep disturbance. Manifestations of mood and behavioral health problems include: impaired peer relationships, impaired romantic relationships, poor school or work performance, difficulty getting or keeping a job.  Persons may struggle with inconsistent medical follow-up, inconsistent compliance, and substance abuse. Predictors & Prevalence of Depression / Anxiety: Defect Severity (mild, moderate, great complexity) was not associated with depression or anxiety. Similarly, physician diagnosed NYHA Class was not associated with depression/anxiety [2]. Known predictors: patient-reported physical health status impacts symptoms of depression/anxiety [2].There is also a link between social wellbeing and psychological well-being. Other studies have highlighted that perceived health status is an important predictor. Risk Stratification All patients with congenital heart disease are at risk for mental health disorders and need to be screened. Those at heightened risk include patients with genetic syndromes (in particular, those with 22q11 deletion, associated with more severe psychiatric disorders), prematurity, longer hospital stays, and those with lower family socioeconomic status. Patients who have undergone cardiopulmonary bypass have higher likelihood of neurologic insults (CVA), but also cognitive dysfunction following surgery. In research, Apolipoprotein E has been predictive of neurodevelopmental dysfunction following cardiac surgery.  Other factors, including the number of surgeries, and how often they were separated from peers growing up might also impact mental health well-being in adults. Quality of Life (QoL) and Assessment Approach-IS Study International Study looking at patient-reported outcomes in adults with CHD. Over 4,000 patients from 15 countries were enrolled. Self-Reported Questionnaires administered to gain information on perceived health status, psychological functioning, health behaviors, quality of life (Scale 0-100) [9]  Patients have lived with CHD their entire life, and report relatively high QoL Older age, lack of employment, never having married, and worse NYHA functional class (self- reported) are associated with lower QoL Alternative Assessment for Nonverbal Patients: Concerns may come from caregivers or parents May demonstrate behavioral changes: outbursts, changes in feeding/eating habits or weight loss/gain, changes in sleeping patterns, fatigue, low mood, anhedonia Screening should begin early in childhood (early assessment and diagnosis allows for enrollment in beneficial social / developmental programs) Cardiac Neurodevelopmental Outcome Collaborative (CNOC): recommend screenings for various ages and provide suggested screening algorithms. Transition to Adult Teams: process that occurs during early adolescence Goals: stay in uninterrupted health care throughout their lives, avoid lapses in care, have an established process, allow patients to develop knowledge and skills to assume maximal responsibility for their healthcare management, and adapt information delivery as necessary The I <3 Change Website provides information for people transitioning from pediatric to adult cardiology teams Beginning in adolescence, pediatric provider is recommended to speak independently with their cardiologist at every visit. Transition is a family process: parents are involved in care and successful transition to help bridge the gap towards independence for the patient Strategies to Ensure Treatment Success Education is Key: Parents and caregivers need an understanding of what CHD concerns are, expected follow up needs, etc. Engage all stakeholders in Medical Home: home health aide, caregiver, primary care physician, etc. Utilize Screening Tools and Implement Routine Screening Refer to Mental Health Provider when Appropriate Embed mental health professional into the Team: identify providers who have an interest in mental health (psychologist / psychiatrist) who are qualified to treat patients with congenital heart disease Improves access and reduces stigma Allows for ease of access / rapid consultation Encourage appropriate physical activity: exercise and physical activity has physiologic and mental health benefit, improves mood, stress, anxiety, etc. Mental health benefit is present regardless of type / intensity / duration of activity Ask patients if they avoid particular activities and provide reassurance Offer opportunities for peer interaction: patient education sessions, etc. Provide Positive Reinforcement: comment on patients’ resilience and effective coping. Destigmatize It! Practice of carefully worded Key Sentences help to destigmatize mental health disorders: “Does thinking about your health every make you worried or depressed?” “How are you doing from a psychological perspective?” “I know that patients sometimes struggle with low mood or anxiety. If that ever happens to you, let me know, and we can discuss it.” References – Congenital Heart Disease and Psychosocial Wellbeing Gonzalez, V.J., et al., Mental Health Disorders in Children With Congenital Heart Disease. Pediatrics, 2021. 147(2). PubMed CrossRef Kovacs, A.H., et al., Depression and anxiety in adult congenital heart disease: predictors and prevalence. Int J Cardiol, 2009. 137(2): p. 158-64. PubMed  CrossRef Gaynor, J.W., et al., Validation of association of the apolipoprotein E ε2 allele with neurodevelopmental dysfunction after cardiac surgery in neonates and infants. J Thorac Cardiovasc Surg, 2014. 148(6): p. 2560-6. PubMed CrossRef Schmithorst, V.J., et al., Organizational topology of brain and its relationship to ADHD in adolescents with d-transposition of the great arteries. Brain Behav, 2016. 6(8): p. e00504. PubMed CrossRef Cassidy, A.R., et al., Executive Function in Children and Adolescents with Critical Cyanotic Congenital Heart Disease. J Int Neuropsychol Soc, 2015. 21(1): p. 34-49. PubMed CrossRef Kolaitis, G.A., M.G. Meentken, and E. Utens, Mental Health Problems in Parents of Children with Congenital Heart Disease. Front Pediatr, 2017. 5: p. 102. PubMed CrossRef Boukovala, M., et al., Effects of Congenital Heart Disease Treatmenton Quality of Life. Am J Cardiol, 2019. 123(7): p. 1163-1168. PubMed CrossRef Müller, J., J. Hess, and A. Hager, Sense of coherence, rather than exercise capacity, is the stronger predictor to obtain health-related quality of life in adults with congenital heart disease. Eur J Prev Cardiol, 2014. 21(8): p. 949-55. PubMed CrossRef Apers, S., et al., Assessment of Patterns of Patient-Reported Outcomes in Adults with Congenital Heart disease – International Study (APPROACH-IS): rationale, design, and methods. Int J Cardiol, 2015. 179: p. 334-42. PubMed CrossRef 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. A curated library of conference and grand rounds recordings for continuing medical education. Learn more at www.heartuniversity.org/ CardioNerds Adult Congenital Heart Disease Production Team Amit Goyal, MD Daniel Ambinder, MD

CardioNerds (Amit Goyal and Dan Ambinder) join Dr. Radi Zinoviev, Dr. Josh Cohen, and Dr. Tiffany Dong (CardioNerds Ambassador) from the Cleveland Clinic for a day on Edgewater beach. They discuss the following case of the evaluation and management of prosthetic tricuspid valve stenosis in a patient with a history of Ebstein Anomaly. The expert commentary and review (ECPR) is provided by Dr. Jay Ramchand, staff cardiologist with expertise in multimodality cardiovascular imaging at the Cleveland Clinic. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. This episode is supported by the 5th Annual Going Back to the Heart of Cardiology (A MedscapeLIVE Conference). Join co-chairs Dr. Robert Harrington and Dr. Fatima Rodriguez January 24-26, 2025 at the Fontainebleau Hotel in Miami Beach, Florida. The agenda will explore the latest advancements in cardiology including cardiovascular prevention, atherosclerosis and thrombosis, cardiovascular dysfunction, arrhythmias, and valvular heart disease. Network, attend engaging presentations by renowned cardiologists, visit the exhibit and poster hall, participate in an exclusive immersive experience, and earn up to 13 CME/CE credits. Register today with code CARDIONERDS for 30% OFF your registration. Click here for more information. Jump to: Case media – Case teaching – 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 CXR ECG TTE RHC Final TTE TTE 1 TTE 2 TTE 3 Follow up TTE 1 Follow up TTE 2 Episode Schematics & Teaching Pearls – Tricuspid Valve Stenosis Tricuspid stenosis is uncommon (<1% of the US population) and thus we have a lack of evidence as well as guideline recommendations. While there are no official diagnostic criteria for severe tricuspid stenosis, some echocardiographic features include flow acceleration across the valve, a mean pressure gradient of ≥ 5mmHg and an inflow VTI of > 60cm. Structural findings that support the presence of severe tricuspid stenosis include a moderately dilated RA and a dilated IVC, though these are not specific. Right heart catheterization hemodynamics that support tricuspid stenosis include a high right atrial pressure and gradual “y” descent. Bioprosthetic tricuspid valves are generally favored over mechanical valves due to risk of thrombosis and longevity of these valves in the tricuspid position. Notes – Tricuspid Valve Stenosis What are causes of tricuspid stenosis? Causes of tricuspid stenosis can be divided into congenital and acquired causes. Congenital causes include tricuspid atresia or stenosis. Acquired causes include rheumatic heart disease, carcinoid syndrome, endocarditis, prior radiation, or fibrosis from endomyocardial procedures or placement of electrical leads. Rheumatic heart disease is the most common cause of tricuspid stenosis and is usually associated with mitral valvulopathy. What are the symptoms and physical exam findings of tricuspid stenosis? Findings revolve around right sided congestion or heart failure symptoms such as peripheral edema, abdominal distension with ascites, hepatomegaly, and jugular venous distension. When examining the jugular vein, you may see prominent a-waves and an almost absent or slow y descent reflective of delayed emptying of the right atrium (in the absence of tricuspid regurgitation). The murmur of tricuspid stenosis includes an opening snap and low diastolic murmur at the left lower sternal border with inspiratory accentuation. Patients may also report fatigue due to decreased cardiac output from obstruction. On echocardiography, what are the features supportive of severe tricuspid stenosis? Qualitatively, the leaflets may be thickened with reduced mobility and there may be diastolic dooming of the valve. Doppler may show high gradients of ≥ 5 mmHg, which may be elevated if there is coexisting tricuspid regurgitation and lower with decreased cardiac output. Associated structural changes include dilated right atrium and inferior vena cava. What is expected on right heart catheterization for tricuspid stenosis? Assuming the patient remains in sinus rhythm, patients with tricuspid stenosis would display high right atrial pressures and a gradual “y” descent. A diastolic gradient may be measured with dual catheters in the right atrium and the right ventricle. What are the treatment options for tricuspid stenosis? Medical management of tricuspid stenosis includes diuretics and addressing the underlying cause. Intervention is indicated for symptomatic severe tricuspid stenosis although the current 2020 ACC/AHA Valve Guidelines do not address tricuspid stenosis. The 2014 ACC/AHA guidelines give a class I indication for tricuspid stenosis surgery during left sided surgery while there is a class I indication for isolated tricuspid stenosis if symptomatic. Percutaneous options include balloon valvotomy while those who are surgical candidates are eligible for valve repair or replacement. Surgical options include repair or replacement with bioprosthetic favored over mechanical given the latter’s susceptibility to thrombosis. References – Tricuspid Valve Stenosis Nishimura, R. A., et al. (2014). “2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.” Circulation 129(23): 2440-2492. Otto, C. M., et al. (2021). “2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.” Circulation 143(5): e35-e71.