Cardionerds: A Cardiology Podcast

This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Sections 4.3.2 and 4.4 of the 2025 ACS Guidelines. The question is asked by Thomas Jefferson medical student and CardioNerds Academy Intern Dr. Grace Qiu, answered first by University of Miami cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Saahil Jumkhawala, and then by expert faculty Dr. Binita Shah. Dr. Binita Shah is an associate professor of medicine, interventional cardiologist, Director for research in Interventional Cardiology, and Director of the Department of Medicine Clinical Investigator Track at NYU. She is also an associate director of interventional cardiology and director of the transcatheter valve program at the VA New York Harbor Healthcare System. She was a member of the 2025 ACS Guidelines writing committee. Question #4 A 78-year-old man with a history of hypertension and controlled type 2 diabetes presents to a rural emergency department with 90 minutes of persistent, crushing, substernal chest pain. His ECG reveals 3-mm STE in leads V1 through V4. The nearest PCI-capable center is approximately 140 minutes away by ground transport, and air transport is unavailable due to weather. The patient refuses transfer to another facility for the duration of this admission. The clinical team decides to proceed with fibrinolytic therapy using weight-based Tenecteplase (TNK). Which of the following is the most appropriate initial antithrombotic regimen to accompany the fibrinolytic agent? A Clopidogrel 300 mg loading dose; Enoxaparin 30 mg IV bolus followed by 1.0 mg/kg SC every 12 hours. B Clopidogrel 75 mg (no loading dose); Enoxaparin 0.75 mg/kg SC every 12 hours (no IV bolus). C Ticagrelor 180 mg loading dose; Unfractionated heparin (UFH) weight-based IV bolus and infusion. D Prasugrel 10mg (no loading dose); Fondaparinux 2.5 mg IV bolus followed by 2.5 mg SC daily. Answer #4 Explanation (3-8 min to read) The correct answer is B.  Clopidogrel is the only P2Y12 inhibitor with a Class 1 recommendation for use alongside fibrinolytic therapy to reduce death and MACE (Class 1, LOE A). Of note, pharmacodynamic variability in response to clopidogrel has been well described, and hyporesponders may be at increased risk of MACE and stent thrombosis when treated with clopidogrel after PCI. Other P2Y12 inhibitors such as ticagrelor and prasugrel are more potent than clopidogrel and achieve more rapid onset of inhibition of platelet activation but with increased risk of bleeding compared with clopidogrel. When administered concurrently with fibrinolytic as the reperfusion strategy, clopidogrel is recommended to be administered with a loading dose (300 mg, then 75 mg daily) for patients <75 years of age and starting without a loading dose (75 mg daily) for patients ≥75 years of age. In patients treated with a fibrinolytic agent who are undergoing subsequent PCI, either clopidogrel or ticagrelor (age <75 years, within 24 hours after a fibrinolytic agent) or prasugrel (>24 hours after a fibrinolytic agent) are alternatives to support PCI.  Parenteral anticoagulation is recommended for all patients with ACS, irrespective of the initial treatment strategy, to treat the underlying pathophysiologic process (coronary atherothrombosis) and reduce the risk of recurrent MACE. The choice of a parenteral anticoagulant can be complex because it is influenced by various factors, including vascular access site, renal function, and concomitant use of other antiplatelet or anticoagulant agents. In patients with STEMI treated with fibrinolytic therapy, parenteral anticoagulation is recommended before and after fibrinolytic therapy to reduce ischemic events. In patients with STEMI who received fibrinolytic therapy and who are not planned for an invasive approach (as with the patient in the question stem), enoxaparin is the preferred anticoagulant over UFH. In the ExTRACT-TIMI 25 study, enoxaparin until hospital discharge or for a maximum of 8 days (whichever came first) was compared with UFH administered for at least 48 hours. The primary endpoint of death or nonfatal recurrent MI through 30 days occurred in 12% in the UFH group compared with 9.9% in the enoxaparin group. In a meta-analysis of 14 randomized trials, UFH did not reduce reinfarction or death in patients treated with fibrinolytic therapy. In contrast, low-molecular- weight heparin reduced the risk of reinfarction and death compared with placebo and the risk of reinfarction.  In patients >75 years of age, the dosing must be modified: Omit the initial 30 mg IV bolus. Reduce the subcutaneous dose to 0.75 mg/kg (instead of the standard 1.0 mg/kg). The first two SC doses should also be capped at a maximum of 75 mg each. After receiving the fibrinolytic and adjusted antithrombotics, the patient should be transferred to a PCI center to facilitate immediate or early catheterization depending on the clinical circumstances, if this is in-line with the patient’s wishes. Hospitals should have transfer protocols in place to allow for a seamless transfer to the PCI-capable facility as soon as it is safe to do so. A detailed assessment of clinical status is critical to determine the timing of angiography.  A is incorrect: This is the standard dose for patients under 75 years of age. In a 78-year-old, the IV bolus of Enoxaparin and the Clopidogrel load significantly increase the risk of a fatal brain bleed. B is incorrect: Ticagrelor is not recommended as an adjunct to fibrinolysis in the 2025 ACS guidelines. D is incorrect: While fondaparinux may be used alongside lytic therapy when not planning an invasive strategy, prasugrel does not have a Class 1 recommendation for use with fibrinolytic therapy. Main Takeaway – Clopidogrel is the only P2Y12 inhibitor with a Class 1 recommendation for use alongside fibrinolytic therapy Guideline Loc. Sections 4.3.2 and 4.4 Table 10  

This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes.  The following question refers to Section 3.2 of the 2025 ACS Guidelines. The question is asked by Thomas Jefferson medical student and CardioNerds Academy Intern Dr. Grace Qiu, answered first by Cleveland Clinic interventional and structural cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Eunice Dugan, and then by expert faculty Dr. Binita Shah. Dr. Binita Shah is an associate professor of medicine, interventional cardiologist, Director for research in Interventional Cardiology, and Director of the Department of Medicine Clinical Investigator Track at NYU. She is also an associate director of interventional cardiology and director of the transcatheter valve program at the VA New York Harbor Healthcare System. She was a member of the 2025 ACS Guidelines writing committee. Question #3 A 55-year-old woman is brought to the Emergency Department after an out-of-hospital cardiac arrest. She had a witnessed collapse with an initial shockable rhythm. Return of Spontaneous Circulation (ROSC) was achieved after 15 minutes of Advanced Cardiac Life Support (ACLS). Her post-resuscitation ECG shows diffuse ST-segment depression but no ST-segment elevation. She remains comatose. Which of the following is the most appropriate next step in her management regarding coronary angiography? A Immediate emergency coronary angiography (within 2 hours) should be performed. B Routine emergency coronary angiography is not recommended in the absence of ST-segment elevation or hemodynamic instability. C Coronary angiography should be delayed for at least 72 hours to allow for neurological recovery. D Fibrinolytic therapy should be administered immediately if the patient cannot reach a cath lab within 90 minutes. Answer #3 Explanation The correct answer is B. In resuscitated patients who are comatose after cardiac arrest, electrically and hemodynamically stable, and without evidence of STEMI, immediate angiography is not recommended due to lack of benefit (Class 3: No Benefit; LOE A) Patients who have been resuscitated after cardiac arrest and are noncomatose or who are comatose with favorable prognostic features and with evidence of STEMI, should undergo PPCI to improve survival. (Class 1; LOE B-NR). For patients such as this one, a delayed or selective approach should be taken once the patient is stabilized. Early angiography should not be denied solely based on a comatose state, but it should be deferred if there are clear non-cardiac causes for the arrest or if the patient’s overall prognosis is futile. A is incorrect because recent evidence shows no benefit to “emergency” PPCI for stable patients without ST-elevation. C is incorrect because while we wait for stability, we don’t necessarily have a fixed 72-hour “mandatory” delay for the heart if ischemia is suspected. D is incorrect, as fibrinolysis is generally not indicated for post-arrest patients without clear STEMI and carries risks in a post-CPR setting due to potential trauma. The MIRACLE2 Score is a tool for neuroprognostication. It helps clinicians estimate the likelihood of a poor neurological outcome at 6 months. A high score suggests that the benefit of an invasive procedure may be outweighed by the severity of the brain injury. Components of MIRACLE2: M – Missed (unwitnessed) arrest I – Initial non-shockable rhythm R – Reactive pupils at ROSC A – Age (points increase significantly at >60 and >80) C – Rhythm change (e.g., VF to PEA) L – Low pH (pH < 7.20) E – Epinephrine (any dose given) Clinical Threshold: A score of >5 indicates a high risk of poor neurological recovery, which may lead a Heart Team to favor stabilization over immediate emergency angiography in patients without ST-elevation. Early recognition of STEMI in resuscitated patients and direct transfer to a PCI-capable center is associated with improved survival. Survival-to-hospital discharge in the patient who is comatose with out-of-hospital cardiac arrest is <10% regardless of etiology. Those with a witnessed arrest and a shockable rhythm have improved survival.  Outcomes for patients with STEMI who are awake after resuscitated cardiac arrest are comparable to patients with STEMI who were not in cardiac arrest. For this reason, patients with cardiac arrest who have achieved return of spontaneous circulation (ROSC) and are awake with STEMI on ECG are candidates for PPCI. However, care should be individualized in the comatose patient with rapid assessment of the patient’s clinical features and cardiac arrest characteristics before proceeding with invasive angiography. In contrast, patients who are stable without ST-segment elevation after out-of-hospital cardiac arrest do not require immediate coronary angiography. Coronary angiography in this setting can be deferred pending further risk stratification. Main Takeaway Patients with cardiac arrest and STEMI who have been resuscitated should preferentially be transferred by EMS to a PPCI-capable center. Certain prognostic scores can help risk stratify patients prior to catheterization. Guideline Loc. Section 3.2. Management of Patients Presenting With Cardiac Arrest

CardioNerds (Drs. Dr. Natalie Marrero, Dr. Ritika Tuli, and Dr. Rafael Toro Manotas) discuss multimodality imaging for risk stratification, evaluation, and management of chronic coronary artery disease with Dr. Panithaya Chareonthaitawee. Audio editing by CardioNerds intern Iman Razeghian. This episode was produced as part of the CardioNerds Academy curriculum by House Taussig under the guidance of House Chief, Dr. Natalie Marrero and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course. In this episode, we discuss the pathophysiology and risk stratification of chronic coronary artery disease (CAD), as well as the current landscape of non-invasive evaluation of this condition. CAD remains a leading cause of morbidity and mortality despite advances in pharmacological and non-pharmacological strategies for the prevention and treatment of atherosclerotic disease. The concept of chronic CAD has shifted from the traditional model of stable, obstructive, flow-limiting disease, toward the current understanding of a dynamic process that extends beyond obstructive epicardial lesions to include non-obstructive plaque, diffuse atherosclerosis, and microvascular disease. Similarly, the imaging modalities used to evaluate CAD have evolved, and clinicians now have an extensive menu of options, each with distinct advantages and limitations, that must be selected carefully to maximize diagnostic accuracy and optimize treatment guidance, while also considering resource availability, local expertise, and high-value care. By the end of the episode, listeners will understand the pathophysiology of chronic CAD, risk-stratify patients with suspected CAD, recognize the advantages and pitfalls of each non-invasive diagnostic modality, and select the most appropriate diagnostic tool for a given clinical scenario. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls: Chronic CAD is a complex process that extends beyond obstructive epicardial stenosis to include non-obstructive disease, dynamic plaque burden and ischemia, diffuse atherosclerosis, microvascular dysfunction, vasospasm, among others. When evaluating patients with suspected CAD, the diagnostic process should be guided by a specific and appropriate clinical question before ordering any tests. The current diagnostic tool arsenal is broadly divided into anatomic and functional imaging modalities. These are complementary, each with distinct properties and limitations, addressing different clinical questions and assessing different aspects of disease. Local availability and expertise, along with patient-specific considerations and contraindications, determine the choice of diagnostic modality. No single test is best for every patient. INOCA and coronary microvascular dysfunction represent a common and increasingly recognized entity that is diagnosable and treatable; initial evaluation includes non-invasive testing such as stress PET and stress CMR. References Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;144(22):e368-e454. doi:10.1161/CIR.0000000000001029 https://pubmed.ncbi.nlm.nih.gov/34709879/ Vrints C, Andreotti F, Koskinas KC, et al. 2024 ESC Guidelines for the management of chronic coronary syndromes. Eur Heart J. 2024;45(36):3415-3537. doi:10.1093/eurheartj/ehae177 https://pubmed.ncbi.nlm.nih.gov/39210710/ Virani SS, Newby LK, Arnold SV, et al. 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2023;148(9):e9-e119. doi:10.1161/CIR.0000000000001168 https://pubmed.ncbi.nlm.nih.gov/37471501/ Edvardsen T, Asch FM, Davidson B, et al. Non-Invasive Imaging in Coronary Syndromes: Recommendations of The European Association of Cardiovascular Imaging and the American Society of Echocardiography, in Collaboration with The American Society of Nuclear Cardiology, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2022;35(4):329-354. doi:10.1016/j.echo.2021.12.012 https://pubmed.ncbi.nlm.nih.gov/35379446/ Douglas PS, Hoffmann U, Patel MR, et al. Outcomes of anatomical versus functional testing for coronary artery disease. N Engl J Med. 2015;372(14):1291-1300. doi:10.1056/NEJMoa1415516 https://pubmed.ncbi.nlm.nih.gov/39210710/ Sharma A, Coles A, Sekaran NK, et al. Stress Testing Versus CT Angiography in Patients With Diabetes and Suspected Coronary Artery Disease. J Am Coll Cardiol. 2019;73(8):893-902. doi:10.1016/j.jacc.2018.11.056 https://pubmed.ncbi.nlm.nih.gov/30819356/ SCOT-HEART Investigators, Newby DE, Adamson PD, et al. Coronary CT Angiography and 5-Year Risk of Myocardial Infarction. N Engl J Med. 2018;379(10):924-933. doi:10.1056/NEJMoa1805971 https://pubmed.ncbi.nlm.nih.gov/30145934/ Li Z, Xu T, Wang Z, et al. Prognostic Significance of Computed Tomography-Derived Fractional Flow Reserve for Long-Term Outcomes in Individuals With Coronary Artery Disease. J Am Heart Assoc. 2025;14(2):e037988. doi:10.1161/JAHA.124.037988 https://pubmed.ncbi.nlm.nih.gov/39791423/ Bateman TM, Al-Mallah MH, et al. Clinical indications for positron emission tomography myocardial perfusion imaging and myocardial blood flow quantification: An American Society of Nuclear Cardiology position statement. J Nucl Cardiol. 2026;57:102619. doi:10.1016/j.nuclcard.2025.102619 https://pubmed.ncbi.nlm.nih.gov/41482140/ Taqueti VR, Di Carli MF. Coronary Microvascular Disease Pathogenic Mechanisms and Therapeutic Options: JACC State-of-the-Art Review. J Am Coll Cardiol. 2018;72(21):2625-2641. doi:10.1016/j.jacc.2018.09.042 https://pubmed.ncbi.nlm.nih.gov/30466521/ Taqueti VR, Hachamovitch R, Murthy VL, et al. Global coronary flow reserve is associated with adverse cardiovascular events independently of luminal angiographic severity and modifies the effect of early revascularization. Circulation. 2015;131(1):19-27. doi:10.1161/CIRCULATIONAHA.114.011939 https://pubmed.ncbi.nlm.nih.gov/25400060/ Mehta PK, Huang J, Levit RD, Malas W, Waheed N, Bairey Merz CN. Ischemia and no obstructive coronary arteries (INOCA): A narrative review. Atherosclerosis. 2022;363:8-21. doi:10.1016/j.atherosclerosis.2022.11.009 https://pubmed.ncbi.nlm.nih.gov/36423427/ Kunadian V, Chieffo A, Camici PG, et al. An EAPCI Expert Consensus Document on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary Pathophysiology & Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group. EuroIntervention. 2021;16(13):1049-1069. doi:10.4244/EIJY20M07_01 https://pubmed.ncbi.nlm.nih.gov/32624456/

CardioNerds (Dr. Apoorva Gangavelli, Dr. Cory Sejo, and Dr. Joseph Kassab), discuss tricuspid regurgitation evaluation and management with Dr. Sunil Mankad. This episode was produced as part of the CardioNerds Academy curriculum by House Einthoven under the guidance of House Chief, Dr. Apoorva Gangavelli and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course.  Audio editing by CardioNerds intern Emma Winakur. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Key Points: Tricuspid regurgitation is common and associated with increased mortality at every stage, regardless of etiology. Outcomes are worse with worsening severity, so accurate grading is critical. Etiology is critical to guide treatment decisions. Etiology includes primary vs secondary (atrial or ventricular) vs CIED-related TR. 3D echocardiography can be very helpful in determining TR etiology, especially in CIED-related TR. Diuresis with the goal of euvolemia is step one. Additionally, underlying contributory conditions (eg. pulmonary HTN, HFrEF, atrial fibrillation) should be addressed, if appropriate, and then TR severity reassessed. The choice between T-TEER and TTVR hinges on anatomy, RV function, pulmonary hypertension, and the ability to tolerate anticoagulation. T-TEER is generally first line in atrial functional TR with appropriate anatomy, in patients with poor RV function who cannot tolerate a sudden increase in RV afterload, or in patients who cannot tolerate the necessary anticoagulation with TTVR. TTVR is preferred with wide coaptation gaps and CIED-related TR. This is a team sport. Multidisciplinary discussions utilizing imaging (TTE/TEE, CT), risk scores (TRI-SCORE or TRIO), patient preference, and prior institutional experience are essential for the effective treatment of severe TR. Notes: What is the clinical importance of tricuspid regurgitation? TR is very common with approximately 4% of people over 75 having moderate or greater severity. TR (even mild) is associated with increased mortality. Those outcomes worsen as the TR severity worsens, and this phenomenon is independent of the mechanism of regurgitation. What is unique about the tricuspid valve compared to the other cardiac valves? It is at an anterior location which allows it to be imaged well with transthoracic echocardiography It is the largest valve and composed generally of 3 leaflets (but very often can have 4+ leaflets). Importantly, the RV is compliant and changes size and shape readily based on loading conditions. The TV annulus similarly changes size and shape based on hemodynamic conditions such as preload. What is a good framework for approaching the causes of tricuspid regurgitation? Determine the presence and define the severity of TR. Using TTE, we want to measure the right atrial size, the RV size, and any other concomitant valvular lesions.  Use TTE (2D and 3D) to characterize leaflet anatomy and characteristics. Subtypes of TR mechanisms (many times etiology is mixed). Primary: primary leaflet abnormality, occurs in ~10% of cases. Look for prolapse, flail, endocarditis, etc. Secondary/functional: leaflets normal but surrounding structures are abnormal. Atrial: RA and tricuspid annular dilation but normal RV size/shape, and can be related to arrhythmias like atrial fibrillation. Ventricular: RV dilated and/or dysfunctional with leaflet tethering. Can be related to pulmonary hypertension or primary RV disease. Cardiac implantable electronic device (CIED): Related to device (usually pacemakers or ICD) interaction with TV leaflets. Includes perforation, entanglement in subvalvular apparatus, impingement, etc. 3D TTE particularly helpful to evaluate How do we grade TR severity? It is very important to grade the severity of TR, and this is generally done with echocardiography. There are both quantitative and qualitative methods which use Doppler and various equations to estimate TR severity. Current recommendations have expanded TR severity beyond mild/moderate/severe to include “massive” and “torrential” categories. The most important parameters measured/calculated are vena contracta width, regurgitant volume, regurgitant fraction, and effective regurgitant orifice area. Helpful qualitative metrics include hepatic venous flow reversal. When should additional studies beyond transthoracic echocardiography, such as transesophageal echocardiography (TEE), cardiac computed tomography (CT), and cardiac magnetic resonance imaging (MRI) be pursued? TEE is particularly helpful if TTE views are poor. Since TEE is used during transcatheter intervention, a pre-procedure TEE to define anatomy, determine procedure candidacy, and plan for the procedure is critical.  CT is also helpful for procedure planning and has particular strengths in defining annulus size and geometry. A CT is required prior to transcatheter tricuspid valve replacement (TTVR). MRI is helpful for measuring RV volumes and function, but is not generally used to assess TR severity.  What is the approach to the treatment for severe tricuspid regurgitation? The first step is to try to determine the etiology. For secondary TR, treating the underlying condition is indicated. For example, pulmonary vasodilators for pulmonary HTN or guideline therapy for heart failure with reduced ejection fraction. Diuretics are the mainstay for treatment, with the goal to obtain euvolemia. This may require inpatient admission to optimize volume status and medication regimen. Once reversible etiologies are addressed, if the patient is still symptomatic from TR, additional therapies can be considered. What is the role of right heart catheterizations (RHC) in patients with severe TR? RHC is very helpful for many reasons. We use it in TR to help determine volume status, cardiac output, and RV function. Additionally, identifying and characterizing pulmonary hypertension (with pulmonary artery pressures and calculating pulmonary vascular resistance) is an important factor when choosing future therapies.  With severe tricuspid regurgitation, when should we refer for intervention (either with surgery or transcatheter repair or replacement)? Once reversible etiologies are addressed and euvolemia has been achieved, if the patient is still symptomatic from TR despite aggressive medical optimization, additional therapies can be considered. Once euvolemic, a repeat TTE should be ordered to reassess the severity of the TR. Use calculators (for example, either the TRI-SCORE or TRIO score) to predict operative mortality for isolated TR surgery. What are our transcatheter treatment options in severe tricuspid regurgitation, and how do we choose between them? The primary approved transcatheter treatment options for severe TR include transcatheter tricuspid edge-to-edge repair (T-TEER) and transcatheter tricuspid valve replacement (TTVR), of which the Edwards EVOQUE valve is the only one currently approved by the FDA. There are other TTVR device under investigation. These decisions should be made with a multi-disciplinary team including representation from cardiac imaging, interventional cardiology, and cardiothoracic surgery. Factors that go into the decision between T-TEER and TTVR include anatomy (annulus width, coaptation gap, leaflet length), RV reserve, pulmonary hypertension presence, ability to tolerate anticoagulation, patient preference, and institutional experience.  T-TEER is generally the first line with atrial functional and suitable anatomy. It is successful at reducing TR but does not generally eliminate it.  TTVR with EVOQUE is preferred in certain anatomic considerations like a large coaptation gap or when there is CIED-related TR (as this was excluded in T-TEER trials). Patients must be suitable for anticoagulation to receive TTVR as there is risk of leaflet thrombosis without it. If moderate/severe pulmonary hypertension is present, or there is poor RV function, TTVR may be avoided as the sudden elimination of TR causes a sudden increase in RV afterload which may not be tolerated. What is the role in advanced metrics for evaluating RV function? Advanced metrics like RV/PA coupling are under investigation but have not made it into the guidelines. The clinical utility is not yet known.  Assessing the RV function is important as stated above. Dr. Mankad prefers using 3D TTE to calculate an RVEF, or tracking RV longitudinal free wall strain. If you do encounter CIED-related TR, how do you treat it? Evaluate with TTE or TEE. 3D is very helpful to identify relative anatomy and leaflet-device interactions. There is no clear consensus about treatment if CIED-related TR is the primary mechanism of severe TR. If recently implanted, repositioning may be a valid option, but requires discussions with multiple teams including electrophysiology, advanced cardiac imaging, CT surgery, and interventional cardiology. References O’Gara PT, Lindenfeld J, Hahn RT, et al. 10 Issues for the Clinician in Tricuspid Regurgitation Evaluation and Management: 2025 ACC Expert Consensus Decision Pathway. J Am Coll Cardiol. 2025;S0735-1097(25)07047-0. O’Gara PT, Little SH, Badhwar V, et al. Operator and Institutional Recommendations and Requirements for Tricuspid Interventions: 2026 ACC/AHA/ASE/HRS/STS Expert Consensus Systems of Care Document. J Am Coll Cardiol. 2026;S0735-1097(26)05481-1. Hahn RT. Tricuspid Regurgitation. N Engl J Med. 2023;388(20):1876-1891. Davidson LJ, Tang GHL, Ho EC, et al. The Tricuspid Valve: A Review of Pathology, Imaging, and Curr

CardioNerds (Dr. Apoorva Gangavelli, Dr. Rebecca Garber, and Dr. Tina Reddy), discuss pre-pregnancy risk stratification and counseling with Dr. Katie Young across a range of risks.  This episode was produced as part of the CardioNerds Academy curriculum by House Einthoven under the guidance of House Chief, Dr. Apoorva Gangavelli and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course. Audio editing by CardioNerds intern, Dr. Patrick Pekyi-Boateng. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Notes:  Why is pregnancy considered a “physiologic stress test,” and why does risk extend beyond delivery? Blood volume, heart rate, and cardiac output rise while systemic vascular resistance falls, peaking in the late second/early third trimester; underlying (even undiagnosed) heart disease can be unmasked or worsened. Postpartum (“fourth trimester”) is a high-risk period, not a safe zone – fluid shifts, rising SVR, and bleeding risk can precipitate decompensation in patients with heart failure, pulmonary hypertension, valvular disease, or aortopathy. Adverse pregnancy outcomes (hypertensive disorders, gestational diabetes, preterm birth, fetal growth restriction, peripartum cardiomyopathy) are markers of future cardiovascular risk and warrant long-term preventive follow-up. What is the practical framework for approaching pre-pregnancy cardiovascular risk? Four broad categories: (1) patients who may need cardiac screening before pregnancy, (2) patients needing risk-factor/medication optimization, (3) known cardiovascular disease where pregnancy is reasonable with structured risk stratification, and (4) high-risk disease where pregnancy may need to be delayed, modified by intervention, or discouraged. Testing should be targeted, not blanket – reserved for symptoms, abnormal exam, concerning family history, or reduced functional capacity. How is risk stratified in patients with known cardiovascular disease? Use a combination of tools per 2025 ESC guidelines: mWHO 2.0 (broad maternal risk category), CARPREG II (additional predictors of maternal cardiac events), and ZAHARA (useful in congenital heart disease). Key lesion-specific factors: aortic size/growth, valve severity, ventricular function, symptoms, blood pressure, and family history of dissection. Translate risk into practical terms for patients rather than leading with a numerical score. Which cardiovascular medications require review before conception? ACE inhibitors, ARBs, and ARNIs should be transitioned off before pregnancy; statins, MRAs, and SGLT2 inhibitors also need review. DOACs are contraindicated in pregnancy and lactation; mechanical valve anticoagulation requires individualized shared decision-making, as no strategy is risk-free for mother and fetus. Medication changes are best made proactively, before conception, rather than reactively. This is not an exhaustive list! The medication list needs to be reviewed carefully. Which conditions carry high or prohibitive risk in pregnancy? Pulmonary arterial hypertension, Eisenmenger syndrome, severe ventricular dysfunction, prior peripartum cardiomyopathy with residual LV dysfunction, severe left-sided obstructive valve disease (e.g., severe mitral stenosis), mechanical valves, significant aortopathy, cyanotic congenital heart disease, and Fontan physiology. Common theme: limited cardiovascular reserve and high risk of decompensation, thrombosis, arrhythmia, heart failure, aortic dissection, or death. These patients need expert multidisciplinary evaluation before pregnancy. Severe mitral stenosis is poorly tolerated because tachycardia shortens diastolic filling time and raises left atrial pressure, risking pulmonary edema and decompensation. When should genetic testing or counseling be offered? Consider when a diagnosis may be inherited or affect the patient, pregnancy, or family members: inherited cardiomyopathies, aortopathies, channelopathies, select congenital heart disease, and some pulmonary hypertension syndromes. Recurrence risk of congenital heart disease in offspring is roughly 6-10% when the mother has CHD; fetal echocardiography should be offered. How should contraception be approached in high-risk cardiac patients? Frame contraception as part of the cardiac care and reproductive safety plan to prevent unplanned high-risk pregnancy. Long-acting reversible contraception is often preferred; progestin-only methods are generally safer than estrogen-containing options with thrombosis risk, pulmonary hypertension, or mechanical valves. What are key delivery-planning considerations for cardiac patients? Vaginal delivery is preferred unless there is an obstetric indication for cesarean or a specific cardiac reason (e.g., unstable maternal status, therapeutic INR) to avoid labor. Planning should address delivery location, anesthesia involvement, telemetry needs, fluid management, and postpartum monitoring, clearly communicated across the multidisciplinary team in advance. How should clinicians counsel patients when pregnancy is discouraged but strongly desired? Acknowledge the patient’s goals and the emotional weight of the conversation; separate the goal (family building) from the timeline (safety now vs. after optimization). If pregnancy remains prohibitively risky, discuss alternatives for family building and ensure adequate patient support. What are the key gaps and future directions in cardio-obstetric risk stratification? Current risk tools (mWHO, CARPREG II, ZAHARA) provide common language but do not fully capture functional status, prior pregnancy history, or how risk evolves over time. Future direction: individualized, dynamic risk prediction incorporating imaging, biomarkers, exercise capacity, and social drivers of health, with better long-term links between pregnancy complications and cardiovascular prevention. References 1. European Society of Cardiology. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. 2. Mehta LS, et al. Cardiovascular Considerations in Caring for Pregnant Patients: A Scientific Statement From the American Heart Association. Circulation. 2020;141:e884-e903. PMID: 32362133. doi:https://doi.org/10.1161/CIR.0000000000000772 3. ACOG Practice Bulletin No. 212. Pregnancy and Heart Disease. Obstet Gynecol. 2019;133(5):e320-e356. PMID: 31022123. doi:https://doi.org/10.1097/AOG.0000000000003243