Cardionerds: A Cardiology Podcast

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

  1. 17h ago

    475. Case Report: The Walls Have a Story: Rapidly Progressive AL Cardiac Amyloidosis – Georgetown/Washington Hospital Center

    CardioNerds guest hosts Dr. Apoorva Gangavelli and Dr. Georgia Vasilakis, alongside Dr. Flavia Tejada, Dr. Ahmad Ahmad, and Dr. Blanca Simon Frances from MedStar Washington Hospital Center/Georgetown University for a case discussion on rapidly progressive heart failure and the urgency of recognizing infiltrative cardiomyopathy. They discuss a 65-year-old man with newly diagnosed HFrEF and CKD who presented with acute decompensated heart failure, low-voltage ECG, concentric LV thickening, renal dysfunction, and abnormal lambda free light chains. His course was complicated by PEA arrest when laid supine, cardiogenic shock physiology, bilateral pleural effusions, and biopsy-confirmed AL cardiac amyloidosis. The episode focuses on clinical red flags, diagnostic algorithms, hemodynamic fragility, and why suspected AL amyloidosis is a hematologic and cardiac emergency. Expert commentary is provided by Dr. Ajay Kadakkal. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. “To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Pearls The combination of low voltage on ECG and increased wall thickness on echocardiogram should always raise suspicion for an infiltrative cardiomyopathy, not hypertensive heart disease. A negative SPEP does not exclude a plasma cell dyscrasia; serum free light chains and urine immunofixation are required, and PYP should only be used to support a noninvasive ATTR diagnosis after a monoclonal process has been excluded. Nearly one in four ATTR patients have a coexisting MGUS, making serum markers alone insufficient to distinguish AL from ATTR; when cardiac involvement is suspected, endomyocardial biopsy remains the gold standard for confirming amyloid deposition. Preload dependence and low stroke volume in cardiac amyloidosis create extreme sensitivity to volume shifts and positional changes, requiring a much narrower margin of safety than typical heart failure. In advanced cardiac AL amyloidosis, delays in initiating anti-plasma cell therapy can rapidly narrow the therapeutic window, making urgent multidisciplinary coordination essential. Notes Notes were drafted by Dr. Flavia Tejada Frisancho, Dr. Ahmad Ahmad and Dr. Blanca Simon Frances. 1. What clinical features should raise suspicion for cardiac amyloidosis in a patient presenting with heart failure? Cardiac amyloidosis should be considered when the clinical picture does not behave like typical hypertensive, ischemic, or dilated cardiomyopathy. In this case, the key clue was pattern recognition: new heart failure, rapid progression, low-voltage ECG, severe concentric LV thickening, small LV cavity, biventricular dysfunction, renal dysfunction, pleural effusions, and abnormal light chains.  Shared cardiac red flags include increased LV wall thickness out of proportion to hypertension or valvular heart disease, diastolic dysfunction, biatrial enlargement, restrictive filling physiology, biventricular involvement, atrial fibrillation or conduction disease, elevated natriuretic peptides and troponin out of proportion to symptoms, and intolerance of standard heart failure therapies.  Extracardiac manifestations can provide important clues and include proteinuria, peripheral or autonomic neuropathy, bilateral carpal tunnel syndrome, lumbar spinal stenosis, and spontaneous biceps tendon rupture.  AL-predominant clues include rapid clinical progression over weeks to months, fatigue, weight loss, nephrotic-range proteinuria or renal dysfunction, pleural effusions, hypotension or shock physiology, low-voltage ECG, and evidence of a monoclonal protein or abnormal serum free light chains.  Pathognomonic extracardiac findings for AL amyloidosis include macroglossia, periorbital purpura, and acquired factor X deficiency.  ATTR-predominant clues often evolve over years and include bilateral carpal tunnel syndrome, lumbar spinal stenosis, spontaneous biceps tendon rupture, aortic stenosis, and HFpEF with increased wall thickness. Low-voltage ECG can occur but is less common in ATTR than AL.  The key bedside teaching point is to lean into the inconsistency. Hypertension can cause LVH, but hypertension does not fully explain low voltage, rapid biventricular failure, renal dysfunction with monoclonal light chains, pleural effusions, and severe hemodynamic fragility.  2. Once cardiac amyloidosis is suspected, how should we approach the diagnosis? The diagnostic approach begins with suspicion and then immediately separates two pathways: rule out AL amyloidosis  evaluate for ATTR amyloidosis 3. Why is it so important to rule out AL amyloidosis early? AL amyloidosis is both a hematologic and cardiac emergency.  The underlying plasma cell clone produces misfolded immunoglobulin light chains that: deposit as amyloid fibrils  exert direct cardiotoxic effects on cardiomyocytes  Light chains impair lysosomal function, disrupt autophagy, increase oxidative stress, and contribute to progressive cellular injury and death.  Cardiac involvement is the primary determinant of prognosis in AL amyloidosis.  Risk stratification commonly incorporates: troponin  NT-proBNP  serum free light chain burden  Mayo staging systems use these biomarkers to estimate prognosis and identify patients at especially high early mortality risk.  Patients with advanced cardiac involvement can deteriorate over days to weeks, particularly when there is hypotension, markedly elevated NT-proBNP, elevated troponin, renal dysfunction, low output physiology.  Early hematology involvement is essential because treatment targets the plasma cell clone.  Daratumumab combined with bortezomib, cyclophosphamide, and dexamethasone (D-VCd) is now considered standard first-line therapy for newly diagnosed AL amyloidosis.  The addition of daratumumab has been associated with deeper, faster responses, improved organ outcomes and improved survival.  Treatment logistics matter. In advanced cardiac AL amyloidosis, delaying therapy until outpatient follow-up may be dangerous if the patient is unstable or has high-risk features.  The practical takeaway: once AL is suspected, do not wait for every outpatient test to return before escalating care. send the full monoclonal protein workup. involve hematology and amyloid specialists early. expedite tissue diagnosis and treatment planning. 4. How does cardiac amyloidosis affect hemodynamics and response to therapy? Amyloid infiltration produces restrictive cardiomyopathy characterized by: impaired ventricular compliance, elevated right- and left-sided filling pressures, low stroke volume, preload dependence, afterload intolerance, and limited ability to augment cardiac output. Because stroke volume is fixed, heart rate becomes an important contributor to cardiac output. Beta blockers, non-dihydropyridine calcium channel blockers, and aggressive vasodilators may be poorly tolerated, particularly in AL cardiac amyloidosis with hypotension or advanced restrictive physiology. Patients may appear profoundly volume overloaded while remaining severely forward-flow limited. This explains why diuresis can be difficult until perfusion improves, and why inotropes may produce a dramatic improvement in urine output in selected patients with low-output physiology. Right heart catheterization can help characterize the physiology. In this case, invasive hemodynamics showed elevated filling pressures and pulmonary hypertension due to left-sided disease: RA 12 mmHg, PA 58/26 mmHg, mean PA 39 mmHg, PCW 20 mmHg, and cardiac index approximately 2.2-2.3 L/min/m2. Positioning and respiratory mechanics matter. In this case, lying supine during renal ultrasound likely worsened respiratory mechanics in the setting of large pleural effusions and restrictive physiology, contributing to hypoxia and PEA arrest.  This case highlights how patients with cardiac amyloidosis can be extremely hemodynamically fragile. 5. What management principles are important once AL cardiac amyloidosis is suspected or confirmed? Management requires multidisciplinary coordination among Advanced Heart Failure, Hematology/Oncology, Nephrology, Critical Care, Pathology, and, when needed, amyloid specialty clinics. Supportive heart failure therapy centers on careful volume management. Loop diuretics are often needed, sometimes with sequential nephron blockade, but the margin between congestion and underfilling is narrow due to preload dependence.  Guideline-directed medical therapy for conventional HFrEF may be limited by hypotension, renal dysfunction, low stroke volume, and autonomic dysfunction. The goal is not to force standard HFrEF therapy when the physiology does not support it. Pleural effusions may be large and recurrent. Drainage can improve respiratory mechanics, but it does not treat the underlying restrictive cardiomyopathy or plasma cell disorder. For AL amyloidosis, definitive therapy targets the plasma cell clone. Cardiac stabilization and chemotherapy planning must proceed in parallel, because ongoing light-chain production can drive rapid organ injury even after temporary hemodynamic improvement. The major clinical pearl from this case is that AL cardiac amyloidosis should be

  2. 3d ago

    474. Cardiothoracic Surgery in Pulmonary Embolism with Dr. Joshua Goldberg

    In this episode, the CardioNerds (Dr. Dinu Balanescu, Dr. Billy Joe Mullinax, and Dr. Akiva Rosenzveig) take a deep dive into the world of the surgical management of pulmonary embolism (PE) with faculty expert, Dr. Joshua Goldberg. We start from the pathophysiology of PE and its impact on right ventricular, and thereby left ventricular, hemodynamics. We then discuss the management of high-risk PE and where catheter-based therapies, surgical management and mechanical circulatory support via ECMO find their roles. Dr. Goldberg also provides a historical overview of the evolution of the surgical management of PE. We conclude by briefly discussing the management of chronic thromboembolic pulmonary hypertension (CTEPH) as a long-term complication of PE. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes.  NOTE: this episode was recorded before the publication of the 2026 AHA/ACC Acute PE Guidelines. Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium.   Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Pulmonary Embolism Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Pearls: Beware of the RV death spiral. Hypotension occurs late in the acute PE pathophysiology as the LV function is preserved. A patient becomes hypotensive once all compensatory mechanisms have failed. Don’t just treat the clot. Support the RV as well and think more seriously about ECMO. One needs to be very careful intubating these patients, as sedating them will counteract many of the hemodynamic compensatory mechanisms and will lead to cardiac arrest.  With the increasing role of catheter-based therapies, surgery’s role in acute PE is becoming more nuanced. Surgery is most useful in those patients with predominantly subacute clot, which is difficult to extract via catheter-based therapies. Notes: Notes: Notes drafted by Dr. Akiva Rosenzveig. What is the hemodynamic consequences of high-risk PE and what is the Right ventricular (RV) “death spiral?” Sudden increase in RV afterload which leads to RV volume and pressure overload which leads to neurohormonal activation, increased oxygen demand and RV ischemia, reduced RV contractility leading to reduced left ventricular (LV) preload and reduced cardiac output What is the role of ECMO in acute PE? We need to focus on not only treating the clot but supporting the RV concurrently. This is analogous to supporting the LV with mechanical circulatory support while also opening the culprit coronary lesion in acute myocardial infarction related cardiogenic shock (AMI-CS). The reason why High-risk/Massive PE has historically had poor outcomes may be because treatment modalities focused on treating the clot and not supporting the RV as well. When is surgical embolectomy considered in the treatment of acute PE? With the increased role of catheter-based therapies, the role of surgery is narrowing to a more nuanced patient population. Surgery should be considered when we don’t have other treatment options. It remains especially useful in more subacute clots where it is more difficult to extract with catheter-based interventions. In those cases, surgical pulmonary embolectomy can be useful as you have direct visualization of the pulmonary arteries and its branches. What is the historical evolution of surgical management of PE? In the early 1900’s, the Trendelenburg procedure was performed but had a very high mortality rate. This was because they waited for the patients to decompensate and then once the patient was peri-arrest, they would take them urgently to the operating room, snare the aorta and pulmonary artery and open the artery and remove the clot. By manipulating the PA in this way they detrimentally increased the RV afterload on an already failing RV. In the 1930’s, John Gibbon started working on developing cardiopulmonary bypass. Now, surgeons can put the patient on cardiopulmonary bypass and create incisions on both the left and right pulmonary arteries to extract the clot. Can we be reassured if the patient does not have a saddle embolus? Contrary to what we are used to hearing, the lack of a saddle PE shouldn’t be comforting. The more distal clot is more concerning as that’s where there is more significant flow resistance. The saddle embolus takes up a small proportion of the PA cross-sectional area and, therefore, the flow obstruction does not come from there. References: Goldberg JB, Spevack DM, Ahsan S, et al. Survival and Right Ventricular Function After Surgical Management of Acute Pulmonary Embolism. J Am Coll Cardiol. 2020;76(8):903-911. doi:10.1016/j.jacc.2020.06.065 Goldberg JB, Giri J, Kobayashi T, et al. Surgical Management and Mechanical Circulatory Support in High-Risk Pulmonary Embolisms: Historical Context, Current Status, and Future Directions: A Scientific Statement From the American Heart Association. Circulation. 2023;147(9):e628-e647. doi:10.1161/CIR.0000000000001117 Delcroix M, Pepke-Zaba J, D’Armini AM, et al. Worldwide CTEPH Registry: Long-Term Outcomes With Pulmonary Endarterectomy, Balloon Pulmonary Angioplasty, and Medical Therapy. Circulation. 2024;150(17):1354-1365. doi:10.1161/CIRCULATIONAHA.124.068610

  3. 6d ago

    473. ACS Guidelines Question #11 with Dr. Venu Menon

    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 8.2 of the 2025 ACS Guidelines. The question is asked by Johns Hopkins pre-medical undergraduate and CardioNerds Academy Intern Joshua Khorsandi, answered first by University of Wisconsin cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Shikha Jha, and then by expert faculty Dr. Venu Menon. Dr. Menon is the Section Head of Clinical Cardiology, Director of the Cardiac Intensive Care Unit, and Program Director of Cardiology Fellowship at the Cleveland Clinic. He is the Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine. He was also a member of the 2025 ACS Guidelines writing committee. Question #11 A 58-year-old man with a past medical history of hypertension, hyperlipidemia, schizophrenia, atrial fibrillation (on apixaban), and prior tobacco use presents to the emergency department with chest tightness. ECG shows ST elevations in leads II, III, and aVF with reciprocal depressions in leads I and aVL. Emergency coronary angiography demonstrates 100% occlusion of the proximal RCA, and he undergoes PCI. Transthoracic echocardiogram afterward reveals normal LV function with inferior hypokinesis. On day 2, the patient experienced lightheadedness and has frequent melanic stools. His hemoglobin returns at 6 gm/dL (initial hemoglobin 11 g/dL). He undergoes EGD and colonoscopy with successful endoscopic treatment of a small gastric ulcer.  True or False: it is reasonable to administer 3-4 units of packed red blood cells for a goal Hb ≥ 10 g/dL. True False Answer #11 Explanation  The correct answer is True – it would be reasonable to administer 3-4 units of packed red blood cells for a goal Hb ≥ 10 g/dL. Anemia is common in patients with ACS and is associated with worse short- and long-term outcomes. Anemia is associated with adverse outcomes irrespective of whether the anemia is chronic and due to comorbid conditions, or acute and the result of bleeding related to antithrombotic therapy and/or invasive procedures. The adverse effects of anemia may be due to decreased myocardial oxygen delivery, increased myocardial oxygen demand due to increased cardiac output, or the avoidance of potentially beneficial antithrombotic drugs and/or procedures. Randomized trials in medically ill patients and those undergoing cardiac surgery have demonstrated similar or better outcomes with a restrictive transfusion strategy (targeting a blood hemoglobin level around 8 g/dL) than with a liberal transfusion strategy (targeting a blood hemoglobin level around 10 g/dL). However, randomized trial evidence for populations with ACS suggests possible clinical benefit for a more liberal transfusion strategy targeting a hemoglobin level above 10 g/dL compared with targeting a hemoglobin level above 7 g/dL to 8 g/dL  The MINT (Myocardial Ischemia and Transfusion) trial randomly assigned 3,504 patients with acute STEMI or NSTEMI and anemia with a blood hemoglobin level of 10 g/dL in patients with ACS and acute or chronic anemia to reduce cardiovascular events. Main Takeaway In patients with ACS and acute or chronic anemia, blood transfusion to achieve a hemoglobin level of more than 10 g/dL may be reasonable to reduce cardiovascular events. Guideline Loc. Section 10.2

  4. Oct 21

    471. ACS Guidelines Question #9 with Dr. Venu Menon

    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 9.2 of the 2025 ACS Guidelines. The question is asked by Johns Hopkins pre-medical undergraduate and CardioNerds Academy Intern Joshua Khorsandi, answered first by University of Wisconsin cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Shikha Jha, and then by expert faculty Dr. Venu Menon. Dr. Menon is the Section Head of Clinical Cardiology, Director of the Cardiac Intensive Care Unit, and Program Director of Cardiology Fellowship at the Cleveland Clinic. He is the Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine. He was also a member of the 2025 ACS Guidelines writing committee. Question #9 A 74-year-old man with past medical history significant for hyperlipidemia, obstructive sleep apnea, hypertension, tobacco use, type 2 diabetes mellitus, and chronic obstructive pulmonary disease presents to the emergency department with two days of chest tightness and worsening shortness of breath at rest. He is found to have ST elevations in the anterolateral leads. Emergent coronary angiography demonstrates 90% stenosis of proximal to mid LAD and he is treated with two drug-eluting stents. Transthoracic echocardiograms during hospitalization showed an LVEF of 25% with anterior and apical wall motion abnormalities. He is discharged on dual antiplatelet therapy along with metoprolol, valsartan, spironolactone, SGLT2 inhibitor, and rosuvastatin. At follow-up 3 months later, he reports home BP readings in 90s/50s mm Hg with intermittent shortness of breath and lightheadedness. Blood pressure in the office is 92/54 mmHg. ECG shows normal sinus rhythm with anterior Q waves, a narrow QRS, and no acute ST-segment or T-wave changes.  Repeat transthoracic echocardiogram shows an LVEF of 30%. What is the most appropriate next step? A Switch valsartan to sacubitril-valsartan B Consider implantable cardioverter defibrillator (ICD) placement C Consider cardiac resynchronization therapy  D Consider additional cardiac rehabilitation sessions Answer #9 Explanation  The correct answer is B – consider implantable cardioverter defibrillator (ICD) placement. Generally, arrhythmic complications increase both morbidity and mortality rates in patients after ACS. Patients who present with AMI with reduced LVEF (≤40%) have increased risk of new-onset atrial fibrillation, bradyarrhythmias, and ventricular arrhythmias. Ventricular arrhythmias are common after ACS and more common in patients with reduced LVEF. The MADIT II trial (Multicenter Automatic Defibrillator Implantation Trial) demonstrated a 31% reduction in all-cause mortality (HR, 0.69 [95% CI, 0.51-0.93]) for prophylactic implantation of a cardiac defibrillator in patients with an LVEF ≤30% who were at least 30 days after MI or 3 months after revascularization for MI and had an anticipated life expectancy longer than 1 year. A mortality benefit for prophylactic ICD implantation has also been shown in patients with an LVEF ≤35% and New York Heart Association class II or III HF symptoms, as well as in patients with inducible ventricular tachycardia or ventricular fibrillation and an LVEF ≤40%. This patient has an LVEF of 48 hours and within 40 days post-MI to improve survival (LOE 2a, LOE C-EO). Some may wonder about the use of a temporary wearable cardioverter-defibrillator after the initial presentation. In the VEST trial, this strategy did not significantly reduce the primary endpoint, a composite of sudden death or death from ventricular tachyarrhythmias at 90 days) in patients with AMI and LVEF ≤ 35%. Notably, there was a lower incidence of death from any cause in the wearable vest group compared to the no-device group and overall, greater benefit was seen in those who were compliant with the device. As such, use of a wearable cardioverter-defibrillator could be considered in high-risk patients with reduced LVEF as a bridge to consideration for the need for an ICD. Per the guidelines, in patients early after MI, usefulness of a temporary wearable cardioverter-defibrillator is uncertain in patients with an LVEF ≤35% to improve survival (COR 2b, LOE B-R). Main Takeaway In patients post MI, implantable cardioverter defibrillator (ICD) implantation is recommended in selected patients with an LVEF of less than or equal to 40% at least 40 days post MI and at least 90 days post revascularization to reduced death. Guideline Loc. Section 9.2

  5. Oct 20

    470. ACS Guidelines Question #8 with Dr. Venu Menon

    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 9.1 of the 2025 ACS Guidelines. The question is asked by Johns Hopkins pre-medical undergraduate and CardioNerds Academy Intern Joshua Khorsandi, answered first by Washington University cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Colin Martz, and then by expert faculty Dr. Venu Menon. Dr. Menon is the Section Head of Clinical Cardiology, Director of the Cardiac Intensive Care Unit, and Program Director of Cardiology Fellowship at the Cleveland Clinic. He is the Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine. He was also a member of the 2025 ACS Guidelines writing committee. Question #8 A 65-year-old female with no significant prior cardiac history presents to the emergency department with 3 days of chest tightness associated with shortness of breath. ECG demonstrates anterior ST-segment elevation with reciprocal depressions. Coronary angiography reveals 100% occlusion of the mid left anterior descending artery. She undergoes PCI of the LAD. Two days later, she develops worsening shortness of breath. Her HR is 115 and BP 95/50. Lungs are clear on auscultation. Cardiac examination is significant for a harsh systolic murmur at the left sternal border with a palpable thrill. Transthoracic echocardiogram showed ventricular septal rupture with left-to-right shunt and Qp:Qs estimated at 2.5:1. What is the best next step? A Continue medical management B Proceed with repeat coronary angiogram and right heart catheterization with shunt run C Percutaneous ventricular septal defect closure D Intra-aortic balloon pump placement and cardiac surgical consultation Answer #8 Explanation  The correct answer is D – placement of an intra-aortic balloon pump and CT surgical consultation. Timely reperfusion therapy has reduced the incidence of mechanical complications (ventricular septal rupture, mitral valve insufficiency due to papillary muscle infarction or rupture, or free wall rupture) after AMI. Although occasionally found incidentally, mechanical complications commonly present with recurrent or refractory chest pain or a new murmur accompanied by disproportionate heart failure, cardiogenic shock, or sudden cardiac death on clinical presentation within the first week after an AMI. Medical therapy alone is associated with high risk of early death; definitive surgical correction is frequently the treatment of choice. Mortality rates with surgery are highest in subjects with cardiogenic shock and in those requiring early emergency/urgent intervention after AMI. Observed mortality rates following delayed surgery (>7 days) are lower but patient selection and survivor bias contribute to this observation. The 2025 ACS guidelines give a Class 2a, LOE B-NR recommendation for the use of short-term MCS devices in patients with mechanical complications of ACS for hemodynamic stabilization and bridge to surgery. The availability of temporary MCS devices has led to increasing trends for delayed surgery due to concerns for the initial degree of extensive tissue destruction. Delayed surgical intervention may enable hemodynamic stabilization, lead to recovery of end-organ injury, and promote infarct tissue healing and maturation that could facilitate definitive repair. Percutaneous approaches toward repair have been used in patients with prohibitive surgical risk or contraindications to surgery as a primary or temporizing option in the setting of acute mitral regurgitation and ventricular septal rupture and remain an evolving area of investigation. This patient is not at prohibitive risk for surgery. Select patients with mechanical complications of ACS may be considered for cardiac transplantation or durable LVAD as a primary or bailout treatment strategy to improve survival.  No RCTs evaluate the role of transfer of patients with mechanical complications after MI to dedicated centers with cardiac surgical expertise. Although overall surgical mortality is approximately 40%, it remains the treatment strategy of choice. Hemodynamic deterioration is unpredictable and can be precipitous in previously stable subjects. Consequently, transfer to a Level 1 cardiac intensive care unit (CICU) with access to various temporary MCS devices and multidisciplinary experienced teams of surgical, interventional, HF, and palliative care specialists is recommended. The guidelines give a Class 1, LOE C recommendation for management of patients with mechanical complications of ACS at centers with cardiac surgical expertise. Main Takeaway Patients with mechanical complications of ACS should be managed in a center with cardiac surgical expertise. In such patients, short-term MCS devices are reasonable for hemodynamical stabilization as a bridge to surgery. Guideline Loc. Section 9.1, Figure 9

  6. Oct 19

    469. ACS Guidelines Question #7 with Dr. Venu Menon

    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 8.2 of the 2025 ACS Guidelines. The question is asked by Johns Hopkins pre-medical undergraduate and CardioNerds Academy Intern Joshua Khorsandi, answered first by University of Wisconsin cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Shikha Jha, and then by expert faculty Dr. Venu Menon. Dr. Menon is the Section Head of Clinical Cardiology, Director of the Cardiac Intensive Care Unit, and Program Director of Cardiology Fellowship at the Cleveland Clinic. He is the Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine. He was also a member of the 2025 ACS Guidelines writing committee. Question #7 A 72-year-old gentleman with past medical history significant for hypertension, hyperlipidemia, type 2 diabetes, and tobacco use is brought to the ED with chief complaint of chest tightness. He is found to have ST elevations in leads V1 to V4 and is taken for emergency coronary angiography, which demonstrates 99% proximal LAD occlusion. During the procedure, he becomes hypotensive (BP 74/55 mm Hg) and tachycardic (HR 122 bpm). Norepinephrine is initiated. Right heart catheterization demonstrates elevated left and right-sided filling pressures with low cardiac index. Besides immediate revascularization, which of the following would be the best next step?  A Cannulate for VA-ECMO B Placement of microaxial intravascular flow pump C Administration of intravenous fluid D Placement of an intraaortic balloon pump Answer #7 Explanation  The correct answer is B – Placement of microaxial intravascular flow pump. Cardiogenic shock is estimated to occur in approximately 10% of patients with STEMI and is associated with an early mortality rate of 40% to 50%. Several types of devices for temporary mechanical circulatory support (MCS) are available and have been studied in patients with cardiogenic shock, with variable efficacy and increased risk of vascular complications. IABP counterpulsation improves coronary perfusion and reduces cardiac afterload. It is relatively easy to use and has a smaller insertion profile (8 French), which is associated with lower rates of vascular access site complications when compared with other MCS devices. Left ventricular percutaneous microaxial flow pumps unload the LV by draining blood from the LV and pumping it to the ascending aorta. They are dependent on adequate right ventricular function to fill the LV and require adequate oxygenation of blood. VA-ECMO provides both blood flow and gas exchange, providing full cardiopulmonary bypass, but increases afterload.  Randomized trials of MCS devices remain challenging to conduct due to relative lack of equipoise on the part of treating physicians, leading to selective patient enrollment and limiting the generalizability of study results. The DanGer-Shock randomized 360 patients presenting with STEMI and cardiogenic shock of 24 hours duration to either microaxial flow pump or standard of care. The trial demonstrated a 26% reduction of all-cause mortality at 180 days (HR, 0.74 [95% CI, 0.55-0.99]; P = 0.04; absolute risk reduction, 12.7%; number needed to treat = 8) compared with standard of care. However, this came at the cost of increased risk of complications like bleeding, limb ischemia and renal replacement therapy in the microaxial flow pump group. In light of this and other trial data, the guidelines give a Class 2a, LOE B recommendation for the use of a microaxial intravascular flow pump in patients with STEMI complicated by severe or refractory cardiogenic shock to reduce mortality. These patients should be noncomatose and have adequate peripheral vasculature to accommodate large-bore access. Answer choice A is not correct as the use of VA-ECMO cannulation in this setting has been given a class 3 recommendation for lack of benefit. VA-ECMO has not been shown to reduce death compared with medical therapy alone in patients with cardiogenic shock in the setting of MI but increases major bleeding and vascular complications. In the absence of severe concomitant respiratory failure requiring oxygenation support, this strategy is not indicated in the patient described here. Further fluid resuscitation (answer choice C) is not likely to be helpful as right heart catheterization demonstrated elevated filling pressures. Placement of an intraaortic balloon pump (IABP) is not the next best step.  The IABP-SHOCK II trial, which randomized patients with acute MI and severe cardiogenic shock to IABP or medical therapy showed no differences at 30 days or at long-term follow-up in the primary outcome of all-cause death. The use of IABP has a class 3 recommendation for lack of benefit in patients with cardiogenic shock secondary to acute myocardial infarction. Main Takeaway In selected patients with STEMI and severe or refractory cardiogenic shock, insertion of microaxial intravascular flow pump is reasonable to reduce death in a noncomatose patient with adequate vascular access.  Guideline Loc. Section 8.2

  7. Oct 12

    468. 2026 Acute Pulmonary Embolism Guidelines with Dr. Mark Creager

    CardioNerds (Drs. Billy Joe Mullinax, Dinu Balanescu, and Saahil Jumkhawala) discuss the 2026 American Heart Association (AHA)/American College of Cardiology (ACC) multisocietal guidelines for the evaluation and management of acute pulmonary embolism (PE) with Dr. Mark Creager, Director Emeritus of the Heart and Vascular Center at Dartmouth Health, past president of the AHA, and Chair of the Writing Committee for the 2026 AHA/ACC PE Guidelines. Audio editing by CardioNerds intern, Dr. Patrick Pekyi-Boateng. Pulmonary embolism is one of the most rapidly evolving conditions in cardiovascular medicine. The 2026 AHA/ACC multisocietal guideline, endorsed by ten professional societies, is the first de novo comprehensive guideline dedicated exclusively to acute PE in adults. It introduces a new five-category A-E risk classification system, a Class I recommendation for the Pulmonary Embolism Response Team (PERT), updated guidance on anticoagulation and advanced reperfusion therapies, and a structured framework for post-PE follow-up and chronic thromboembolic pulmonary hypertension (CTEPH) screening. This episode walks through all of it, using a high-risk clinical case as the backbone. Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium.   Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Pulmonary Embolism Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron! Pearls: The 2026 guideline replaces “massive/submassive/low-risk” language with a new five-category A-E classification. Category A is subclinical/incidental PE; B is symptomatic with a low clinical severity score; C1-C3 stratifies intermediate-risk patients by right ventricular (RV) function and biomarkers; D1-D2 captures incipient cardiopulmonary failure (transient hypotension vs. normotensive shock with end-organ dysfunction); and E1-E2 is frank cardiopulmonary failure up to cardiac arrest. Each category carries a respiratory modifier (R) for hypoxemia, tachypnea, or need for supplemental oxygen. PERT receives a Class I recommendation. Registry data show PERT reduces time to therapeutic anticoagulation, decreases unnecessary inferior vena cava (IVC) filter use, and shortens hospital and intensive care unit (ICU) length of stay. PERT is most impactful when advanced therapy decisions are on the table. Low molecular weight heparin (LMWH) is now preferred over unfractionated heparin (UFH) for initial parenteral anticoagulation in most patients (Category C and above), given superior venous thromboembolism (VTE) recurrence reduction, predictable pharmacokinetics, no routine monitoring, and lower heparin-induced thrombocytopenia (HIT) risk. UFH is still preferred when imminent reperfusion is planned, in severe renal failure, or when rapid reversal may be needed. Categories A and B go straight to a direct oral anticoagulant (DOAC). Advanced reperfusion therapies – systemic thrombolysis, catheter-directed thrombolysis (CDT), mechanical thrombectomy (MT), and surgical embolectomy – carry Class 2B recommendations for Category D PE because available trials used surrogate endpoints only. HI-PEITHO, which showed a composite 7-day benefit for CDT plus anticoagulation vs. anticoagulation alone, was published in March 2026 after guideline lock and could not influence the current document. More trials are coming (PEERLESS 2, PE-TRACT, PERSEVERE, TORPEDO). Post-PE follow-up is now structured: outreach within 1 week of discharge, office visit with a PE-experienced clinician by 3 months, and active chronic thromboembolic pulmonary disease (CTEPD) and CTEPH screening at every visit for at least 1 year. Persistent symptoms or functional limitation beyond 3 months should trigger evaluation with a ventilation-perfusion (V/Q) scan, echocardiogram, and right heart catheterization (RHC). Notes: Notes drafted by Dr. Saahil Jumkhawala. Why did the writing committee believe a new classification system was necessary in 2026? The 2011 AHA scientific statement used “low-risk,” “submassive,” and “massive” categories – broad, imprecise, and insufficient for guiding modern management decisions. The 2019 European Society of Cardiology (ESC) guideline improved on this with low, intermediate-low, intermediate-high, and high-risk categories, but still did not capture many clinical, imaging, and laboratory variables with reliable prognostic data. The writing committee wanted a classification system that: Was more nuanced and captured the full clinical spectrum of PE severity Incorporated the clinical, laboratory, and imaging variables with the strongest outcome data Mapped directly to management decisions and could serve as a shared communication tool The result is a five-category A-E system with subcategories and a respiratory modifier, easier to memorize and use in practice. How do we apply the new five-category system at the bedside? What data points drive category assignment, and what is the significance of the respiratory modifier? Category A – Subclinical/Incidental PE Asymptomatic; PE found incidentally (e.g., on staging computed tomography (CT) for cancer) Often subsegmental; typically appropriate for outpatient management Category B – Symptomatic, Low Severity Chest pain or dyspnea, but simplified Pulmonary Embolism Severity Index (sPESI) = 0 B1: subsegmental PE; B2: non-subsegmental PE Outpatient management appropriate unless confounding comorbidity present Category C – Symptomatic, Elevated Severity Score (analogous to ESC intermediate risk) C1: normal RV size/function, normal biomarkers C2: abnormal RV function OR elevated biomarker (one of the two) C3: both abnormal RV function AND at least one elevated biomarker Respiratory modifier (R): oxygen saturation (SpO2) 30, or need for supplemental O2 Category D – Incipient Cardiopulmonary Failure D1: transient hypotension (systolic blood pressure (SBP) 90 mmHg but with end-organ dysfunction (elevated lactate, rising creatinine) Respiratory modifier (R): >6 L nasal cannula O2 or non-rebreather mask required Category E – Frank Cardiopulmonary Failure E1: recurrent or persistent hypotension with cardiogenic shock E2: refractory cardiogenic shock or cardiac arrest Respiratory modifier (R): hypoxemic or ventilatory respiratory failure Mr. Osis (our case patient): tachycardic, transient SBP 84 mmHg, lactate 3.4, requiring 3L O2 – classified as D1R. What is the evidence behind the Class I PERT recommendation, and when should PERT be involved in the context of the new triage system? PERT provides: Improved risk stratification through multidisciplinary input Expert guidance on selection and timing of advanced therapies Implementation of evidence-based protocols Education of the broader care team PERT composition varies by institution but may include: pulmonary/critical care, general cardiology, interventional cardiology, cardiac surgery, vascular surgery, hematology/oncology, emergency medicine, and pharmacy. Published data supporting Class I recommendation: Reduced time to therapeutic anticoagulation Decreased unnecessary IVC filter placement Shorter hospital and ICU length of stay Possible mortality reduction (data conflicting across registries) PERT is most impactful in Category C3 and above, particularly when advanced therapy decisions are being contemplated – though the guideline does not restrict PERT activation to any specific category threshold. What does the 2026 guideline say about initial anticoagulation choice (UFH vs. LMWH)? LMWH is the preferred initial parenteral anticoagulant for most patients with acute PE (Category C and above). Meta-analytic evidence: LMWH reduces recurrent VTE more effectively than UFH without increasing bleeding Predictable pharmacokinetics – no routine activated partial thromboplastin time (aPTT) monitoring required Lower incidence of HIT UFH is preferred when: Imminent advanced reperfusion is anticipated (systemic lysis, MT, surgical embolectomy, or extracorporeal membrane oxygenation (ECMO) cannulation) Severe renal dysfunction (unpredictable LMWH pharmacokinetics) Rapid reversibility needed Categories A and B: proceed directly to a DOAC (no parenteral bridge needed). DOACs are preferred over vitamin K antagonists (VKA) for long-term therapy in most patients, including most with cancer-associated PE. Exception: LMWH preferred for luminal gastrointestinal (GI) or genitourinary (GU) malignancies due to bleeding risk DOACs are contraindicated in pregnancy; LMWH is generally used throughout gestation and for at least 6 weeks postpartum How does the guideline navigate Category D1-D2 patients? What is the evidence base for the Class 2B recommendation for advanced therapies, and how do we choose between CDT and MT? All advanced reperfusion therapies carry a Class 2B recommendation for Category D PE: Class 2B = “may be considered” – the intervention can be used, but evidence is less certain Applies to: systemic thrombolysis, CDT, MT, and surgical embolectomy Why Class 2B? Available trials at the time of guideline finalization (early fall 2025) relied on surrogate endpoints: ULTIMA: CDT vs. anticoagulation alone – surrogate RV/LV ratio endpoint OPTALYSE: CDT dose-finding – surrogate endpoints STORM-PE: surrogate endpoints PEERLESS (New England Journal of Medicine, 2024): MT vs. CDT – included mortality, intracranial hemorrhage (ICH), major bleed, ICU admission, but was not vs. anticoagulation alone HI-PEITHO (published March 2026 at the ACC annual meeting – after guideline lock): 7-day composite of PE-related death, clinical decompensation/collapse, or PE recurrence Primary o

  8. Sep 23

    467. ACS Guidelines Question #6 with Dr. Binita Shah

    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 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 #6 A 64-year-old male with a history of hypertension and dyslipidemia presents to the emergency department with crescendo angina. His ECG shows ST-segment depression in leads V4–V6, and high-sensitivity troponin levels are significantly elevated. A diagnosis of NSTE-ACS is made, and the patient is scheduled for an early invasive strategy with percutaneous coronary intervention (PCI). Which of the following parenteral anticoagulants is NOT recommended for use as a standalone agent during the PCI procedure itself? A Fondaparinux B Bivalirudin C Unfractionated Heparin D Enoxaparin Answer #6 Explanation The correct answer is A.  The choice of parenteral anticoagulation for a patient with Non-ST-Elevation Acute Coronary Syndrome (NSTE-ACS) undergoing Percutaneous Coronary Intervention (PCI) is governed by both efficacy in preventing ischemic events and the safety profile regarding bleeding. The following are the recommended Agents for PCI: Unfractionated Heparin (UFH): In patients with NSTE-ACS, intravenous unfractionated heparin (UFH) is useful to reduce ischemic events (Class 1, LOE C-EO). Bivalirudin: This direct thrombin inhibitor is recommended as an alternative to UFH. In patients with NSTE-ACS undergoing PCI, bivalirudin may be reasonable as an alternative to UFH to reduce bleeding and mortality (Class 2b, LOE B-R) Enoxaparin: In patients with ACS, intravenous enoxaparin may be considered as an alternative to UFH at the time of PCI to reduce ischemic events (Class 2B, LOE B) In patients with ACS, fondaparinux should not be used to support PCI because of the risk of catheter thrombosis (Class 3: Harm; LOE B-R). The primary reason is due to the risk of catheter thrombosis. Large-scale trials (notably the OASIS-5 trial) demonstrated that using fondaparinux alone during PCI led to a significantly higher rate of thrombus formation on the diagnostic and therapeutic catheters. In the OASIS-5 trial, an increase was observed in the rate of catheter-related thrombus with fondaparinux compared with enoxaparin (0.9% versus 0.4%). Similar results were observed in the OASIS-6 trial, in which a higher rate of guiding-catheter thrombosis and more coronary complications with fondaparinux were observed when used during PCI. Main Takeaway – Parenteral anticoagulation for a patient with Non-ST-Elevation Acute Coronary Syndrome (NSTE-ACS) undergoing Percutaneous Coronary Intervention (PCI) is governed by both efficacy in preventing ischemic events and the safety profile regarding bleeding. Expert Suggestions When to consider AC other than UFH prior to and during PCI. Considerations around patients with HIT. Guideline Loc. Section 4.4

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