Cardiovascular Medicine Flashcards

A 58-year-old woman with hypertrophic obstructive cardiomyopathy (HOCM) presents with worsening dyspnea and near-syncope. Echocardiography shows a resting LVOT gradient of 55 mmHg. She is currently on metoprolol 100 mg daily. Which of the following is the most appropriate next step?

Answer: Add disopyramide to her current regimen

Disopyramide is a Class IA antiarrhythmic with significant negative inotropic properties, making it highly effective for reducing LVOT obstruction in HOCM when added to a beta-blocker. The combination of metoprolol + disopyramide is guideline-recommended for symptomatic patients with persistent gradients despite beta-blocker monotherapy. Loop diuretics reduce preload and would worsen obstruction. Verapamil is an alternative to beta-blockers, not an add-on. Septal reduction therapy (ablation or myectomy) is reserved for patients who fail maximal medical therapy.

A 72-year-old man with systolic heart failure (EF 30%) and LBBB (QRS 158 ms) undergoes CRT-D implantation. Six months later, he remains persistently symptomatic and repeat echo shows EF 32%. Device interrogation confirms >98% biventricular pacing. Which of the following is the most likely explanation for non-response?

Answer: True electrical non-responder due to extensive scar burden

Approximately 30% of patients who receive CRT are non-responders. When biventricular pacing is confirmed at >98% and AV/VV intervals are optimized, persistent non-response most often reflects extensive myocardial fibrosis or scar burden (commonly from prior MI) that prevents mechanical resynchronization despite electrical correction. Lead dislodgement would reduce pacing percentages. AV delay optimization is a consideration but is less likely when pacing percentages are adequate. Tachycardia-mediated cardiomyopathy would require uncontrolled rapid rates, which are not suggested here.

A 45-year-old man is found to have isolated severe aortic regurgitation on echocardiography. He is completely asymptomatic with an LV end-systolic diameter of 48 mm and EF of 58%. He exercises vigorously without limitation. What is the most appropriate management?

Answer: Referral for aortic valve replacement

Per 2021 ACC/AHA Valvular Heart Disease Guidelines, aortic valve replacement is indicated in asymptomatic severe AR when the LV end-systolic diameter (LVESD) reaches ≥50 mm (Class I) or when LVESD is 45–49 mm in patients undergoing cardiac surgery for another reason, OR when LVESD ≥45 mm with evidence of progressive LV enlargement. At 48 mm LVESD with preserved (but not normal) EF, this patient meets criteria for surgery referral under the ≥50 mm threshold approached — notably, guidelines also support surgery at LVESD index ≥25 mm/m². Surveillance alone is insufficient at this dilation level. ACE inhibitors do not have proven benefit in asymptomatic severe AR with preserved EF.

A 63-year-old woman with known coronary artery disease presents with an acute inferior STEMI. Primary PCI is performed successfully to the right coronary artery. Post-procedure, she develops hypotension (BP 78/50) with clear lung fields, elevated JVP, and a new pansystolic murmur loudest at the left lower sternal border. ECG shows sinus bradycardia. What is the most likely diagnosis?

Answer: Ventricular septal rupture

Post-MI ventricular septal rupture (VSR) classically presents 3–5 days after MI (though can be earlier) with sudden hemodynamic deterioration and a new harsh pansystolic murmur at the left lower sternal border, reflecting left-to-right shunting. Inferior MI commonly causes posterior VSR. Right ventricular infarction causes hypotension with clear lungs and elevated JVP but does not produce a new pansystolic murmur. Acute MR from papillary muscle rupture produces a murmur, but it is often apical/radiating to the axilla. Cardiac tamponade causes muffled heart sounds and pulsus paradoxus, not a new murmur.

A 55-year-old man with long-standing hypertension and type 2 diabetes is started on sacubitril/valsartan for HFrEF (EF 35%). Two weeks later, he presents with angioedema of the lips and tongue. He was previously on lisinopril, which was discontinued 24 hours before initiating sacubitril/valsartan. What is the most likely mechanism of this adverse event?

Answer: Cross-reactive angioedema from residual ACE inhibitor effect

Sacubitril inhibits neprilysin, which normally degrades bradykinin and substance P. When sacubitril is initiated too soon after an ACE inhibitor (which also prevents bradykinin degradation), overlapping mechanisms cause dangerous bradykinin accumulation, leading to angioedema. Guidelines mandate a 36-hour washout period between discontinuing an ACE inhibitor and starting sacubitril/valsartan. In this case, only 24 hours elapsed — insufficient to clear ACE inhibitor activity, resulting in combined bradykinin potentiation. Valsartan (an ARB) does not directly affect bradykinin. Mast cell degranulation describes allergic/IgE-mediated angioedema, a different mechanism.

A 38-year-old competitive cyclist presents with exertional chest discomfort and is found to have an anomalous origin of the left coronary artery from the right sinus of Valsalva (ALCAPA from right sinus) with an interarterial course. Cardiac MRI shows a perfusion defect in the LAD territory with stress. He is currently asymptomatic at rest. What is the most appropriate management?

Answer: Surgical coronary reimplantation or unroofing procedure

Anomalous origin of a coronary artery from the opposite sinus (ACAOS) with an interarterial course carries a significant risk of sudden cardiac death, particularly during exertion, due to compression of the anomalous vessel between the aorta and pulmonary artery. When there is objective evidence of ischemia (as shown by perfusion defect on stress MRI), surgical correction — either reimplantation or unroofing of the intramural segment — is strongly indicated regardless of symptom status at rest. This is a Class I recommendation in current guidelines. Beta-blockers alone are insufficient. PCI is not appropriate for this anatomical variant. Annual surveillance without correction is inadequate given confirmed ischemia.