Cardiovascular Disease Flashcards

A 58-year-old man with ischemic cardiomyopathy (EF 25%) presents with dyspnea. He is on maximally tolerated GDMT including carvedilol 25 mg BID, sacubitril/valsartan 97/103 mg BID, and eplerenone. His resting heart rate is 68 bpm and he remains in sinus rhythm. Which additional therapy has demonstrated mortality benefit in this specific scenario?

Answer: Ivabradine

Ivabradine (SHIFT trial) reduces cardiovascular mortality and HF hospitalization in patients with HFrEF (EF ≤35%), sinus rhythm, and resting heart rate ≥70 bpm on maximally tolerated beta-blocker. Although this patient's HR is 68, note the stem specifies sinus rhythm and maximally tolerated beta-blocker — in practice ivabradine is indicated at HR ≥70. However, among the choices, ivabradine is the only agent with demonstrated mortality benefit as an add-on to modern GDMT including ARNI. Digoxin reduces hospitalizations but not mortality. Hydralazine-nitrate is reserved for patients intolerant of ACEi/ARB/ARNI. Amiodarone has no mortality benefit in HFrEF and increases non-cardiovascular mortality.

A 72-year-old woman is admitted with NSTEMI and found to have a 90% stenosis of the proximal LAD and a 70% stenosis of the mid-RCA. She undergoes PCI to the LAD with drug-eluting stent placement. Four days later she develops recurrent chest pain. ECG shows 2 mm ST elevations in V1-V4. Emergent angiography reveals a patent LAD stent with TIMI-3 flow but a new 100% occlusion of the mid-RCA. What is the most likely explanation for the RCA occlusion?

Answer: In-hospital stent thrombosis of an untreated lesion due to heightened platelet reactivity

This scenario illustrates 'vulnerable plaque progression' — after an ACS index event, systemic inflammation and heightened platelet/coagulation activation increase the risk of thrombosis at non-culprit lesions with moderate stenosis. The 70% RCA lesion, while not treated initially (guideline-concordant in stable non-culprit vessel), subsequently developed acute plaque rupture and thrombosis in the peri-PCI hypercoagulable state. This phenomenon (culprit-only PCI leaving vulnerable non-culprit lesions exposed) is distinct from stent thrombosis of a treated vessel. Plaque shift causing distal embolism to a separate vessel is not a recognized mechanism. Spontaneous dissection propagation and contrast spasm do not explain a new total occlusion 4 days post-procedure.

A 45-year-old man with hypertrophic obstructive cardiomyopathy (HOCM), LVOT gradient of 80 mmHg at rest, and NYHA class III symptoms despite maximally tolerated disopyramide and metoprolol presents for further management. He has a 22 mm anterior mitral valve leaflet and septal thickness of 28 mm. Which statement best characterizes the comparative outcomes of septal myectomy versus alcohol septal ablation (ASA) in this patient?

Answer: Myectomy is preferred because ASA cannot adequately address concomitant SAM-related mitral regurgitation and produces equivalent long-term gradient reduction

In patients with HOCM and concomitant intrinsic mitral valve pathology (elongated anterior leaflet >17 mm, as in this case), systolic anterior motion (SAM) of the mitral valve contributes significantly to both LVOT obstruction and MR. Surgical myectomy allows direct visualization and repair/resection of abnormal mitral apparatus anatomy — including papillary muscle realignment and anterior leaflet plication — which ASA cannot address. Additionally, with severe septal hypertrophy (≥28 mm) and complex anatomy, ASA targets only one segment and may produce incomplete gradient relief. Regarding CHB: ASA actually carries a higher risk of complete heart block (up to 10-20%) than surgical myectomy (1-2%), not the reverse. Both procedures are not equivalent in patients with complex anatomy.

A 66-year-old woman is started on amiodarone for persistent atrial fibrillation. Six months later she presents with dyspnea and is found to have bilateral pleural effusions and a diffuse interstitial infiltrate on CT chest. PFTs show a restrictive pattern with DLCO 52% predicted. Bronchoscopy with BAL shows foamy macrophages. Which of the following is the most appropriate next step?

Answer: Discontinue amiodarone, switch to an alternative antiarrhythmic, and initiate corticosteroids

Amiodarone pulmonary toxicity (APT) is a life-threatening complication occurring in 1-5% of patients. The combination of new restrictive physiology, reduced DLCO, bilateral infiltrates, and foamy macrophages on BAL (pathognomonic phospholipidosis from drug accumulation) confirms the diagnosis. Management requires: (1) discontinuation of amiodarone — dose reduction is insufficient as the drug's half-life is 40-55 days and tissue accumulation persists; (2) initiation of corticosteroids (prednisone 40-60 mg/day) because inflammation-mediated injury responds to steroids and untreated APT has >10% mortality; (3) substitution with an alternative rhythm control agent (e.g., dofetilide, dronedarone, or rate control strategy). Continuing amiodarone even with steroids allows ongoing pulmonary injury. Corticosteroids ARE indicated given the severity of presentation.

A 52-year-old man with a mechanical aortic valve (on-X bileaflet) and no other risk factors (no AF, no prior thromboembolism, no LV dysfunction) has been maintained on warfarin with a target INR of 2.0-3.0. His last 12 INR values over 18 months have been 100% in range. Based on updated evidence, what change to his anticoagulation regimen should be considered?

Answer: Lower INR target to 1.5-2.0 combined with aspirin 100 mg daily, based on the PROACT Xa trial data

The PROACT Xa trial (2023) specifically evaluated the On-X bileaflet mechanical aortic valve — an FDA-approved trial demonstrating non-inferiority of INR 1.5-2.0 plus aspirin 100 mg versus standard INR 2.0-3.0 in low-risk patients (no AF, no prior TE, preserved EF, no additional risk factors). On-X valves have superior hemodynamic and flow characteristics (nearly central flow, reduced thrombogenicity) compared to older mechanical valves. The FDA approved a labeling change for On-X AVR specifically. This is the ONLY mechanical valve with approved lower INR targeting. DOACs (rivaroxaban, apixaban) are contraindicated in ALL mechanical valves (RE-ALIGN trial showed excess thrombosis and bleeding). Adding aspirin to an already optimally anticoagulated patient increases bleeding without benefit in this low-risk scenario.

A 61-year-old man with diabetes, CKD stage 3b (eGFR 38), and established ASCVD is on maximally tolerated rosuvastatin 20 mg (higher doses worsen myalgias) with LDL-C of 88 mg/dL. He had an MI 8 months ago. His cardiologist adds ezetimibe. After 3 months his LDL-C is 71 mg/dL. According to current ACC/AHA very-high-risk ASCVD guidelines, what is the most appropriate next step?

Answer: Add a PCSK9 inhibitor (evolocumab or alirocumab) to achieve LDL-C <55 mg/dL

This patient is very-high-risk ASCVD (recent MI within 12 months + diabetes + CKD): the 2022 ACC Expert Consensus Decision Pathway sets an LDL-C goal of <55 mg/dL for very-high-risk patients. At LDL-C 71 mg/dL on statin + ezetimibe, he remains above goal. The next step is addition of a PCSK9 inhibitor. The FOURIER (evolocumab) and ODYSSEY OUTCOMES (alirocumab) trials demonstrated further cardiovascular event reduction beyond statin therapy in post-ACS patients. Icosapent ethyl (REDUCE-IT) reduces ASCVD events via triglyceride/pleiotropic mechanisms independent of LDL-C and is additive but does not address the LDL-C target gap — it would be a complementary addition, not the 'next step' for LDL control. The LDL-C goal of <70 mg/dL (older standard) is no longer sufficient for very-high-risk ASCVD.