100+ Free Cert Cardiology(SA) Phys Practice Questions

Explanation: When primary PCI cannot be performed within 120 minutes of STEMI diagnosis (as in this case with an estimated 3.5-hour transfer delay), guideline-directed therapy requires immediate fibrinolysis (preferably with a weight-based bolus of tenecteplase within 10 minutes of diagnosis) followed by immediate transfer to a PCI-capable center for rescue PCI if lysis fails or routine pharmacoinvasive angiography within 2-24 hours if successful.

Explanation: High-risk NSTEMI patients—defined by a GRACE score >140, dynamic ST-T segment changes, or troponin elevation—should undergo an early invasive strategy within 24 hours. Immediate angiography (<2 hours) is reserved for very high-risk features (hemodynamic instability, cardiogenic shock, refractory chest pain, life-threatening arrhythmias, acute heart failure, or ST elevation on aVR/V1).

Explanation: Potent P2Y12 inhibitors (ticagrelor or prasugrel) are superior to clopidogrel in acute coronary syndromes undergoing PCI, reducing ischemic events, stent thrombosis, and all-cause mortality (PLATO and TRITON-TIMI 38 trials). Prasugrel is contraindicated in patients with a prior history of stroke/TIA.

Explanation: Post-MI papillary muscle rupture (most commonly posteromedial papillary muscle due to single blood supply from the PDA/RCA) presents with acute pulmonary edema, cardiogenic shock, and severe MR. Emergency surgical repair/replacement combined with hemodynamic stabilization (IABP/Impella and vasopressors/afterload reduction) is mandatory as medical therapy alone carries >80% mortality.

Explanation: Right ventricular infarction (RVI) causes RV failure, reducing RV stroke volume and LV preload. Treatment relies on aggressive volume expansion (IV isotonic saline) to optimize RV preload and maintain cardiac output. Nitrates, diuretics, and opioids lower preload and are dangerous in RVI.

Explanation: Cardiac Magnetic Resonance (CMR) imaging is the cornerstone gold-standard diagnostic tool in MINOCA. It identifies the cause in >85% of patients by distinguishing true myocardial infarction (subendocardial/transmural LGE), acute myocarditis (subepicardial/mid-wall LGE with T2 edema), Takotsubo syndrome (apical ballooning without LGE), or non-ischemic cardiomyopathies.

Explanation: LV free wall rupture typically occurs between day 3 and 7 post-MI (especially in elderly females, first MI, hypertension, or delayed reperfusion). It manifests as sudden electromechanical dissociation / PEA collapse due to acute hemopericardium and cardiac tamponade.

Explanation: This patient has Dressler syndrome (post-cardiac injury syndrome). In post-MI pericarditis, high-dose aspirin (500–1000 mg every 8 hours) combined with colchicine (0.5 mg daily for 3 months) is the treatment of choice. Non-aspirin NSAIDs (like ibuprofen or indomethacin) are avoided post-MI as they impair myocardial scar formation and increase rupture risk.

Explanation: When heart rate is already low (<60 bpm) on beta-blockers, adding heart rate-reducing drugs like Ivabradine, Diltiazem, or Verapamil is contraindicated or ineffective (Ivabradine requires HR >70 bpm; Diltiazem/Verapamil cause severe bradycardia and AV block when combined with beta-blockers). Second-line antianginals that do not lower heart rate, such as long-acting nitrates, ranolazine, or nicorandil, are indicated.

Explanation: In diabetic patients with multivessel CAD, especially with high SYNTAX scores (>22) or proximal LAD involvement, CABG provides significant survival benefits and lower rates of repeat revascularization and MI compared to PCI (FREEDOM trial, SYNTAX 10-year extended follow-up).