A 66-year-old man presents to the cardiology clinic for follow-up 8 weeks after hospitalization for an anterior ST-elevation myocardial infarction. During his admission, he underwent successful percutaneous coronary intervention to the left anterior descending artery and was discharged on aspirin, ticagrelor, atorvastatin, metoprolol, and lisinopril. Since discharge, he has noticed mild exertional dyspnea but denies recurrent chest pain. He has been compliant with all medications. Temperature is 36.8°C (98.2°F), blood pressure is 122/74 mm Hg, pulse is 72/min, and respiratory rate is 14/min. Physical examination demonstrates a laterally displaced point of maximal impulse. No murmurs are present. ECG demonstrates persistent ST-segment elevation in leads V1-V4, unchanged from an ECG obtained 6 weeks earlier. Troponin levels are normal. Transthoracic echocardiography reveals a thinned, dyskinetic segment of the anterior left ventricular wall that bulges outward during systole.
Which of the following complications is this patient at greatest risk of developing?
The correct answer is:
B) Left ventricular mural thrombus with systemic embolization
This patient has a left ventricular aneurysm, a late complication of transmural myocardial infarction. The diagnosis is suggested by persistent ST-segment elevation weeks after infarction and echocardiographic evidence of a thinned, dyskinetic ventricular wall that paradoxically bulges during systole.
Unlike the acute mechanical complications of myocardial infarction, ventricular aneurysms develop over weeks as infarcted myocardium is replaced by fibrotic scar tissue. Because scar tissue lacks contractile function, the affected ventricular segment becomes dyskinetic and may impair overall systolic performance.
One of the most important complications of ventricular aneurysms is formation of a left ventricular mural thrombus. Blood stasis within the aneurysmal segment promotes thrombus formation, which can subsequently embolize to the systemic circulation. Patients may present with ischemic stroke, acute limb ischemia, mesenteric ischemia, or other arterial embolic events. Additional complications include heart failure due to reduced systolic function and ventricular arrhythmias caused by scar-mediated reentry circuits.
Answer choice A: Cardiac tamponade due to ventricular free wall rupture, is incorrect.
Free wall rupture is an acute complication that generally occurs 3–7 days after a transmural myocardial infarction, when inflammatory degradation weakens the infarcted myocardium. It causes hemopericardium and cardiac tamponade. Eight weeks after infarction, the infarcted myocardium has already undergone fibrotic healing, making free wall rupture highly unlikely.
Answer choice C: Papillary muscle rupture causing acute mitral regurgitation, is incorrect.
Papillary muscle rupture usually occurs within 2–7 days after myocardial infarction and presents with sudden pulmonary edema, cardiogenic shock, and a new apical holosystolic murmur. This patient’s stable outpatient presentation and chronic ventricular remodeling are inconsistent with this acute mechanical complication.
Answer choice S: Ventricular fibrillation due to acute coronary occlusion, is incorrect.
Ventricular fibrillation can occur during acute ischemia and is a common cause of sudden cardiac death in the early phase of myocardial infarction. Although ventricular aneurysms may predispose patients to ventricular arrhythmias, this answer specifically describes arrhythmia due to acute coronary occlusion rather than the chronic complication most directly associated with the aneurysm seen in this patient.
Answer choice W: Ventricular septal rupture causing a left-to-right shunt, is incorrect.
Ventricular septal rupture also occurs within the first week after infarction and presents with a new harsh holosystolic murmur, palpable thrill, and cardiogenic shock. Once scar formation is complete, the risk of septal rupture dramatically decreases.
Key Learning Point
A left ventricular aneurysm is a late complication of transmural myocardial infarction characterized by persistent ST-segment elevation and a dyskinetic scarred ventricular wall. Major complications include mural thrombus formation, systemic embolization, heart failure, and ventricular arrhythmias.
