A 68-year-old man is admitted to the coronary care unit after undergoing successful percutaneous coronary intervention for an inferior ST-elevation myocardial infarction. He is started on aspirin, ticagrelor, atorvastatin, metoprolol, and lisinopril. His hospital course is initially uncomplicated. On hospital day 3, he develops sudden-onset shortness of breath. He reports severe dyspnea and is unable to lie flat. He denies recurrent chest pain. Temperature is 37.0°C (98.6°F), blood pressure is 84/52 mm Hg, pulse is 124/min, respiratory rate is 30/min, and oxygen saturation is 88% on room air. Physical examination reveals marked respiratory distress. Jugular venous pressure is elevated. Cardiac examination demonstrates a new high-pitched holosystolic murmur best heard at the cardiac apex and radiating to the axilla. Diffuse crackles are present throughout both lung fields. ECG shows persistent Q waves in leads II, III, and aVF without new ST-segment elevations. Troponin levels are decreasing compared with prior values.
Which of the following is the most likely cause of this patient’s acute deterioration?
The correct answer is:
B) Acute rupture of the posteromedial papillary muscle
This patient has acute papillary muscle rupture, a catastrophic mechanical complication of myocardial infarction that typically occurs 2–7 days after infarction. The diagnosis is suggested by the sudden development of cardiogenic shock, severe pulmonary edema, and a new holosystolic murmur consistent with acute mitral regurgitation.
The posteromedial papillary muscle is particularly vulnerable because it receives blood supply from a single coronary artery, most commonly the right coronary artery. Inferior myocardial infarctions therefore place patients at increased risk for papillary muscle ischemia and rupture.
When papillary muscle rupture occurs, the mitral valve abruptly loses structural support, causing severe acute mitral regurgitation. Blood is ejected backward into the left atrium during systole, leading to a rapid increase in left atrial and pulmonary venous pressures. Because the left atrium has not had time to adapt, patients develop fulminant pulmonary edema, hypotension, and cardiogenic shock.
Urgent echocardiography is required, and definitive treatment is surgical repair or replacement of the mitral valve.
Answer choice A: Acute rupture of the left ventricular free wall, is incorrect.
Free wall rupture usually occurs within the first week after transmural myocardial infarction and often results in hemopericardium and cardiac tamponade. Patients typically develop sudden hypotension, jugular venous distention, and pulseless electrical activity. A new apical holosystolic murmur and severe pulmonary edema are more characteristic of acute mitral regurgitation due to papillary muscle rupture.
Answer choice C: Left ventricular aneurysm formation, is incorrect.
A ventricular aneurysm is a late complication that generally develops weeks to months after infarction. Patients may develop heart failure, persistent ST-segment elevation, ventricular arrhythmias, or mural thrombus formation. It would not explain this patient’s abrupt deterioration on hospital day 3.
Answer choice D: Reinfarction due to acute stent thrombosis, is incorrect.
Acute stent thrombosis can cause recurrent myocardial infarction and recurrent chest pain with new ischemic ECG changes and rising troponin levels. This patient has no recurrent chest pain, no new ischemic ECG findings, and decreasing troponin levels. The new murmur strongly suggests a mechanical complication rather than recurrent infarction.
Answer choice E: Ventricular septal rupture, is incorrect.
Ventricular septal rupture is another mechanical complication occurring 2–7 days after MI and can also cause cardiogenic shock and a new holosystolic murmur. However, the murmur is usually loudest along the left sternal border and is often accompanied by a palpable thrill. Severe pulmonary edema with an apical murmur radiating to the axilla is more characteristic of acute mitral regurgitation due to papillary muscle rupture.
Key Learning Point
Patients who develop sudden pulmonary edema, cardiogenic shock, and a new apical holosystolic murmur 2–7 days after an inferior myocardial infarction should be presumed to have papillary muscle rupture causing acute severe mitral regurgitation.
