Resident University of North Carolina at Chapel Hill Chapel Hill, North Carolina, United States
Disclosure(s):
Emily A. Parks, MD: No financial relationships to disclose
Background: Papillary muscle rupture is a rare mechanical complication of myocardial infarction that has become less common (0.05 to 0.26%) since the development of reperfusion strategies (1). Prompt recognition of acute papillary muscle rupture is essential to stabilize and support the patient prior to urgent surgical intervention
Methods: A 62-year-old male with past medical history of hypertension and hyperlipidemia presented to his primary care provider with two days of worsening dyspnea and chest discomfort. Electrocardiography revealed an acute inferior ST-segment elevation myocardial infarction (STEMI) prompting transfer to the hospital. He was found to be hypoxic with evidence of pulmonary edema on chest x-ray. He required intubation shortly after arrival to the emergency department due to worsening respiratory failure. Initial laboratory workup was notable for marked troponin elevation and bedside echocardiography showed a hyperdynamic left ventricle with estimated left ventricular ejection fraction (LVEF) >70%. Following admission to the cardiac intensive care unit, urgent transesophageal echocardiogram (TEE) revealed severe mitral regurgitation with a large flail portion of the posterior leaflet consistent with papillary muscle rupture. Left heart catheterization demonstrated multi-vessel coronary artery disease including an occluded right coronary artery, likely leading to ischemia of the posteromedial papillary muscle. He developed cardiogenic shock prompting initiation of vasopressors and inotropes and an intra-aortic balloon pump was placed. Cardiothoracic surgery was consulted and emergently performed coronary artery bypass to the right posterior descending artery and left anterior descending artery territories followed by mitral valve replacement.
Outcome: Post-operative transesophageal echocardiogram showed moderately reduced LVEF of 45-55%, moderate right ventricular dysfunction and no mitral regurgitation with the bioprosthetic valve in place. The patient remained on inotropic support and discharged home with cardiac rehabilitation.
Conclusion: This case describes acute papillary muscle rupture following inferior STEMI, resulting in severe mitral regurgitation and cardiogenic shock. Preserved or hyperdynamic left ventricular function with pulmonary edema and shock after myocardial infarction represents a distinctive presentation that should prompt suspicion for papillary muscle rupture.
