Abstract
Mitral valve rupture secondary to ischemic papillary muscle necrosis is rare in the contemporary era due to improved revascularization techniques. However, when it does occur, prompt diagnosis and urgent surgical intervention can be lifesaving. A 69-year-old male with morbid obesity, hypothyroidism, and a family history of coronary artery disease presented to the hospital with chest pain and dyspnea that began five hours prior. He had an acute infero-postero-lateral myocardial infarction due to total occlusion of the left circumflex artery that was revascularized with the deployment of a drug-eluting stent. Two days after the myocardial infarction, the patient had an episode of ventricular tachycardia. He subsequently went into respiratory distress from flash pulmonary edema and developed cardiogenic shock due to acute mitral valve rupture. The patient underwent surgical mitral valve replacement, extracorporeal membranous oxygenation (ECMO), and hemodialysis. His course was complicated by an acute lower gastrointestinal bleed that progressed into multiorgan failure and eventually his demise. This case highlights the need to include papillary muscle rupture high on the differential when evaluating a hemodynamically unstable patient in the setting of an acute myocardial infarction (MI). Rapid diagnosis by urgent bedside echocardiogram and surgical intervention is crucial.
Highlights
Papillary muscle rupture is a rare and fatal complication of acute ST-segment elevation myocardial infarction in the contemporary age
Mitral valve rupture secondary to ischemic papillary muscle necrosis is rare in the contemporary era due to improved revascularization techniques
He subsequently went into respiratory distress from flash pulmonary edema and developed cardiogenic shock due to acute mitral valve rupture
Summary
Papillary muscle rupture is a rare and fatal complication of acute ST-segment elevation myocardial infarction in the contemporary age. The patient was steadily improving until post-infarction day two when he developed sudden onset ventricular tachycardia requiring one synchronized cardioversion with conversion to sinus tachycardia He subsequently developed respiratory distress, hypoxia with oxygen saturation of 85% on room air, and hypotension with blood pressure 80s/50s mmHg, and sinus tachycardia with heart rate in the range of 130140 beats per minute. At this point, the differential diagnosis included ventricular free wall rupture, papillary muscle rupture, or recurrent myocardial infarction resulting in flash pulmonary edema and cardiogenic shock. An urgent transesophageal echocardiogram (TEE) confirmed flail anterior mitral leaflet and chordae due to posteromedial papillary muscle rupture, as well as severe posteriorly directed mitral valve regurgitation (Figure 4). The patient expired on postoperative day twelve
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