Case Presentation: A 74-year-old woman with morbid obesity presented with chest pain for three hours. Chest pain was constant, pressure sensation, located in her left chest and accompanied with shortness of breath. Her blood pressure was 106/91 mmHg, pulse rate was 71 /min, respiratory rate was 28 /min, and oxygen saturation was 78% on 15L of oxygen through non-rebreather mask. Physical examination showed bilateral crackles without cardiac murmur, jugular venous distention or leg edema. EKG revealed sinus rhythm and ST elevation in inferior leads without Q-wave. Patient was in respiratory distress and subsequently intubated. Patient was diagnosed with ST elevation myocardial infarction and taken to an emergency cardiac catheterization, which showed a total occlusion of right coronary artery. Patient successfully underwent percutaneous coronary intervention. Initial troponin I value was 2.4 µg/ml and troponin elevated up to 208 µg/ml after cardiac catheterization. Patient became hypotensive and required high-dose catecholamine and intra-aortic balloon pump support. Transthoracic echocardiography showed preserved ejection fraction with regional motion abnormality in inferior wall, but an evaluation of mitral valve was suboptimal due to severe obesity. No cardiac murmur was appreciated on serial physical examinations. On day 3, trans-esophageal echocardiography was performed because of a lack of the improvement, which revealed papillary muscle rupture and severe mitral regurgitation. Her condition failed to improve in spite of the medical treatment, and she underwent mitral valve replacement on day 5. Postoperative course was complicated by pneumonia and acute kidney injury. After a prolonged duration of hospital stay, the patient was discharged to sub-acute rehabilitation facility.
Discussion: The present case highlighted the importance of thorough workup for a mechanical complication following myocardial infarction. Acute mitral regurgitation caused by papillary muscle rupture is a rare but life-threatening complication of myocardial infarction. Papillary muscle rupture usually occurs in patients with an inferior infarction with right coronary artery as a culprit two to seven days after the infarction, as in the present case. The present case was, however, atypical in terms of the physical exam findings. Though careful physical examination is usually the first step for early recognition for this rare complication, in the present case, mechanical noise sound due to intra-aortic balloon pump and patient body habitus made it difficult to appreciate cardiac murmur. Only trans-esophageal echocardiography was able to reveal severe mitral regurgitation. Our study suggested that mechanical complication should be investigated when a patient with inferior myocardial infarction develops persistent hypotension and heart failure, even when a cardiac murmur is not evident. Urgent surgical intervention remained the treatment of choice of this complication, as the mortality rate of medically managed patient is high.
Conclusions: The present case highlighted the importance of thorough workup for a mechanical complication following myocardial infarction. In some cases, a cardiac murmur is not evident even on serial physical examinations. Papillary muscle rupture can happen after a patient is transferred to general medicine floor, and therefore recognizing this complication is important for hospitalists to provide appropriate care to patients with recent myocardial infarction.