Unruptured left coronary sinus of Valsalva aneurysm causing mitral valve obstruction.

A 77-year-old man was admitted for congestive heart failure. He had started to have palpitations after eating supper 2 days before the admission and had experienced dyspnea on exertion since then. He visited his family physician, who referred him to the cardiology clinic of our hospital. The patient was under the family physician’s care for diabetes mellitus, hypertension, and paroxysmal atrial fibrillation. He had never been diagnosed as having any organic heart disease. He was an ex-smoker and drank alcohol on social occasions. The patient was on -blockers and Coumadin. His cardiovascular physical examination was significant for a 3/6 systolic murmur and a rapid, irregular heart beat. His ECG showed atrial fibrillation with a ventricular rate of 150 bpm. His portable chest x-ray (Figure 1A) showed bilateral pleural effusion and pulmonary edema. An emergency transthoracic echocardiogram showed normal left and right ventricular function. A large mass in the left atrium was seen that was causing functional mitral stenosis. The patient was admitted to the hospital, given digoxin, and started on intravenous diuresis. His ECG on normal sinus rhythm (Figure 1B), which was recorded 2 weeks after the admission, showed P mitrale, suggesting significant overload of the left atrium. A complete transthoracic echocardiogram after conversion to normal sinus rhythm revealed a large aneurysm in the left coronary sinus of Valsalva measuring 58 48 mm that was protruding into the left atrium. There was a thrombus inside the aneurysm. The aneurysm was prolapsing into the mitral valve, thus resulting in obstruction of the left ventricular inflow. The mitral valve orifice area measured by the pressure–half-time method was 0.8 cm. No mitral regurgitation was observed at this time. The estimated right ventricular systolic pressure was 47 mm Hg. Significant tricuspid regurgitation was present. Aortic regurgitation was trivial. Transesophageal echocardiography showed the same pathophysiological findings (Movie I in the online-only Data Supplement). The patient was further evaluated by computed tomography of the ascending aorta and the heart (Figure 2). This imaging modality further confirmed the findings from the echocardiogram.