A 67-year-old man presenting with chest discomfort and nausea was transferred to the nearby hospital. He was diagnosed with acute myocardial infarction; an intra-aortic balloon pump (IABP) was inserted, and he was taken to the catheter room. His angiogram findings revealed left anterior descending coronary artery occlusion with a thrombus that was aspirated immediately. Echocardiography revealed a pericardial effusion suggestive of left ventricular rupture, and he was referred to our unit for surgery. The patient had been consulting a local physician for hypertension, diabetes mellitus, and hyperlipidemia. He had a 47-year history of daily smoking. His blood pressure was 143/92 mmHg, and the pulse rate was 86 beats/min. His blood oxygen saturation (SpO2) level was 98% with 8 L/min of oxygen therapy. His chest radiography findings showed remarkable cardiomegaly with pulmonary congestion. The 12-lead electrocardiogram findings demonstrated sinus rhythm with ST elevation and poor R progression in leads V1–4. Laboratory findings showed that the cardiac enzymes, creatine kinase and creatine kinase-MB, were elevated at 196 and 17 IU/L (peak level of creatine kinase-MB), respectively, and reached 2223 and 14 IU/L 3 days later. Troponin I level was remarkably elevated at 19.26 ng/mL on admission. A median sternotomy was performed, and he underwent drainage of the pericardial bleeding and hemostasis of the left ventricular oozing rupture without cardiopulmonary bypass. A tissue-sealing seat was applied to the left ventricle epicardium using human fibrinogen, thrombin, and aprotinin. During surgery, we performed a transesophageal echocardiogram (TEE), which revealed a small slit formation of the ventricular septum; however, it showed no shunt between the right and left ventricles. The patient was transferred to the intensive care unit in a stable condition. A transthoracic echocardiogram showed akinetic regions of the large anterior segment and apex of the left ventricle. Although the slitted interventricle septum was depicted with fluttering motions, no shunt was indicated (Additional file 1: Video S1). However, 15 h later, he presented with sudden cardiogenic shock requiring extra-corporeal membrane oxygenation (ECMO). The patient could not be weaned from ECMO, and a TEE performed 5 days later showed the new onset of a left ventricular septal aneurysm (Fig. 1, Additional file 2: Video S2). The left ventriculogram also revealed a saccular aneurysm-like protrusion at the ventricular septum (Fig. 2), which caused severe left ventricular acute failure and ECMO support dependence. Then, the patient was taken to the operating room for surgical repair. Re-sternotomy was performed, and cardiopulmonary bypass was instituted from the superior and inferior veins to the ascending aorta. A left ventricular vent tube was inserted via the right upper pulmonary vein. The ascending aorta was clamped and the heart was arrested with antegrade cardioplegia. Then, the left ventricle was incised at the lateral portion of the left anterior descending coronary artery. The ventricular septal wall had a dissection with a single tear into the left ventricle, forming a large aneurysm (Fig. 3a, c). The septal dissection was obliterated with a large suture through the right ventricle from the septum using 3-0 polypropylene suture with Teflon felt (Fig. 3d). Inside the left ventricle, a 4 × 6-cm oval fabric patch was placed over the infarcted septal wall, including the rupture, and was sutured with pledget 3-0 polypropylene (Fig. 3b, e–g). An additional aortocoronary bypass graft with a saphenous vein graft was performed. Cardiopulmonary bypass was weaned off with ECMO and IABP. Hemostasis was secured, and the surgery was completed. The patient was weaned off ECMO on postoperative day (POD) 1. The IABP was removed on POD 5, and the patient was extubated on POD 15. He was complicated by a small left temporal lobe infarction. After 4 months, he was transferred to another hospital for rehabilitation and was discharged 1 year later.
