A Case of Acute Myocardial Infarction with Myocardial Damage Caused by Thrombi Originally Located in the Non-culprit Lesion

Abstract

An 81-year-old woman presented to the emergency room with back pain. The patient had been in her normal state of health until three days before presentation, when exertional chest pain developed and lasted for approximately five minutes. On the day of presentation, she woke up due to back pain and called an ambulance because the pain did not resolve. Her previous medical history was diabetes, which was well controlled with diet therapy alone. She did not take any medication. The patient did not drink, smoke, or use illicit drugs, and had no known allergies. There was no family history of cardiovascular diseases. On examination, she was alert and oriented. Her vital signs were normal except for a blood pressure of 190/80 mmHg. Neither additional heart sounds nor murmurs were heard on auscultation, and the remaining examinations were normal. Electrocardiography demonstrated ST-segment elevations in leads V1 to V4. Anteroposterior chest radiography was normal. The complete blood cell counts were normal, as were the renal and liver function tests. Although the creatinine kinase level was 128 U/L, the heart-type fatty acid binding protein was positive and the high-sensitivity cardiac troponin T level was 0.181 ng/dL (reference value, ≤0.100). The level of brain natriuretic peptide was elevated to 303.3 pg/mL (reference value, ≤18.4). In addition, echocardiography demonstrated hypokinesis in the anterior wall and the apex of the left ventricle. A diagnosis of ST-segment elevation acute myocardial infarction was made, and oral clopidogrel (300 mg), oral aspirin (200 mg), and intravenous heparin (10,000 units) were administered. Emergency coronary angiography demonstrated total occlusion in the mid-portion of the left anterior descending coronary artery and severe stenosis in the mid-portion of the right coronary artery (Fig. 1). Collateral flow to the right coronary artery from the first septal perforator of the left anterior descending coronary artery, which branched before the total occlusion of the left anterior descending coronary artery, was observed. After thrombus aspiration, recanalization of the left anterior descending coronary artery was obtained. Unexpectedly, thrombi migrating to the distal part of the right coronary artery was observed (Fig. 2, videos Case Report