OBJECTIVES: Data regarding the distribution of vulnerable lesions in the coronary arteries are scarce. The aim was to evaluate the frequency and distribution of culprit lesions in patients with ST-segment elevation acute myocardial infarction. In addition, the location of culprit lesions was related to infarct size. METHODS: Consecutive patients (N=1533, mean age 61±12 years) were evaluated. All patients were treated with primary percutaneous coronary intervention and underwent two-dimensional echocardiography less than 48 h after admission. RESULTS: The majority of the culprit lesions were located in the left anterior descending coronary artery (LAD, 45%), followed by the right coronary artery (RCA, 38%), and left circumflex coronary artery (LCX, 14%). Subanalysis demonstrated that patients with a culprit lesion in the LAD and LCX had significantly higher-peak cardiac enzymes compared with patients with culprit lesions in the RCA. In addition, patients with proximal LAD and LCX lesions had significantly worse left ventricular function compared with patients with mid or distal lesions. CONCLUSION: Plaque rupture resulting in acute myocardial infarction is more likely to occur in the proximal parts of the LAD and RCA. In addition, the location of culprit lesions was related to infarct size. Therefore, knowledge of the distribution of vulnerable lesions is important for identifying patients at risk for acute coronary events.
OBJECTIVES: Data regarding the distribution of vulnerable lesions in the coronary arteries are scarce. The aim was to evaluate the frequency and distribution of culprit lesions in patients with ST-segment elevation acute myocardial infarction. In addition, the location of culprit lesions was related to infarct size. METHODS: Consecutive patients (N=1533, mean age 61±12 years) were evaluated. All patients were treated with primary percutaneous coronary intervention and underwent two-dimensional echocardiography less than 48 h after admission. RESULTS: The majority of the culprit lesions were located in the left anterior descending coronary artery (LAD, 45%), followed by the right coronary artery (RCA, 38%), and left circumflex coronary artery (LCX, 14%). Subanalysis demonstrated that patients with a culprit lesion in the LAD and LCX had significantly higher-peak cardiac enzymes compared with patients with culprit lesions in the RCA. In addition, patients with proximal LAD and LCX lesions had significantly worse left ventricular function compared with patients with mid or distal lesions. CONCLUSION: Plaque rupture resulting in acute myocardial infarction is more likely to occur in the proximal parts of the LAD and RCA. In addition, the location of culprit lesions was related to infarct size. Therefore, knowledge of the distribution of vulnerable lesions is important for identifying patients at risk for acute coronary events.