ercutaneous coronary intervention (PCI) is an effective treatment in the early phase of acute myocardial infarction (AMI), 1-3 but the unstable plaque and coronary arterial thrombi that are involved in the onset of AMI sometimes induce the no-reflow phenomenon after PCI whereby there is insufficient reperfusion. 4 There is reportedly a high incidence of the no-reflow phenomenon or slow flow in AMI in which the right coronary artery (RCA) is the culprit lesion. 4-6 The greater susceptibility of

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... he RCA to developing large thrombi makes successful reperfusion more difficult to achieve. It is possible that the state of the thrombi affects the onset of complications related to PCI, but there have not been any reports investigating the differences in the images of pathological thrombi according to the infarct-related coronary artery. It is now possible to aspirate coronary arterial thrombi using coronary arterial thrombectomy, 7-9 and to evaluate the pathological images in vivo. 10,11 So we investigated the characteristics of the pathological images of coronary arterial thrombi according to the infarct-related coronary artery. Methods Subjects Subjects were 231 patients with AMI who had sought treatment at Toyama Prefectural Central Hospital during a 30-months period from September 2000 to February 2003 and who had undergone emergency coronary angiography. AMI was diagnosed when chest pain persisted for at least 30 min and the 12-lead ECG confirmed ST elevation of at least 2 mm in at least 2 leads in succession, and there was confirmation by initial coronary angiography of occlusion or sub-occlusion of the infarct-related artery. Of the 199 patients indicated for PCI, 129 underwent thrombectomy. Patients who were scheduled for coronary bypass surgery (multivessel disease and left main trunk lesion), patients who could not undergo coronary arterial thrombectomy because of serious complications (fatal arrhythmia, cardiogenic shock, and pulmonary edema), and patients who had undergone thrombolytic therapy before emergency coronary angiography were excluded from the study. Of the 129 patients who underwent coronary arterial thrombectomy, there were 77 cases in which the coronary artery thrombi could be extracted for study within 24 h of the onset of AMI. Cardiac Catheterization and Coronary Intervention Written informed consent was obtained from all patients, after the patients and their families were informed of the Background Unstable plaque and coronary arterial thrombi sometimes induce a no-reflow phenomenon after intervention whereby there is sufficient reperfusion. The greater susceptibility of the right coronary artery to development of large thrombi makes successful reperfusion more difficult, therefore the characteristics of the pathological images of coronary arterial thrombi according to the infarct-related coronary artery were investigated. Methods and Results Coronary arterial thrombi were extracted from 77 patients with acute myocardial infarction (AMI) using a thrombectomy catheter. The 36 patients had a thrombus containing atherosclerotic cells. Platelets, fibrin, and neutrophils were seen in all cases. The mean ratios of structural components of thrombi were 51.0±29.5% (mean ± SD) of the platelet component, 19.9±25.7% of the erythrocyte component and 11.9±22.5% of atherosclerosis component. Erythrocyte-rich thrombi and mixed thrombi mainly composed of erythrocytes were seen in 14 of the 30 cases involving the right coronary artery, 6 of the 35 cases in the left anterior descending artery, 2 of the 11 cases of the left circumflex artery, and in the 1 case of saphenous vein bypass graft. There was significantly more erythrocyte component in the thrombi from the right coronary artery (28.7±30.1%) than in those from the left coronary artery (12.1±18.4%). Conclusion Coronary artery thrombi in AMI are composed principally of platelets. Atherosclerotic cells were identified within thrombi from some patients. In the right coronary artery there were many more thrombi that were rich in erythrocytes than in thrombi from the left coronary artery. (Circ J 2004; 68: 308 -314)