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To investigate the pathogenesis of acute myocardial infarction (AMI) and values of intracoronary aspiration thrombectomy (ICAT), we applied ICAT to reperfusion therapy using generally available intracoronary catheters to aspirate intracoronary occlusive tissues. We assigned ICAT or primary percutaneous transluminal coronary angioplasty (PTCA) to patients with evolving AMI (Thrombolysis In Myocardial Infarction (TIMI) trial grade 0), and investigated primary histopathologic, clinical, and angiographic outcomes in 43 patients treated with ICAT alone or followed by PTCA, and compared the outcomes with those in 48 patients treated with primary PTCA. No major complications (procedural death, emergent bypass graft surgery) occurred. Reconalization (TIMI grade 3 and 2) was achieved in 25 patients (58%) with ICAT alone and in 39 patients (91%) with ICAT alone or followed by PTCA. Aspirated thrombi were defined as recent thrombi in 21 cases (49%), atheroma in 6 (14%), no thrombi in 13 (30%), and organized thrombi in 1 case. In cases of recent thrombi, ICAT alone provided recanalization more frequently than in those of atheroma or no thrombi (18 of 21 [86%], 3 of 6 [50%], 4 of 13 [31%], respectively; p < 0.05; recent thrombi vs atheroma or no thrombi). There were no significant differences in primary recanalization rate (ICAT alone or followed by PTCA vs primary PTCA; 91% vs 92%) or incidence of complications between the 2 strategies. These results indicate that although the pathogenesis of AMI is heterogeneous in each individual case, intracoronary thrombus contributes little to the pathogenesis of average AMI, and therefore mechanical approaches may be feasible to maximize reperfusion therapies for AMI.

Objectives: The purpose of this study was to test the hypothesis that the diameter of the recipient coronary artery of the well developed collateral circulation in patients with acute myocardial infarction increases because of the augmented intravascular pressure caused by subsequent collateral development., Background: It is well known that collateral circulation develops after acute myocardial infarction. However, some patients have a well developed collateral circulation at the onset of infarction, which may limit the angiographic evaluation of further development of collateral circulation., Methods: We measured the diameter of the donor and recipient arteries of the collateral circulation by means of a computer-assisted analysis system in seven patients with acute myocardial infarction who had a totally occluded infarct-related coronary artery during the acute and chronic stages of infarction. All coronary angiograms were obtained after the administration of sublingual nitroglycerin. The measurement was repeated immediately after (within 6 h) and late after (42 +/- 11 days) the onset of acute myocardial infarction., Results: The diameter of the donor artery remained unchanged (1.32 +/- 0.98 vs. 1.42 +/- 1.12 mm). In contrast, the diameter of the recipient artery increased from 1.25 +/- 0.63 to 1.55 +/- 0.61 mm (p < 0.01). These changes in coronary artery diameter were associated with an improvement in regional myocardial wall motion at rest in infarct areas (6.7 +/- 7.0% vs. 13.6 +/- 10.7%, p < 0.05)., Conclusions: These findings indicate that serial measurement of coronary artery diameter is useful for the evaluation of collateral development after acute myocardial infarction.

The incidence and pathologic features of cardiac lesions in 184 autopsied aged patients with disseminated intravascular coagulation (DIC) were reported. Coronary thrombosis was noted in 31 (16.8%), fresh myocardial necrosis in 60 (32.6%) and massive myocardial hemorrhage in 49 (26.6%) of these patients. Fresh myocardial infarction was present in 16 (8.7%) patients, 13 of whom manifested coronary thrombosis. The site of thrombi deposition was closely related to preexisting stenotic lesions of the coronary arteries. Only 3 of 16 patients with disseminated intravascular coagulation and acute myocardial infarction had typical cardiac symptoms. In most patients, the electrocardiographic changes were equivocal or not diagnostic for the diagnosis of acute myocardial infarction. We suggest the possibility that coronary thrombi in disseminated intravascular coagulation may gradually increase in extent and severity, leading to confluent areas of myocardial necrosis. The possibility of death due to heart failure, arrhythmia or cardiac rupture, points to the importance of recognizing the frequent cardiac involvement in aged patients with disseminated intravascular coagulation.

Influence of vasodilator therapy on prognosis of acute myocardial infarction complicated by left heart failure (in Killip classes II and III) was studied in 22 aged patients (mean age; 75.7 years). The patients were retrospectively divided into 2 groups: Group I; 12 patients were treated with isosorbide dinitrate and/or chlorpromazine and Group II; 10 patients were treated with other conventional medical measures. Initial hemodynamic changes on admission were not significantly different between 2 groups. With these treatments mortality rate within 2 weeks of treatment was lower in Group I than in Group II (p less than 0.01), however, cumulative cardiac mortality rate within 18 months did not differ significantly. The present study demonstrated beneficial influence of vasodilator therapy on early prognosis in aged patients, but failed to show prolonged influence on later mortality.