title: The pathogenesis of an impending infarction and its treatment--an angioscopic analysis.
abstract: To clarify the pathogenesis of an impending infarction and to investigate the difference between the pathogenesis of an acute myocardial infarction and an impending infarction, we have performed percutaneous transluminal coronary angioscopy in 13 patients with an impending infarction and in 13 patients with an acute myocardial infarction. As a result, coronary thrombi were observed in 12 of the 13 patients with an impending infarction, and a similar frequency of thrombi was observed in the patients with an acute myocardial infarction. Further, grayish white thrombi were observed in 9 of 12 patients with an impending infarction, but no such thrombi were noted in those with an acute myocardial infarction. Reddish thrombi, however, were observed in all patients with acute myocardial infarction, whereas such thrombi were observed in only 3 of 12 patients with an impending infarction. Informatively, occlusive thrombi occurred more frequently in patients with an acute myocardial infarction than in those with an impending infarction. As a thrombus plays an important role in an impending infarction, we also evaluated the effect of anticoagulant and thrombolytic therapy for an impending infarction in 79 patients. The incidence of recurrent angina and a subsequent acute myocardial infarction were significantly higher in non-heparin-treated patients and in thrombolytic-treated patients than in heparin-treated patients. In conclusion, a thrombus plays an important role in the pathogenesis of an impending infarction and in an acute myocardial infarction, though the characteristics of the thrombus differ in each instance. This difference may account for the differing results of thrombolytic therapy. Heparin was found an effective treatment for myocardial ischemia in an impending infarction.
authors.affiliation: Department of Emergency Medicine, National Defense Medical College, Saitama, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Mizuno
authors.forename: H
authors.initials: H
authors.lastname: Hikita
authors.forename: A
authors.initials: A
authors.lastname: Miyamoto
authors.forename: K
authors.initials: K
authors.lastname: Satomura
authors.forename: T
authors.initials: T
authors.lastname: Shibuya
authors.forename: K
authors.initials: K
authors.lastname: Arakawa
authors.forename: A
authors.initials: A
authors.lastname: Kurita
authors.forename: H
authors.initials: H
authors.lastname: Nakamura
mesh_terms: D017546:Angioscopy; D003328:Coronary Thrombosis / Q000150:complications; D003331:Coronary Vessels / Q000473:pathology*; D004562:Electrocardiography; D006493:Heparin / Q000008:administration & dosage; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D015912:Thrombolytic Therapy; D014568:Urokinase-Type Plasminogen Activator / Q000008:administration & dosage
chemical_list: D006493:Heparin; D014568:Urokinase-Type Plasminogen Activator