Myocardial infarction induced by coronary venous thrombosis--an experimental study.
In a previous study, we proved experimentally that transmural infarction was produced in the area of the left anterior descending artery (LAD) by coronary sinus occlusion attributable to thrombus formation. In an attempt to produce infarction due to thrombus formation and to investigate the influence of thrombosis, the anterior interventricular vein (AIV) was occluded in this study. In each of 6 adult mongrel dogs, a balloon-tipped catheter was wedged in the AIV via the jugular vein. After the occlusion of blood flow by inflation of the balloon, thrombin (30-50 IU) was injected into the AIV to produce thrombi and the balloon was removed 60 min later. As a result, ischemic changes of ST and T in an ECG were clearly observed in all 6 dogs, and serum levels of myocardial enzymes supported the development of myocardial necrosis. Coronary arteriography performed 48 hours after the occlusion of the AIV showed normal findings in all 6 dogs, and residual thrombi in the AIV were observed in 5 dogs by coronary venography. In these 5 dogs, very local contraction band necrosis (CBN) was noted in the epicardium surrounding the AIV. These experimental findings indicate the following: 1) CBN can also be induced by coronary venous occlusion, 2) once the occlusive mechanism acts on the coronary venous system, the changes which are clinically similar to myocardial infarction can be induced regardless of its causes, 3) ischemic changes in myocardium can be localized in the epicardium irrespective of its causes. Therefore, these findings are considered to be important in the investigation of the clinical onset mechanism of myocardial infarction.
Miyahara
K
K
Cardiovascular Division, Shinkyoh Hospital, Kagoshima, Japan.
Sakamoto
H
H
Sakamoto
H
H
Satoh
E
E
D000818:Animals; D002404:Catheterization; D003328:Coronary Thrombosis / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D004285:Dogs; D004562:Electrocardiography; D009203:Myocardial Infarction / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D010496:Pericardium / Q000473:pathology