A Study for Hemodynamic Mechanism of Myocardial Infarction following Aortic Dissection.
- Author:
Young Jik LEE
;
Ji Shin LEE
;
Jong Tae PARK
- Publication Type:Case Report
- MeSH:
Adult;
Aorta;
Aortic Rupture;
Aortic Valve;
Arteries;
Atherosclerosis;
Autopsy;
Brachiocephalic Trunk;
Coronary Vessels;
Dilatation, Pathologic;
Elastic Tissue;
Giant Cell Arteritis;
Heart;
Heart Atria;
Hematoma;
Hemodynamics*;
Histiocytes;
Humans;
Hypertension;
Hyperthyroidism;
Infarction;
Male;
Marfan Syndrome;
Muscle, Smooth;
Myocardial Infarction*;
Myocardium;
Necrosis;
Pregnancy;
Sinoatrial Node;
Thorax;
Wounds and Injuries
- From:Korean Journal of Legal Medicine
1997;21(1):97-104
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Aortic dissection may be considered the result of a discrepancy between the strength of the aortic wall and the intramural pressure. And factors that predispose to aortic dissection may include systemic hypertension, cystic medial necrosis, Marfan's syndrome, atherosclerosis, disease of aortic valve, pregnancy, giant cell arteritis, hyperthyrosis, disease of aortic valve, pregnancy, giant cell arteritis, hyperthyroidism, and blunt chest trauma. A few of aortic dissection may extend retrograde toward the aortic valve and involve the coronary arteries. Coronary artery occlusions due to mural dissection are an uncommon but well documented cause of myocardial infarction. Although rare, extramural hematoma compressing the coronary artery is another cause of myocardial infarction. At autopsy of 43 years old male who had no critical external wound, pericardial sac was distended and contained 400ml of dark red and clotted blood. Examination of the aorta revealed only minute atherosclerosis, intact aortic valve, and patent coronary ostia. 0.5cm sized aortic rupture was noted at the 3.5cm distal to the aortic valve. DeBakey type II aortic dissection was found to involve the ascending aorta and brachiocephalic trunk. Three intimal tears were 1.5cm, 8cm. 11.5cm distal to the aortic valve and two false lumens which had intact area between them extended 3.5cm distal to the third intimal tear and proximally in a retrograde fashion to the aortic root. Microscopically, sections of aorta showed relatively intact arrangement of smooth muscle and elastic fibers, except mild vascular ectasia and scattered several foci of the small sized aggregation of foamy histiocytes, and there was no evidence of cystic medial degeneration in aorta. Sections of both coronary arteries did not show mural dissection or atherosclerosis. Sections of right atrium and sinus node showed inflammatory reaction, extensive replacement of myocardium by active fibrous tissue consistent with infarction. There was no histologic evidence of myocardial infarction in the walls of other chambers or septum of the heart. We believe that extramural compression of the artery to sinus m\node by the dissecting hematoma was the cause of myocardial infarction involving the right atrium and the sinus node.
