1975 Volume 2 Issue 4 Pages 217-223
A total of 390 aortas with widely scattered age range in Japanese autopsy cases was morphologically studied for intimal thrombosis. The internal surface of the aorta was divided into 6 segments; each two in the aortic arch, thoracic and abdominal aorta, and extent of lipid deposition, fibrous plaque and complicated lesions in the aortic intima was macroscopically estimated as well as that of thrombosis.
The intimal thrombosis appeared first at the fourth decade of male and the sixth decade of female. The incidence of thrombosis was gradually increased with age up to 80% and 60% in the normotensive (lower than 150/90mmHg) oldest male and female respectively. Presence of hypertension accelerated apparently an increase of the incidence and extent of thrombosis. The extent of thrombosis was maximal at the abdominal aorta, the second at the aortic arch and minimal at the thoracic aorta.
The incidence of thrombosis was varied by basic disease or disorders. Its difference was analysed by comparison of the age-corrected incidence of thrombosis. More than average incidence of thrombosis was observed in the ischemic and/or hypertensive heart disease with a special predominancy in male, idiopatic myocardiopathy and diabetes mellitus. Less than average incidence was seen in the rest of disease and significantly less incidence was in renal disease, blood disease and neoplasmas.
If following organization of the intimal thrombosis made a progression or modification of aortic sclerosis, it should make an increase of fibrotic component, because accumulated thrombosis area with age was paralleled with intimal fibrosis area and not with lipidosis area. On the other hand, the thrombosis area per se was fairly paralleled with lipidosis area and not with fibrosis area. This evidence advocated the possibility that the intimal thrombosis could occur on the previously existed atheromatous lesion and its organization could make a fibrous cap or plaque on the atheroma. It suggested that the thrombosis was not primary element for atherogenicity but a modifying or accelerating factor for sclerosis.
The significantly high incidence of thrombosis in male ischemic and/or hypertensive heart disease might postulate existence of thrombophilia or decrease of fibrinolytic activity in the aortic wall in this paticular disease.
