Mural Vascularization in Coronary Arteries, and its Role in Progression of Arteriosclerosis

To study mural vascularization in coronary arteries and its role in progression of coronary sclerosis, three major approaches have been attempted, as one of the most impressive morphological characteristics of coronary atherosclerosis is a localized eccentric intimal thickening, and such characteristic may not be explained by generalized factors such as plasma constituent insudations. Circulatory disturbances within certain points of the arteries may be one of local factors partly responsible for such characteristic.Firstly, 56 coronary arteries from child and adolescent autopsy cases, 10 from adults without significant cardiac diseases, and 35 arteries from cases with myocardial infarction were histologically studied on multiple step sections and serial section for selected occasions. Secondly, silicone perfusion to the arteries obtained from autopsy cases was tried to analyse a morphology of vasa vasorum. Thirdly, ferritin-used tracer electronmicroscopic investigation was carried out in the rabbit coronary arteries to study intramural circulation of arterial walls.Vasa vasorum in the media were often found in the adults even in the non-atheromatous segments of the arteries, and occasionally in the childhood and adolescence. Vasa vasorum were more prominent in the segments of the arteries with intimal thickening, and seemed to have a communication to the adventitial side.In the atherosclerotic areas, mural vessels were often seen also in the thickened intima. These intimal vessels might be produced from the endothelium or as a result of organization of thrombi. However, it was occasionally proven histologically on serial sections that intimal vessels had a direct communication with vessels entering from the adventitia. This presumably meant a possibility that intimal vessels might produce anastomoses with vasa vasorum from the adventitia.In addition, it could be often found that there were focal edema, concentric lamellar fibrosis, small foci of macrophage accumulation, microhemorrhage and hemosiderin deposition around mural vessels, all of which might be a result following local circulatroy distrubances within the arterial walls.Tracer-used EM study revealed a deposition of ferritin particles in the spaces just beneath the internal elastic lamina in the media and also even in the intercellular spaces in the most outer layer of the media close to the adventitia. This result has led to an idea that intramural intercellular fluid circulation may exist in the arterial walls, and there may be venous channels in mural vasculature system, which may play in part a role in progression of coronary sclerosis.