[Morphologic studies following coronary thrombolysis and PTCA].

Compared with those of other species human coronary arteries show a particularly marked diffuse thickening of the intima. Superimposed on this diffuse thickening local sclerotic changes develop. In early stages they contain plenty of lipids which are mainly stored in modified smooth muscle cells, partly also in cells of monocytic origin. Normally ruptures of arteriosclerotic plaques are responsible for thrombotic occlusions in extensive transmural myocardial infarctions. They are caused by ruptures of the fibrous layer covering the necrotic core of the plaque. By thrombolytic therapy platelet thrombi can be dissolved but the causal stenosing plaques remain. Arteriosclerotic stenoses can be dilated by PTCA. In doing so tears in the area of the plaque can be observed. Often there is partial detachment of the intima from the media, sometimes even extensive dissection. Proliferation of smooth muscle cells is important regarding healing of these tears. They build up a neointima and can cause restenoses in cases of massive proliferation. So far it is unknown how often platelet thrombus formations and their successive stages are involved in causing restenoses. In addition it is not yet clear how far stretching of the media and the collagenous fibers of the adventitia contributes to a permanent dilatation of the lumen after PTCA.