Coronary atherosclerosis revisited. A pathologist's view.
For many years the paradigm of coronary atherosclerosis, set by pathologists, was the far-advanced lesion containing extensive atheromatosis with calcifications. From the point of view of understanding atherogenesis, however, it is much more rewarding to study the coronary artery in patients without clinical evidence of obstructive coronary artery disease. In fact, the normal coronary artery is most revealing in showing discrete intimal changes, which consist of a splitting of the internal elastic lamina accompanied by a proliferation of vascular smooth muscle cells. This process eventually results in the formation of the musculo-elastic layer. In time the cellular and muscular appearance of this layer gradually transforms into a more densely packed fibrous texture. It is of interest, from a point of view of atherogenesis, that the early atherosclerotic lesions often display the histologic features of the musculo-elastic layer at the base of the plaque. Hence, these observations support the concept that the basic lesion in coronary atherosclerosis is a proliferation of vascular smooth muscle cells, most likely as a response to injury. To this extent a dysfunction of the endothelial cell barrier may by crucial. The observations also indicate that the mechanisms involved in atherogenesis also may alter vascular tone and hence, may contribute to a "spastic state" of the coronary arteries. A classification of angina pectoris, on the basis of pathogenesis into organic and spastic may thus prove to be simplistic.
D003327:Coronary Disease / Q000473:pathology*; D003329:Coronary Vasospasm / Q000473:pathology; D003331:Coronary Vessels / Q000033:anatomy & histology / Q000473:pathology*; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000473:pathology