[Pathology of AtheroThrombosIS (ATIS)].

Once atherosclerosis develops, stenosis (or occlusion) may occur in the lumen of various arteries of the living body. This can lead to a range of conditions, including myocardial infarction, cerebral infarction, aortic aneurysm and peripheral artery disease. The acronym 'ATIS' (AtheroThrombosIS) is a collective term for diseases characterized by a common course of development based on atherosclerosis. This article reviews pathological findings in atherothrombotic lesions of human coronary, carotid, and vertebrobasilar arteries as well as leg arteries and veins. Histologically, atheromatous plaques of coronary arteries can broadly be typed as fibrous and lipid-rich (atheromatous). Macroscopically, fibrous plaque has a whitish appearance and is composed of smooth muscle cells and collagen fibres. Lipid-rich (atheromatous) plaque, on the other hand, appears yellow macroscopically, with the superficial layer (closer to the lumen) having a white fibrous cap which covers the atheroma. This fibrous cap is quite thin and is likely to rupture. Typical pathological features of such atherothrombosis are narrowing of the vascular lumen due to lipid-rich (atheromatous) plaque, and thrombus formation due to a broken fibrous cap. Such plaque rupture is the underlying cause of acute myocardial infarction in about 70% of patients, while acute myocardial infarction in the remaining patients (30%) results from plaque erosion. In cases of plaque erosion, atheroma is seldom seen, and atherosclerosis manifests in a full-circumferential manner, resulting in thrombus formation due to endothelial cell injury and eventually leading to obstructive thrombi. Thus, thrombus formation associated with myocardial infarction is attributable to plaque rupture if the lesion contains a lipid-rich (atheromatous) plaque. In cases where plaques cause particularly intense injury of endothelial cells, plaque erosion is likely to occur, resulting in formation of obstructive thrombi within the vascular lumen. Primary factors involved in the evolution of ATIS are injury of vascular endothelial cells, inflammation of a vulnerable plaque and intra-plaque haemorrhage. ATIS in other vascular systems has similar pathological features. The continued increase in the aged population and the morbidity of lifestyle-related diseases will make more cases of ATIS intractable. It will be of paramount importance to prevent intractable ATIS in the future.