title: Clinical-pathological correlations of coronary disease progression and regression.
abstract: The initiation of atherosclerosis may result from blood flow oscillatory shear stress in certain vascular sites (bending points, bifurcations, etc.) producing chronic minimal injury resulting in functional alteration of the arterial endothelium type I injury; experimentally, this is potentiated by atherogenic risk factors such as hypercholesterolemia, hypertension, immunocomplexes, viral infections, and tobacco smoke. Such minimal injury leads to accumulation of lipid and monocytes (macrophages), and subsequently, toxic products released by the macrophages produce damage of the intimal surface with denuding endothelium type II injury or damage, which attracts platelets; all of these cells release growth factors, prompting migration and proliferation of smooth muscle cells and producing a "fibro-intimal lesion" or the outside of the capsule of a predominant "lipid lesion." The lipid lesions surrounded by a thin capsule tend to be small and rupture easily, causing type III injury or damage; that is, they are soft and weak, contain large numbers of macrophages, which may release collagenase and elastase to form abscesses, and by their location, are under the effect of flow shear forces. After plaque disruption there is thrombus formation; when thrombi are small, they can become organized and contribute to the growth of the atherosclerotic plaque; when thrombi are large and occlusive, they lead to the acute coronary syndromes. New data suggest that, at the time of plaque disruption, certain "thrombogenic" risk factors modulate the degree of thrombogenicity and, thereby, the growth of the plaque versus the various acute coronary syndromes. Aside from the need for better understanding of the basic biology of atherogenesis, emphasis on identifying and modifying the primary atherogenic and thrombogenic risk factors should continue for primary prevention. Also, new approaches should focus on the identification, stabilization, and regression of the small "lipid plaques" prone to rupture (these are not necessarily angiographically apparent), as well as on the use of better and safer antithrombotic agents for prevention of progression.
authors.affiliation: Cardiac Unit, Massachusetts General Hospital, Harvard Medical School, Boston 02114.
authors.forename: V
authors.initials: V
authors.lastname: Fuster
authors.forename: J J
authors.initials: JJ
authors.lastname: Badimon
authors.forename: L
authors.initials: L
authors.lastname: Badimon
mesh_terms: D002318:Cardiovascular Diseases / Q000145:classification / Q000473:pathology; D002455:Cell Division; D003324:Coronary Artery Disease / Q000473:pathology / Q000503:physiopathology; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology; D006801:Humans; D050356:Lipid Metabolism; D008264:Macrophages / Q000378:metabolism; D009000:Monocytes / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D009203:Myocardial Infarction / Q000503:physiopathology; D010982:Platelet-Derived Growth Factor / Q000378:metabolism / Q000494:pharmacology
chemical_list: D010982:Platelet-Derived Growth Factor