title: Coronary atherosclerosis. A multifactorial disease.
abstract: BACKGROUND
  Several of the theories on the pathogenesis of atherosclerosis may be integrated into a single multifactorial one. According to this theory, the most likely sequence of events involved in early atherosclerosis is vascular dysfunction and/or injury, monocyte recruitment and macrophage formation, lipid deposition, vascular smooth muscle cell proliferation (mitogenic factor mediated), and synthesis of extracellular matrix. The interaction of all these factors will configurate the typical characteristic of the atherosclerotic plaque.
  
  
  RESULTS
  Accumulating experimental and clinical data suggest two pathways in atherosclerotic progression. In some cases, the very slow process of the pathogenesis of early lesions may be significantly accelerated by means of thrombus formation and organization. Thrombosis is a key process in the pathogenesis of late atherogenesis and in the development of acute ischemic syndromes.
  
  
  CONCLUSIONS
  The possibility of retarding human atherosclerosis or even inducing its regression is one of the present therapeutic challenges. Of the different approaches to this question, one approach aims at better control of risk factors, especially plasma lipid levels. Another approach attempts to enhance the removal of lipids from the arterial wall by increasing plasma high density lipoprotein levels. Each of these approaches, by acting on the lipid-rich plaques more prone to rupture, might prevent plaque progression and induce regression to prevent acute coronary events. A third approach, based on the key role of platelet thrombus formation in the conversion of chronic to acute events, would be the use of antithrombotic therapy. This last approach may partially prevent progression of the disease.
authors.affiliation: Cardiac Unit, Massachusetts General Hospital, Harvard Medical School, Boston 02114.
authors.forename: J J
authors.initials: JJ
authors.lastname: Badimon
authors.forename: V
authors.initials: V
authors.lastname: Fuster
authors.forename: J H
authors.initials: JH
authors.lastname: Chesebro
authors.forename: L
authors.initials: L
authors.lastname: Badimon
mesh_terms: D000818:Animals; D001792:Blood Platelets / Q000502:physiology; D003324:Coronary Artery Disease / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D003327:Coronary Disease / Q000150:complications; D006801:Humans; D050356:Lipid Metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000502:physiology; D010982:Platelet-Derived Growth Factor / Q000502:physiology; D012307:Risk Factors
chemical_list: D010982:Platelet-Derived Growth Factor