title: The three mechanisms for coronary artery disease progression: insights into future management.
abstract: The basic mechanisms of atherosclerotic progression have been well elucidated during the last few years. Basic experimental and clinical information has helped define the three stages of progression. In this review we outline the pathologic and clinical differences between slow, rapid, and intermediate progression. The eight morphologically different lesions (types I, II, III, IV, Va, Vb, Vc, and VI) in their various stages are defined. The relationship between specific type of lesion and chronic endothelial injury, cardiac risk factors, and increased vascular permeability to lipids is noteworthy. In regard to the acute coronary syndromes, the fate of plaque rupture and our understanding of "passive" vs. "active" rupture are defined. In addition to the phenomenon of plaque rupture, the thrombogenicity of atherosclerotic plaques in the genesis of coronary syndromes is described. The combination of plaque disruption and a high thrombogenic risk profile--including local and systemic factors--is vital to understanding the genesis of the acute coronary syndromes. In approaching the use of these new insights to arrest or reverse the atherosclerotic process, it is essential to remember that the disease process starts early in life and takes many years to progress to the symptomatic stage. The future holds promise for the development of preventive strategies to halt the progression of coronary disease--the number one killer in the United States.
authors.affiliation: Department of Cardiology, Mount Sinai School of Medicine, New York, NY 10029, USA.
authors.forename: M A
authors.initials: MA
authors.lastname: McLaughlin
authors.forename: V
authors.initials: V
authors.lastname: Fuster
mesh_terms: D000208:Acute Disease; D000328:Adult; D000367:Age Factors; D000789:Angina, Unstable / Q000209:etiology; D002199:Capillary Permeability; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D003328:Coronary Thrombosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D003329:Coronary Vasospasm / Q000209:etiology; D016757:Death, Sudden, Cardiac / Q000209:etiology; D004562:Electrocardiography; D004730:Endothelium, Vascular / Q000473:pathology; D006801:Humans; D050356:Lipid Metabolism; D008055:Lipids / Q000493:pharmacokinetics; D009203:Myocardial Infarction / Q000209:etiology; D012307:Risk Factors; D013314:Stress, Mechanical; D013577:Syndrome
chemical_list: D008055:Lipids