title: Inflammation, platelets, and glycoprotein IIb/IIIa inhibitors.
abstract: Atherosclerosis, with its thromboembolic complications (including sudden cardiac death, myocardial infarction, and other ischemic organ damage such as stroke and ischemic renovascular disease), represents by far the major cause of death, morbidity, and disability for industrialized countries, and is rapidly spreading worldwide. Atherosclerosis is also a paradigm for complex, multifactorial disorders that affect humans in an age-dependent fashion. Atherosclerosis has usually been studied in a descriptive framework of biological and clinical data gathered over more than a century. As such, it is a chronic inflammatory process that selectively affects arterial vessels, and is, at least in part, genetically predetermined. Despite spectacular progress in the cardiovascular discipline, with the development of therapeutic strategies that have substantially improved the outcome of affected patients, several key questions remain unanswered: Why is aging such a powerful risk for coronary artery disease? What is the triggering mechanism for atherosclerotic inflammation? Also, in the context of this and accompanying reviews, do we modify coronary inflammation with glycoprotein IIb/IIIa blockers? Recent progress in our understanding of the underlying process of atherosclerosis has provided us with the opportunity to refine the answers to some of these questions.
authors.affiliation: Division of Cardiology, Department of Medicine, Duke Clinical Research Institute, Duke University Medical Center, Durham, NC, 27710, USA. golds017@mc.duke.edu
authors.forename: Pascal J
authors.initials: PJ
authors.lastname: Goldschmidt-Clermont
authors.forename: David E
authors.initials: DE
authors.lastname: Kandzari
authors.forename: Michael H
authors.initials: MH
authors.lastname: Sketch
authors.forename: Harry R
authors.initials: HR
authors.lastname: Phillips
mesh_terms: D000077284:Abciximab; D000375:Aging / Q000502:physiology; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D018932:Chemokine CCL2 / Q000276:immunology*; D003324:Coronary Artery Disease / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D003328:Coronary Thrombosis / Q000209:etiology / Q000517:prevention & control*; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use*; D009203:Myocardial Infarction / Q000209:etiology / Q000628:therapy*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018932:Chemokine CCL2; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077284:Abciximab