Inflammation, platelets, and glycoprotein IIb/IIIa inhibitors.

Published

Journal Article (Review)

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.

Full Text

Duke Authors

Cited Authors

  • Goldschmidt-Clermont, PJ; Kandzari, DE; Sketch, MH; Phillips, HR

Published Date

  • December 2002

Published In

Volume / Issue

  • 14 Suppl E /

Start / End Page

  • 18E - 25E

PubMed ID

  • 12668859

Pubmed Central ID

  • 12668859

International Standard Serial Number (ISSN)

  • 1042-3931

Language

  • eng

Conference Location

  • United States