Inflammation, platelets, and glycoprotein IIb/IIIa inhibitors

Pascal Goldschmidt-Clermont, David E. Kandzari, Michael H. Sketch, Harry R. Phillips

Research output: Contribution to journalArticle

8 Citations (Scopus)

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? Do platelets promote 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.

Original languageEnglish
JournalJournal of Invasive Cardiology
Volume14
Issue number13 SUPPL. E
StatePublished - Dec 1 2002
Externally publishedYes

Fingerprint

Integrin beta3
Platelet Glycoprotein GPIIb-IIIa Complex
Atherosclerosis
Inflammation
Sudden Cardiac Death
Developed Countries
Coronary Artery Disease
Cause of Death
Blood Platelets
Stroke
Myocardial Infarction
Morbidity

Keywords

  • Atherosclerosis
  • GP IIb/IIIa
  • Inflammation
  • Macrophages
  • PCI
  • Platelets

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Goldschmidt-Clermont, P., Kandzari, D. E., Sketch, M. H., & Phillips, H. R. (2002). Inflammation, platelets, and glycoprotein IIb/IIIa inhibitors. Journal of Invasive Cardiology, 14(13 SUPPL. E).

Inflammation, platelets, and glycoprotein IIb/IIIa inhibitors. / Goldschmidt-Clermont, Pascal; Kandzari, David E.; Sketch, Michael H.; Phillips, Harry R.

In: Journal of Invasive Cardiology, Vol. 14, No. 13 SUPPL. E, 01.12.2002.

Research output: Contribution to journalArticle

Goldschmidt-Clermont, P, Kandzari, DE, Sketch, MH & Phillips, HR 2002, 'Inflammation, platelets, and glycoprotein IIb/IIIa inhibitors', Journal of Invasive Cardiology, vol. 14, no. 13 SUPPL. E.
Goldschmidt-Clermont P, Kandzari DE, Sketch MH, Phillips HR. Inflammation, platelets, and glycoprotein IIb/IIIa inhibitors. Journal of Invasive Cardiology. 2002 Dec 1;14(13 SUPPL. E).
Goldschmidt-Clermont, Pascal ; Kandzari, David E. ; Sketch, Michael H. ; Phillips, Harry R. / Inflammation, platelets, and glycoprotein IIb/IIIa inhibitors. In: Journal of Invasive Cardiology. 2002 ; Vol. 14, No. 13 SUPPL. E.
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