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 language | English |
|---|---|
| Journal | Journal of Invasive Cardiology |
| Volume | 14 |
| Issue number | 13 SUPPL. E |
| State | Published - Dec 1 2002 |
| Externally published | Yes |
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Keywords
- Atherosclerosis
- GP IIb/IIIa
- Inflammation
- Macrophages
- PCI
- Platelets
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
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 journal › Article
}
TY - JOUR
T1 - Inflammation, platelets, and glycoprotein IIb/IIIa inhibitors
AU - Goldschmidt-Clermont, Pascal
AU - Kandzari, David E.
AU - Sketch, Michael H.
AU - Phillips, Harry R.
PY - 2002/12/1
Y1 - 2002/12/1
N2 - 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.
AB - 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.
KW - Atherosclerosis
KW - GP IIb/IIIa
KW - Inflammation
KW - Macrophages
KW - PCI
KW - Platelets
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UR - http://www.scopus.com/inward/citedby.url?scp=0036924801&partnerID=8YFLogxK
M3 - Article
C2 - 12668859
AN - SCOPUS:0036924801
VL - 14
JO - Journal of Invasive Cardiology
JF - Journal of Invasive Cardiology
SN - 1042-3931
IS - 13 SUPPL. E
ER -