REVIEW ARTICLES
Platelets and restenosis
Baskaran Chandrasekar, MDa and
Jean-François Tanguay, MDa
a Division of Interventional Cardiology, Montreal Heart Institute, Montreal, Canada
Manuscript received June 4, 1999;
revised manuscript received September 26, 1999,
accepted November 15, 1999.
Reprint requests and correspondence: Dr. J F Tanguay, Montreal Heart Institute, 5000 Belanger, Montreal H1T 1C8, Canada Tanguay{at}icm.umontreal.ca
Restenosis is currently the major limitation of percutaneous transluminal coronary angioplasty (PTCA). Factors such as elastic recoil, migration of vascular smooth muscle cells from media to intima, neointimal proliferation and vascular remodeling underly the restenotic process. Presently there is no effective therapy available for restenosis. The role of platelets in the development of thrombosis and abrupt closure after PTCA is well recognized. However, the effects of platelets in PTCA extend well beyond the early phase. Although antiplatelet agents such as glycoprotein IIb/IIIa antagonists have been reported to reduce target vessel revascularization, major unresolved controversies still exist. This report reviews the potential role of platelets in restenosis. Various drugs, successfully tested in experimental studies and in a small number of human studies, that inhibit the effect of platelets on the restenotic process are also reviewed.
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Abbreviations and Acronyms
| | AS-OLN | = antisense oligonucleotides | | DNA | = deoxyribonucleic acid | | GP | = glycoprotein | | mRNA | = messenger ribonucleic acid | | PDGF | = platelet-derived growth factor | | PTCA | = percutaneous transluminal coronary angioplasty | | SMC | = smooth muscle cell | | TGF | = transforming growth factor |
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