Although percutaneous transluminal coronary angioplasty is a widely accepted form of therapy for coronary artery disease, there is a 30% restenosis rate associated with it. The pathobiological processes that are triggered following coronary angioplasty are related to platelet-vessel wall interactions, coagulation, endothelial injury and smooth muscle cell modulation and proliferation. These events are reviewed with respect to the role of platelets and the products they release at the site of endothelial injury. Various families of antiplatelet drugs are discussed with regard to the rationale for their use and the results reported in patients undergoing percutaneous transluminal coronary angioplasty. The major conclusion is that a variety of processes are likely to be responsible for restenosis. Acetylsalicylic acid has been shown to be effective in reducin cardiovascular disease conditions associated with thrombosis and may effect reductions in restenosis through its inhibition of this process. Current pharmacologic regimens do not significantly reduce the incidence of smooth muscle cell proliferation, an important feature of long term stenosis. The role of new, more specific antiplatelet drugs as well as innovations in instrumental technology may hold future promise in reducing rates of restenosis.
|Original language||English (US)|
|Number of pages||10|
|Journal||Canadian Journal of Cardiology|
|State||Published - Jan 1 1988|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine