Author + information
- Received April 15, 1996
- Revision received August 5, 1996
- Accepted August 26, 1996
- Published online December 1, 1996.
- Herve Le Breton, MD,
- Edward F. Plow, PhD and
- Eric J. Topol, MD, FACC⁎ ()
- ↵⁎Address for correspondence: Dr. Eric J. Topol, Department of Cardiology, F/25, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195-5066.
The role of platelets in the process of restenosis after percutaneous coronary intervention is not fully understood. After vascular injury there is extensive platelet activation, adhesion, aggregation and secretion. Through the liberation of growth factors, such as platelet-derived growth factor, and surface expression of cell adhesion molecules, such as the glycoprotein Ilb/IIIa integrin, platelets appear to be a pivotal mediator of the vascular injury response. Experimental models have demonstrated that profound, prolonged thrombocytopenia, or blockade of the Ilb/IIIa receptor, may reduce neointimal hyperplasia after arterial balloon injury. However, multiple clinical trials testing conventional or new platelet agents have not yielded any salutary effects. The recent finding that abciximab, a monoclonal antibody fragment directed against Ilb/IIIa, reduced clinical restenosis after coronary angioplasty by 26% in patients raises questions about the mechanism of benefit. The αvβ3 vitronectin receptor is responsible for binding endothelial cells to platelets, and it also has a key role in modulating smooth muscle cell migration. It is possible that the antibody fragment exerts its effect on restenosis by means of αvβ3, because abciximab fully cross-reacts to this integrin owing to the shared β3subunit. To date, the other platelet glycoprotein Ilb/IIIa inhibitors, including Integrelin, Tirofiban, Lamifiban and Xemilofiban, are specific in binding to this particular integrin. Considerable further study is necessary to unravel the effects of platelets on the restenosis process.
From the Department of Cardiology and the Joseph J. Jacobs Center for Thrombosis and Vascular Biology, The Cleveland Clinic Foundation, Cleveland, Ohio. This study was supported by the French Federation of Cardiology (Dr. Le Breton) and the Jacobs Center Endowment, Cleveland, Ohio (Drs. Plow and Topol).
- Received April 15, 1996.
- Revision received August 5, 1996.
- Accepted August 26, 1996.
- American College of Cardiology