Molecular biology: insight into the causes and prevention of restenosis after arterial intervention.

Very little is known about the development of postatherectomy or postangioplasty restenosis. Morphologically, restenosis lesions are primarily composed of smooth muscle cells with associated matrix proteins and develop within 3-6 months. Although some degree of smooth muscle cell proliferation is a necessary part of the healing process after injury, it is unclear why only some individuals develop clinically significant lesions. Platelet deposition and release of growth factors have been postulated to be important in initiating the cellular growth response after vascular injury. Current data suggest that growth factors synthesized locally in the vessel wall may be very important in controlling smooth muscle proliferation. In addition, atherosclerotic plaques contain many procoagulant proteins that are exposed by angioplasty or atherectomy. These proteins stimulate a coagulation response and the activation of thrombin, resulting in platelet aggregation and thrombus formation. Thrombin mediates several biologic responses that may facilitate vascular lesion formation and can act directly as a smooth muscle mitogen. Vascular lesion formation as a result of percutaneous transluminal coronary angioplasty or atherectomy may be stimulated by a combination of factors, including platelet deposition and thrombin action, ultimately generating an autocrine growth response in the vessel wall.