PATHOBIOLOGY OF RESTENOSIS AFTER ANGIOPLASTY

Restenosis is a consequence of a disturbed wound healing process after the vascular trauma of angioplasty or similar intervention. Mechanism s involve clotting, cell recruitment and activation (from the blood, t he vascular wall, and the perivascular tissue), as well as cell prolif eration, matrix synthesis, and tissue contraction. In more than half o f the lesions, these events are coordinated and self-limited, leading to a remodeling of the vessel wall with more stable and viable tissue than the original necrotic and lipid-laden atherosclerotic plaque. Thi s remodeling may he as important as the gain in lumen for long-term pa tency. However, this basically favorable healing process may be distur bed by predominantly local conditions such as poor resulting wound ana tomy, necrotic debris, excessive old plaque material, continued moveme nt and irritation, or poor flow, leading to repetitive activation of a ny of these mechanisms. It is this unpredictable chronic persistence o f these essentially physiologic mechanisms rather than the mechanisms themselves that eventually lead to an exuberant proliferative and synt hetic response, which builds up restenotic mass together with thrombot ic material and the old plaque components.