Pathobiology of restenosis after angioplasty

Restenosis is a consequence of a disturbed wound healing process after the vascular trauma of angioplasty or similar intervention. Mechanisms involve clotting, cell recruitment and activation (from the blood, the vascular wall, and the perivascular tissue), as well as cell proliferation, matrix synthesis, and tissue contraction. In more than half of 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. This remodeling may be as important as the gain in lumen for long-term patency. However, this basically favorable healing process may be disturbed by predominantly local conditions such as poor resulting wound anatomy, necrotic debris, excessive old plaque material, continued movement and irritation, or poor flow, leading to repetitive activation of any of these mechanisms. It is this unpredictable chronic persistence of these essentially physiologic mechanisms rather than the mechanisms themselves that eventually lead to an exuberant proliferative and synthetic response, which builds up restenotic mass together with thrombotic material and the old plaque components.