Intimal Hyperplasia,Arterial Remodeling,and Restenosis: An Overview

Abstract

The occurrence of restenosis due to intimal hyperplasia and arterial remodeling remains an unsolved problem after cardiovascular interventions. All forms of reconstructions, whether interventional or surgical, cause injury to the vessel wall, resulting in a wound healing response. In situations in which it becomes exaggerated it leads to restenosis. This injury may involve the development of intimal hyperplasia (IH), which is defined as the migration and proliferation of smooth muscle cells (SMC) into the subintimal space of the vessel. There is subsequent SMC production and deposition of matrix with some degree of lumen narrowing. This complex process has multiple factors that have been implicated to initiate and promulgate it, including those of the immune system, coagulation system, and local paracrine growth factors and cytokines. Recent studies have shown that, besides IH through its production of a physical mass that encroaches on the lumen, the changes in the artery wall geometry, defined as arterial remodeling, also play an important role in the development of restenosis. As an arterial wound healing response to injury, the total circumference of the artery may change significantly due to fibrotic contraction or compensatory dilatation. This process of arterial remodeling, in addition to the amount of IH, seems to determine whether an artery will develop restenosis.

This overview will define the clinical scope of the problem and provide a description of the pathophysiological mechanisms following vascular injury as well some recent developments of strategies for preventing the occurrence of restenosis.