Cytomegalovirus infection and coronary restenosis.

Abstract

Current techniques of percutaneous transluminal coronary revascularization remain limited by the phenomenon of restenosis. The response of the vessel wall to the iatrogenic injury associated with coronary interventions is a complex and multifactorial process. Experimental and clinical studies suggest that a combination of different mechanisms, such as (1) smooth muscle cell (SMC) proliferation and migration (neointimal hyperplasia), (2) vascular remodeling, and (3) thrombus formation and incorporation, may contribute to the development of restenosis.1 Risk factors for restenosis have been analyzed in a large number of studies and can be categorized into lesion-, procedure-, or patient-related variables. Although consistent results have been published regarding lesion- and procedure-related factors, patient-related factors are less well characterized. Diabetes has long been recognized to be a major risk factor for restenosis after balloon angioplasty.2 3 However, studies that have demonstrated interlesion dependence of restenosis in patients who undergo multilesion intervention (the likelihood of restenosis for a lesion being higher when another companion lesion has also developed restenosis) have provided evidence for the existence of other patient-related factors.4 Evidence of prior cytomegalovirus (CMV) infection in adults is very common and usually asymptomatic. High titers of CMV antibodies are more frequent in patients with atherosclerotic disease than in control patients.5 More than …