Atherosclerosis is
chronic disease, the prevalence of which has increased steadily as the population ages.
Vascular injury is believed to be critical initiating event in pathogenesis of spontaneous
atherosclerosis. Syndrome of accelerated
atherosclerosis has been classically described in patients undergoing
heart transplantation,
coronary artery bypass graft, and percutaneous transluminal coronary angioplasty. In contrast to spontaneous
atherosclerosis, denuding endothelial injury followed by
thrombus formation and initial predominant smooth muscle cell proliferation is believed to be playing a significant role in accelerated
atherosclerosis. There is no universal definition of rapid progression of
atherosclerosis. However most studies describing the phenomenon have used the following definition: (i) > or = 10% diameter reduction of at least one preexisting
stenosis > or = 50%, (ii) > or = 30% diameter reduction of a preexisting
stenosis <50%, and (iii) progression of a lesion to total occlusion within few months. Recent studies have described the role of
coronary vasospasm, human immunodeficiency virus, various inflammatory markers, and some genetic mutations as predictors of rapid progression of
atherosclerosis. As research in the field of vascular biology continues, more factors are likely to be implicated in the pathogenesis of rapid progression of
atherosclerosis.