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REVIEW ARTICLE

Arterial remodeling and coronary artery disease: the concept of "dilated" versus "obstructive" coronary atherosclerosis

^a Cleveland Clinic Foundation, Cleveland, Ohio, USA

Manuscript received January 16, 2001; revised manuscript received April 10, 2001, accepted April 23, 2001.

Reprint requests and correspondence: Dr. E. Murat Tuzcu, The Cleveland Clinic Foundation, F 25, 9500 Euclid Avenue, Cleveland, Ohio 44195
tuzcue{at}ccf.org

Traditionally, the development of coronary artery disease (CAD) was described as a gradual growth of plaques within the intima of the vessel. The outer boundaries of the intima, the media and the external elastic membrane (EEM), were thought to be fixed in size. In this model plaque growth would always lead to luminal narrowing and the number and severity of angiographic stenoses would reflect the extent of coronary disease. However, histologic studies demonstrated that certain plaques do not reduce luminal size, presumably because of expansion of the media and EEM during atheroma development. This phenomenon of "arterial remodeling" was confirmed in necropsy specimens of human coronary arteries. More recently, the development of contemporary imaging technology, particularly intravascular ultrasound, has allowed the study of arterial remodeling in vivo. These new imaging modalities have confirmed that plaque progression and regression are not closely related to luminal size. In this review, we will analyze the role of remodeling in the progression and regression of native CAD, as well as its impact on restenosis after coronary intervention.

Abbreviations and Acronyms   CAD = coronary artery disease   EEM = external elastic membrane   IVUS = intravascular ultrasound   MRI = magnetic resonance imaging   SVG = saphenous vein grafts   TLR = target lesion revascularization rate

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