Atheromatous plaque location and arterial remodelling.

Abstract

See doi:10.1016/S1095-668X(02)00426-8for the article to which this editorial refers. Atherosclerosis is associated with a number of structural and functional changes in the arterial wall. Endothelial dysfunction, oxidised-LDL accumulation, increased concentrations of macrophages, neutrophils and T-cells as well as smooth muscle cell migration are some of the most relevant changes that take place during atherogenesis and coronary artery disease progression. It has been shown that the presence of a space-occupying plaque is commonly associated with the expansion of the arterial wall (‘vessel remodelling’).1 The mechanisms responsible for this phenomenon are speculative. The majority of coronary artery atheromatous plaques are eccentric and tend to grow towards the adventitia before encroaching upon the lumen of the artery. This was shown initially by Glagov et al.1 in a pioneering study, which demonstrated thatleft main coronary arteries enlarge in response to atheromatous plaque growth, a phenomenon termed remodelling. Interest in arterial remodelling grew significantly in recent years with the advent of intravascular ultrasound (IVUS) imaging.2,3 Both ‘positive’ and ‘negative’ types of vascular remodelling have been identified. Positive arterial remodelling is described by pathologists as outward plaque bulging associated with the thinning of the arterial media. Positive remodelling is also defined by IVUS as the (positive) ratio: external elastic membrane (EEM) area measured at thelesion site/EEM measured at a control reference site. Negative remodelling, identified in IVUSstudies, describes a ‘paradoxical wall shrinkage’ at the site of atheromatous plaques. This type of remodelling is more commonly found in peripheral arteries compared to coronary arteries.4–6 There is an apparently erratic behaviour of atheromatous coronary artery segments regarding wall expansion at …