Expansive Arterial Remodeling: Location, Location, Location

Abstract

Abstract-The artery is a dynamic organ capable of changing its geometry in response to atherosclerotic plaque formation.Expansion of the vessel diameter retards luminal narrowing and is considered a compensatory response. However, the expansive remodeling response is a "wolf in sheep's clothes," because expansion is associated with the presence of inflammatory cells, proteolysis, and a thrombotic plaque phenotype. The prevalence and clinical presentation of expansively remodeled lesions may differ among vascular beds. However, it is evident that all types of atherosclerotic arterial expansive lesions share the presence of inflammatory cells and subsequent protease activities. The potential role of inflammation and protease activity in the development of the different remodeling modes is discussed. Key Words: remodeling Ⅲ atherosclerosis Ⅲ toll-like receptor Ⅲ inflammation Ⅲ compensatory enlargement P laque formation has long been considered the only determinant of atherosclerotic luminal narrowing. The arterial wall, however, is not a rigid tube, but rather an organ capable of overall reshaping in response to hemodynamic, mechanical, and biochemical stimuli. For instance, the increase in the circumference of the artery can partially or totally compensate for the encroachment of the lumen caused by formation of atherosclerotic plaques or by intimal hyperplasia after arterial injury. 1-3 However, the arterial wall may also respond with constrictive remodeling, thereby aggravating the luminal narrowing response 4,5 (Figure 1).Scientific interest in the role of arterial remodeling in occlusive arterial disease boomed with the upcoming use of the visualization technique of intravascular ultrasound (IVUS). With IVUS, it became apparent just how ubiquitously remodeling can prevent plaque from encroaching on the lumen and also how failure of an expansive remodeling response accelerates luminal stenosis in de novo atherosclerosis. The role of such geometrical remodeling response in relation to plaque formation is currently appreciated but has been traditionally strongly underestimated as a causal factor for arterial occlusive disease. It has recently become clear that the geometrical change in arterial size and plaque area may equally contribute to the luminal narrowing in atherosclerotic disease 6 (Figure 2). For instance, it is possible to demonstrate that in 5% of patients eligible for coronary intervention, the plaque mass at the culprit lesion is actually smaller than that located at the angiographically normal reference site, indicating that in such lesions the degree of luminal narrowing is determined by the differences in vessel size rather than by the plaque mass. 6 In this brief review, an overview of anatomical localization and local morphology of the different remodeling modes is given. We also discuss available results of mechanistic

Predictors of carotid atherosclerotic plaque progression as measured by noninvasive magnetic resonance imaging

“…Most of the concepts of arterial remodeling are based on histological studies (one time point data) of coronary arteries (2,16,17). Therefore, little is known about the change of arterial wall dimensions in the carotid artery over time.…”

Levels of extra domain A containing fibronectin in human atherosclerotic plaques are associated with a stable plaque phenotype

“…EDA in the plaque may activate Tlr4 and initiate an inflammatory response, like a fraction of EDA is able to activate Tlr4 and initiate an inflammatory cascade [14]. But Tlr4 activation is also important for collagen turnover [20] and VSMC proliferation [30]. EDA might trigger SMC proliferation via Tlr4 activation, leading to stabilization and reorganization of the plaque, which results in conversion of an unstable inflammatory plaque into a stable, smooth muscle cell rich plaque.…”

“…Recently, we and others showed that Tlr4 activation accelerates arterial occlusion by neointima formation, plaque formation, geometrical remodeling and plaque destabilization [18][19][20][21]. It remains unclear which ligands activate Tlr4 and thereby promote atherosclerotic luminal narrowing.…”

Carotid artery plaque assessment using quantitative expansive remodeling evaluation and MRI plaque signal intensity

“…20 Plaque with expansive remodeling has been shown to have a significantly larger lipid core and higher macrophage count than negatively or less positively remodeled plaque. 31 Recent studies have also shown that expansive carotid remodeling was associated with low endothelial stress and plaque rupture 4,5 and was significantly greater in patients with cerebral ischemic symptoms than in asymptomatic patients.…”