Correlation Between Carotid Intimal/Medial Thickness and Atherosclerosis

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Abstract
A widely adopted surrogate for predicting rates of cardiovascular events involves measure of carotid intimal-medial thickness (CIMT) by B mode ultrasound, a technique available since the mid 1980s. The value of this modality remains in its ability to noninvasively assess cardiovascular risk beyond traditional factors identified by the Framingham risk score, and it is among the few available techniques for monitoring the effectiveness of pharmacotherapy on plaques. There are, however, existing limitations to this methodology. Perhaps the most important distinction is that IM thickness measurements are generally acquired in the common carotid artery, whereas advanced atherosclerotic disease occurs predominantly downstream in the internal carotid. Moreover, primary contributors to IM thickening are age and hypertension, which do not necessarily reflect the atherosclerotic process. Initiation of disease-related plaques begins as what is referred to as pathological intimal thickening; lesions characterized by the formation of lipid pools in the absence of a necrotic core. The eventual development of a necrotic core, however, is considered a key indicator of significant plaque advancement and recognized feature of lesion vulnerability. Necrotic cores are thought to arise from macrophage infiltration of lipid pools followed by secondary necrosis where defective clearance of debris, tissue disruption proteases, and intraplaque hemorrhage, likely contribute to its enlargement. Therefore, one of the primary limitations to CIMT is its inability to distinguish lesions with a necrotic core. Moreover, in most cases measures of plaque area or volume are generally considered better predictors of an inflammatory process consistent with atherosclerotic disease rather than intimal medial thickness.

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