C oronary heart disease (CHD) remains the leading cause of death in the United States, and an estimated 1.4 million Americans have a heart attack each year.Over the past 2 decades, the concept of the "vulnerable plaque" (VP) being responsible for the majority of acute coronary syndromes (ACS) has become widely accepted.Coincidentally, there has been rapid expansion of coronary imaging modalities, both invasive and noninvasive, seeking the ability to detect high-risk plaques before their disruption and formation of occlusive thrombus.Histological characteristics of the plaques that are vulnerable to rupture are thin fibrous cap (Ͻ65 m), large lipid pool, and activated macrophages near the fibrous cap, all of which can be detected with highresolution coronary imaging. 1 Cellular mechanisms associated with plaque instability include inflammation, reduced collagen synthesis, local overexpression of collagenase, and smooth muscle cell apoptosis.These pathological processes can alter the plaque surface and its mechanical properties, which also have been targets of recent research.Noninvasive tests, such as CT and MRI are limited by low resolution and are unable to visualize most of the features of VP.At present, only intravascular modalities can potentially distinguish VP from benign types of plaques.In this review, we focus on the recent data from the various types of intravascular modalities currently available or in development and compare their advantages and limitations.
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Suh et al. (2011) studied this question.
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