Abstract
Atherosclerosis is a lipoprotein-driven inflammatory disorder leading to a plaque formation at specific sites of the arterial tree. After decades of slow progression, atherosclerotic plaque rupture and formation of thrombi are the major factors responsible for the development of acute coronary syndromes (ACSs). In this regard, the detection of high-risk (vulnerable) plaques is an ultimate goal in the management of atherosclerosis and cardiovascular diseases (CVDs). Vulnerable plaques have specific morphological features that make their detection possible, hence allowing for identification of high-risk patients and the tailoring of therapy. Plaque ruptures predominantly occur amongst lesions characterized as thin-cap fibroatheromas (TCFA). Plaques without a rupture, such as plaque erosions, are also thrombi-forming lesions on the most frequent pathological intimal thickening or fibroatheromas. Many attempts to comprehensively identify vulnerable plaque constituents with different invasive and non-invasive imaging technologies have been made. In this review, advantages and limitations of invasive and non-invasive imaging modalities currently available for the identification of plaque components and morphologic features associated with plaque vulnerability, as well as their clinical diagnostic and prognostic value, were discussed.
Highlights
Cardiovascular diseases (CVDs), including coronary artery disease (CAD) and subsequent acute coronary syndromes (ACSs), continue to dominate as the principal cause of morbidity and mortality in industrialized countries
This study reported that Intravascular ultrasound (IVUS) was not able to visualize the entire coronary tree, assessing only 53% of the lesions that caused adverse cardiovascular events during the median 3.4-year follow-up period
Positron emission tomography (PET) can facilitate a better understanding of the pathobiology of atherosclerosis, prediction of the high risk of events associated with plaque rupture, and monitoring of the efficacy of drug treatments
Summary
Cardiovascular diseases (CVDs), including coronary artery disease (CAD) and subsequent acute coronary syndromes (ACSs), continue to dominate as the principal cause of morbidity and mortality in industrialized countries. The mechanisms of plaque progression encompass SMC apoptosis, matrix synthesis, angiogenesis, arterial remodeling, fibrous cap rupture, and thrombosis, followed by necrosis and calcification. The most acute cardiovascular events are triggered by the rupture; erosion; or, the least common, calcified nodule, the vulnerable plaque phenotypes, followed by coronary thrombosis. The biological features of two major classes of high-risk (vulnerable) plaques, such as rupture-prone and erosion-prone plaques, were described [8]. Progressive calcification supports the transition from initial high-risk microcalcifications to the end-stage macrocalcifications responsible for plaque stability, which limit the inflammation and only occasionally result in rupture [12]. Plaque erosions become calcified to a minor degree when compared to plaque ruptures [9] We discuss the strengths and limitations of currently available invasive and non-invasive imaging modalities that enable in vivo assessment of different aspects attributed to vulnerable plaques, highlighting their clinical and prognostic value
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