Abstract
Acute coronary syndrome (ACS) mostly arises from so-called vulnerable coronary plaques, particularly prone for rupture. Vulnerable plaques comprise a specific type of plaque, called the thin-cap fibroatheroma (TFCA). A TCFA is characterized by a large lipid-rich necrotic core, a thin fibrous cap, inflammation, neovascularization, intraplaque hemorrhage, microcalcifications or spotty calcifications, and positive remodeling. Vulnerable plaques are often not visible during coronary angiography. However, different plaque features can be visualized with the use of intracoronary imaging techniques, such as intravascular ultrasound (IVUS), potentially with the addition of near-infrared spectroscopy (NIRS), or optical coherence tomography (OCT). Non-invasive imaging techniques, such as computed tomography coronary angiography (CTCA), cardiovascular magnetic resonance (CMR) imaging, and nuclear imaging, can be used as an alternative for these invasive imaging techniques. These invasive and non-invasive imaging modalities can be implemented for screening to guide primary or secondary prevention therapies, leading to a more patient-tailored diagnostic and treatment strategy. Systemic pharmaceutical treatment with lipid-lowering or anti-inflammatory medication leads to plaque stabilization and reduction of cardiovascular events. Additionally, ongoing studies are investigating whether modification of vulnerable plaque features with local invasive treatment options leads to plaque stabilization and subsequent cardiovascular risk reduction.
Highlights
Coronary artery disease (CAD) is one of the most common diseases in developed countries and has a high morbidity and mortality [1]
The vulnerable plaques are characterized by specific high-risk features that increase the risk for plaque rupture and are often referred to as lipid-rich plaque or thin-cap fibroatheroma (TCFA) [7,8]
High-risk intravascular ultrasound (IVUS) features for long-term non-culprit events were plaques that were scored as TCFA based on the aforementioned VH-IVUS definition and plaques with a plaque burden greater than 70%
Summary
Coronary artery disease (CAD) is one of the most common diseases in developed countries and has a high morbidity and mortality [1]. The smooth muscle cells in the intima produce an extracellular matrix consisting of proteoglycans, collagen, and elastine, that forms a fibrous cap to cover the core of necrotic foam cells [22] This stage is often irreversible and accompanied by outward vascular remodeling, preventing the cell accumulation in the intima to cause lumen compromise [27]. In the subsequent stages of vulnerable plaque formation, the necrotic core further enlarges This promotes thinning of the fibrous cap, by the loss of smooth muscle cells and continued influx of macrophages that degrade the cap matrix [28,29]. The aforementioned high-risk plaque features, i.e., large lipid core with thin fibrous cap, the presence of active inflammation (macrophage or T-cell infiltration), together with denudation of the endothelium were defined as major criteria. The definition by Naghavi et al considers lesions with >90% diameter stenosis as vulnerable plaques, since rapid progression would lead to clinical events
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