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6-month versus 12-month or longer dual antiplatelet therapy after percutaneous coronary intervention in patients with acute coronary syndrome (SMART-DATE): a randomised, open-label, non-inferiority trial Non-invasive detection of coronary inflammation using computed tomography and prediction of residual cardiovascular risk (the CRISP CT study): a post-hoc analysis of prospective outcome data Patterns of calcification in coronary artery disease. A statistical analysis of intravascular ultrasound and coronary angiography in 1155 lesions Association of White Matter Hyperintensities and Cardiovascular Disease: The Importance of Microcirculatory Disease Infective Endocarditis After Transcatheter Aortic Valve Replacement Balloon Aortic Valvuloplasty as a Bridge to Aortic Valve Replacement: A Contemporary Nationwide Perspective A Review of the Role of Breast Arterial Calcification for Cardiovascular Risk Stratification in Women Edoxaban-based versus vitamin K antagonist-based antithrombotic regimen after successful coronary stenting in patients with atrial fibrillation (ENTRUST-AF PCI): a randomised, open-label, phase 3b trial Conceptual Framework for Addressing Residual Atherosclerotic Cardiovascular Disease Risk in the Era of Precision Medicine Temporal Trends, Characteristics, and Outcomes of Infective Endocarditis After Transcatheter Aortic Valve Replacement
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EditorialOctober 2017, Volume 10, Issue 10

JOURNAL：Circ Cardiovasc Imaging. Article Link

High-Risk Coronary Atherosclerosis Is It the Plaque Burden, the Calcium, the Lipid, or Something Else?

Akiko Maehara, Gregg W. Stone Keywords: calcium death, sudden, cardiac, humans risk factors

ABSTRACT

Cardiac death and myocardial infarction usually result from thrombotic occlusion of a coronary artery with underlying atherosclerotic plaque. Histologically, most underlying plaques that have resulted in sudden cardiac death or myocardial infarction because of coronary thrombosis (vulnerable plaque) are ruptured thin-cap fibroatheromas with large plaque burden and a lipid-rich necrotic core. Second most common are erosions of proteoglycan-rich plaques with thrombosis, despite an intact fibrous cap. The extent that macroscopic or microscopic calcification contributes to plaque instability and thrombosis is controversial. Both fibroatheromas and erosion-prone plaques may be calcified and, occasionally, an isolated calcified nodule has been associated with coronary thrombosis. Using noninvasive and invasive imaging techniques, new in vivo insights into the role of calcification in patient and plaque vulnerability are emerging. The computed tomography (CT)-derived coronary artery calcium score (CACS) accounts for the area and the maximum density of each detected calcium deposit in the entire coronary tree and has proven useful in predicting future cardiovascular events in asymptomatic patients at intermediate risk. CT angiography has demonstrated that hypolucent plaques with positive remodeling or a napkin-ring sign predict future cardiac death, myocardial infarction, or acute coronary syndromes (ACS; patient-level analysis). Finally, prospective intravascular ultrasound (IVUS) studies have shown that a large plaque burden, small minimal lumen area (MLA), and composition consistent with a thin-cap fibroatheroma by radiofrequency analysis identifies those plaques that are likely to cause future adverse cardiovascular events (lesion-level analysis). In this regard, coronary calcification has been correlated with plaque burden but not luminal stenosis. Reconciling these differences, especially the apparent discordance between plaque burden, coronary calcium, and lipid as risk factors is a matter of importance.
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