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Heart Failure With Preserved, Borderline, and Reduced Ejection Fraction: 5-Year Outcomes Impact of Optimal Medical Therapy on 10-Year Mortality After Coronary Revascularization Association Between Haptoglobin Phenotype and Microvascular Obstruction in Patients With STEMI: A Cardiac Magnetic Resonance Study Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC) Canadian Multicenter Chronic Total Occlusion Registry: Ten-Year Follow-Up Results of Chronic Total Occlusion Revascularization Long-Term Outcomes of Biodegradable Versus Second-Generation Durable Polymer Drug-Eluting Stent Implantations for Myocardial Infarction Randomized Comparison of Ridaforolimus-Eluting and Zotarolimus-Eluting Coronary Stents 2-Year Clinical Outcomes: From the BIONICS and NIREUS Trials Successful catheter ablation of electrical storm after myocardial infarction Best Practices for the Prevention of Radial Artery Occlusion After Transradial Diagnostic Angiography and Intervention An International Consensus Paper
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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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