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A Randomized Trial Evaluating Online 3-Dimensional Optical Frequency Domain Imaging-Guided Percutaneous Coronary Intervention in Bifurcation Lesions Optical Coherence Tomography-Guided Percutaneous Coronary Intervention in ST-Segment-Elevation Myocardial Infarction: A Prospective Propensity-Matched Cohort of the Thrombectomy Versus Percutaneous Coronary Intervention Alone Trial Experimental basis of determining maximum coronary, myocardial, and collateral blood flow by pressure measurements for assessing functional stenosis severity before and after percutaneous transluminal coronary angioplasty Technical aspects of the culotte technique Retrospective Comparison of Long-Term Clinical Outcomes Between Percutaneous Coronary Intervention and Medical Therapy in Stable Coronary Artery Disease With Gray Zone Fractional Flow Reserve - COMFORTABLE Retrospective Study Left main coronary artery compression in pulmonary hypertension Robustness of Fractional Flow Reserve for Lesion Assessment in Non-Infarct-Related Arteries of Patients With Myocardial Infarction Rotational Atherectomy in acute STEMI with heavily calcified culprit lesion is a rule breaking solution Optimal threshold of postintervention minimum stent area to predict in-stent restenosis in small coronary arteries: An optical coherence tomography analysis PCI for obstructive bifurcation lesions the 14th consensus document from the european bifurcation club
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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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