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Validation of High-Risk Features for Stent-Related Ischemic Events as Endorsed by the 2017 DAPT Guidelines 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) Position paper of the EACVI and EANM on artificial intelligence applications in multimodality cardiovascular imaging using SPECT/CT, PET/CT, and cardiac CT Successful catheter ablation of electrical storm after myocardial infarction ST-Segment Elevation Myocardial Infarction Patients in the Coronary Care Unit Is it Time to Break Old Habits? Mortality 10 Years After Percutaneous or Surgical Revascularization in Patients With Total Coronary Artery Occlusions Randomized Comparison of Ridaforolimus-Eluting and Zotarolimus-Eluting Coronary Stents 2-Year Clinical Outcomes: From the BIONICS and NIREUS Trials Right ventricular stroke work correlates with outcomes in pediatric pulmonary arterial hypertension The spectrum of chronic coronary syndromes: genetics, imaging, and management after PCI and CABG Drug-coated balloons for small coronary artery disease (BASKET-SMALL 2): an open-label randomised non-inferiority trial
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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

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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