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In vitro flow and optical coherence tomography comparison of two bailout techniques after failed provisional stenting for bifurcation percutaneous coronary interventions Impact of coronary anatomy and stenting technique on long-term outcome after drug-eluting stent implantation for unprotected left main coronary artery disease Contemporary Use and Trends in Unprotected Left Main Coronary Artery Percutaneous Coronary Intervention in the United States: An Analysis of the National Cardiovascular Data Registry Research to Practice Initiative Association of Sustained Blood Pressure Control with Multimorbidity Progression Among Older Adults Leaflet immobility and thrombosis in transcatheter aortic valve replacement Differences between the left main and other bifurcations Pulmonary Artery Denervation Attenuates Pulmonary Arterial Remodeling in Dogs With Pulmonary Arterial Hypertension Induced by Dehydrogenized Monocrotaline Stent underexpansion and residual reference segment stenosis are related to stent thrombosis after sirolimus-eluting stent implantation: an intravascular ultrasound study Transcatheter Aortic Valve Replacement in Patients With Multivalvular Heart Disease Management of Asymptomatic Severe Aortic Stenosis: Evolving Concepts in Timing of Valve Replacement

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.