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IVUS Guidance

科研文章

荐读文献

Novel predictors of late lumen enlargement in distal reference segments after successful recanalization of coronary chronic total occlusion Coronary plaque redistribution after stent implantation is determined by lipid composition: A NIRS-IVUS analysis Optical coherence tomography and intravascular ultrasound assessment of the anatomic size and wall thickness of a muscle bridge segment Intravascular ultrasound-guided drug-eluting stent implantation is associated with improved clinical outcomes in patients with unstable angina and complex coronary artery true bifurcation lesions Prognostic Value of Intravascular Ultrasound in Patients With Coronary Artery Disease Comparison of plaque characteristics in narrowings with ST-elevation myocardial infarction (STEMI), non-STEMI/unstable angina pectoris and stable coronary artery disease (from the ADAPT-DES IVUS Substudy) Relation between baseline plaque features and subsequent coronary artery remodeling determined by optical coherence tomography and intravascular ultrasound Assessment of coronary atherosclerosis by IVUS and IVUS-based imaging modalities: progression and regression studies, tissue composition and beyond A Combined Optical Coherence Tomography and Intravascular Ultrasound Study on Plaque Rupture, Plaque Erosion, and Calcified Nodule in Patients With ST-Segment Elevation Myocardial Infarction: Incidence, Morphologic Characteristics, and Outcomes After Percutaneous Coronary Intervention Percutaneous Coronary Intervention for Vulnerable Coronary Atherosclerotic Plaque

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.