CBS 2019
CBSMD教育中心
中 文

ASCVD Prevention

Abstract

Recommended Article

The sinus venosus contributes to coronary vasculature through VEGFC-stimulated angiogenesis Regional Heterogeneity in the Coronary Vascular Response in Women With Chest Pain and Nonobstructive Coronary Artery Disease High-Risk Coronary Plaque Regression After Intensive Lifestyle Intervention in Nonobstructive Coronary Disease: A Randomized Study Negative Risk Markers for Cardiovascular Events in the Elderly Associations between Blood Lead Levels and Coronary Artery Stenosis Measured Using Coronary Computed Tomography Angiography Lysed Erythrocyte Membranes Promote Vascular Calcification: Possible Role of Erythrocyte-Derived Nitric Oxide Identifying coronary artery disease patients at risk for sudden and/or arrhythmic death: remaining limitations of the electrocardiogram Glycemic Index, Glycemic Load, and Cardiovascular Disease and Mortality

Recommandation Statement2025 Jun;18(6):709-740.

JOURNAL:JACC Cardiovasc Imaging. Article Link

Vulnerable or High-Risk Plaque: A JACC: Cardiovascular Imaging Position Statement

R Vergallo, SJ Park, IK Jang et al. Keywords: high-risk plaque, ACS, SCD

Abstract

The concept of high-risk plaque emerged from pathologic and epidemiologic studies 3 decades ago that demonstrated plaque rupture with thrombosis as the predominant mechanism of acute coronary syndrome and sudden cardiac death. Thin-cap fibroatheroma, a plaque with a large lipidic core covered by a thin fibrous cap, is the prototype of the rupture-prone plaque and has been traditionally defined as “vulnerable plaque.” Although knowledge on the pathophysiology of plaque instability continues to grow, the risk profile of our patients has shifted and the character of atherosclerotic disease has evolved, partly because of widespread use of lipid-lowering therapies and other preventive measures. In vivo intracoronary imaging studies indicate that superficial erosion causes up to 40% of acute coronary syndromes. This changing landscape calls for broader perspective, expanding the concept of high-risk plaque to the precursors of all major substrates of coronary thrombosis beyond plaque rupture. Other factors to take into consideration include dynamic changes in plaque composition, the importance of plaque burden, inflammatory activation (both local and systemic), healing mechanisms, regional hemodynamic pattern, properties of the fluid phase of blood, and the amount of myocardium at risk subtended by a lesion. Rather than the traditional focus limited to the thin-cap fibroatheroma, the authors advocate a more comprehensive approach that considers both morphologic features and biological activity of plaques and blood. This position paper highlights the challenges to the usual concept of high-risk plaque, proposes a broader definition, and analyzes its key morphologic features, the technological progress of plaque imaging (particularly using intracoronary imaging techniques), advances in pharmacologic therapies for plaque regression and stabilization, and the feasibility and efficacy of focal interventional treatments including preemptive plaque sealing.