CBS 2019
CBSMD教育中心
中 文

科学研究

Abstract

Recommended Article

Single direct oral anticoagulant therapy in stable patients with atrial fibrillation beyond 1 year after coronary stent implantation Detection of Device-Related Thrombosis Following Left Atrial Appendage Occlusion A Comparison Between Cardiac Computed Tomography and Transesophageal Echocardiography​: A Comparison Between Cardiac Computed Tomography and Transesophageal Echocardiography Gut microbiota dysbiosis promotes age-related atrial fibrillation by lipopolysaccharide and glucose-induced activation of NLRP3-inflammasome Left Atrial Appendage Occlusion during Cardiac Surgery to Prevent Stroke Rivaroxaban Is Associated With Higher Rates of Gastrointestinal Bleeding Than Other Direct Oral Anticoagulants: A Nationwide Propensity Score–Weighted Study Management and outcomes of patients with left atrial appendage thrombus prior to percutaneous closure Role of local coronary blood flow patterns and shear stress on the development of microvascular and epicardial endothelial dysfunction and coronary plaque Frailty and Clinical Outcomes of Direct Oral Anticoagulants Versus Warfarin in Older Adults With Atrial Fibrillation: A Cohort Study

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.