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.