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.
