Plaque fissure and calcified nodule: histopathological findings

Abstract

Coronary artery disease remains a leading cause of morbidity and mortality. Precise definitions of the distinct plaque morphologies that contribute to coronary artery disease are essential for a comprehensive understanding of plaque progression and vulnerability. This review clarifies critical and often conflated plaque phenotypes: specifically, plaque fissure vs rupture and calcified nodules vs nodular calcification. Furthermore, it contextualizes these pathologies by examining shifting acute coronary syndrome presentations and evolving culprit lesion morphologies and explores how advanced coronary imaging technologies are revolutionizing their detection and treatment. Plaque fissures are characterized by a lateral tear in an eccentric lesion that traverses a thick fibrous cap and ends in a small necrotic core. In contrast to ruptures, fissures are accompanied by an intraplaque thrombus, typically composed of fibrin, platelets, and red cells, while luminal thrombus is usually absent or small if present. In ruptures, a thin fibrous cap is disrupted and associated with significant infiltration of macrophages and T-lymphocytes. Calcified nodules are fragments of dense calcium interspersed by fibrin that protrude into the vessel lumen and trigger a luminal thrombus that is usually non-occlusive and composed of fibrin and platelets. Calcified nodules typically appear as eccentric lesions with a convex luminal surface that is devoid of fibrous tissue or endothelium. While nodular calcifications have a similar morphology, the overlying thick fibrous cap is intact, lined by endothelial cells, and devoid of thrombus. Clarifying these fundamental differences is crucial for an improved understanding of the pathogenesis of coronary artery disease and developing personalized treatment strategies.