Risk stratification of individual coronary lesions using local endothelial shear stress: a new paradigm for managing coronary artery disease

Purpose of review The purpose of this review is to summarize the role of endothelial shear stress in the natural history of coronary atherosclerosis, and to propose an individualized risk-stratification strategy of atherosclerotic lesions based on the in-vivo characterization of local endothelial shear stress and wall morphology. Recent findings Low endothelial shear stress promotes the development of early fibroatheromas, which subsequently follow an individualized natural history of progression. This individual natural history is critically dependent on the magnitude of low endothelial shear stress, which subsequently regulates the severity of inflammation within the wall and ultimately the vascular remodeling response. Very low endothelial shear stress enhances plaque inflammation, leading to excessive expansive remodeling. Excessive expansive remodeling leads to perpetuation, or even exacerbation, of the local low endothelial shear stress environment, thereby setting up a self-perpetuating vicious cycle among low local endothelial shear stress, inflammation, and excessive expansive remodeling, which transforms an early fibroatheroma to a high-risk plaque. Summary In-vivo assessment of the local endothelial shear stress environment, severity of inflammation and vascular remodeling response, all responsible for individual plaque behavior and natural history, in combination with systemic biomarkers of vulnerability, may allow for detailed risk stratification of individual early atherosclerotic plaques, thereby guiding both systemic and local, lesion-specific therapeutic strategies.