Prediction of sites of coronary atherosclerosis progression: In vivo profiling of endothelial shear stress, lumen, and outer vessel wall characteristics to predict vascular behavior.

PURPOSE OF REVIEW: Native atherosclerosis and in-stent restenosis are focal and evolve independently. The endothelium regulates arterial behavior by responding to its local environment of hemodynamic stresses, in particular, shear stress. Identification of endothelial shear stress and arterial wall characteristics may allow for the prediction of the progression of atherosclerosis. Accurate identification of arterial segments at high risk for progression may permit preemptive intervention strategies to avoid adverse coronary events.

RECENT FINDINGS: In vitro studies indicate that low endothelial shear stress upregulates the genetic and molecular responses leading to the initiation and progression of atherosclerosis, and promotes inflammation and formation of other features characteristic of vulnerable plaque. Physiologic endothelial shear stress is vasculoprotective and fosters quiescence of the endothelium and vascular wall. High endothelial shear stress promotes platelet aggregation. Recent studies have now provided evidence that endothelial shear stress and vascular wall morphology along the course of human coronary arteries can be characterized in vivo, and, in serial studies, may actually predict the focal areas in which atherosclerosis progression occurs.

SUMMARY: Rapidly evolving methodologies are able to characterize the arterial wall and the local hemodynamic environmental factors likely responsible for progression of coronary disease in humans. These new diagnostic modalities allow for identification of plaque progression. Future studies need to identify the factors responsible for vulnerable plaque formation. The current availability of drug-eluting stents with a low risk of restenosis allows for consideration of preemptive intervention strategies for these high-risk vascular sites such that future adverse coronary events can be averted.