Myocardial infarction and sudden cardiac death are usually due to the rapid progression of previously non-flow limiting atherosclerotic plaques that transform to an unstable (i.e., vulnerable) phenotype. Despite considerable advances in medical therapies and treatment modalities for coronary artery disease (CAD), there is no accurate method to predict the site of abrupt lesion progression that can lead to an acute coronary event. Wall shear stress (WSS) has not only been implicated in the development of CAD, but also in its rapid progression [1]. Recent data from our laboratory indicates significant plaque progression in areas of low WSS (<10 dynes/cm2), plaque regression in regions of physiologic WSS (10–25 dynes/cm2), and phenotypic transformation towards an unstable lesion in regions of high WSS (>25 dynes/cm2) [2].

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