Coronary angiography-based shear stress computation to identify high-risk coronary artery plaques: Are we there yet?

In the last number of years there has been increasing interest in identifying coronary artery plaques likely to destabilize and cause a future major adverse cardiac event (MACE), with the ultimate goal to inform, and possibly enable, preemptive intervention strategies to prevent that individual plaque's adverse natural history. Intravascular imaging with intravascular ultrasound (IVUS) and optical coherence tomography (OCT) are the most precise and accurate methods to characterize the plaque, the arterial wall, and the blood flow patterns surrounding the plaque area. These methods have been the basis for computational fluid dynamics (CFD) calculations of local endothelial or wall shear stress (ESS or WSS), the frictional force of blood flowing over endothelial cells that triggers fundamental signaling pathways responsible for vascular and plaque behavior [ [1] Chatzizisis Y.S. Coskun A.U. Jonas M. Edelman E.R. Feldman C.L. Stone P.H. Role of endothelial shear stress in the natural history of coronary atherosclerosis and vascular remodeling: molecular, cellular, and vascular behavior. J. Am. Coll. Cardiol. 2007; 49: 2379-2393https://doi.org/10.1016/j.jacc.2007.02.059 Crossref PubMed Scopus (980) Google Scholar ]. The ability to identify the broad range of focal ESS values is critical since different ranges of ESS values (low, physiologic, high, and supraphysiologically high) trigger very different phenotypic switches driving a plaque to develop a highly inflamed, pro-atherothrombotic area or to remain quiescent [ [2] Koskinas K.C. Feldman C.L. Chatzizisis Y.S. et al. Natural history of experimental coronary atherosclerosis and vascular remodeling in relation to endothelial shear stress: a serial, in vivo intravascular ultrasound study. Circulation. 2010; 121: 2092-2101https://doi.org/10.1161/CIRCULATIONAHA.109.901678 Crossref PubMed Scopus (143) Google Scholar , [3] Antoniadis A.P. Papafaklis M.I. Takahashi S. et al. Arterial remodeling and endothelial shear stress exhibit significant longitudinal heterogeneity along the length of coronary plaques. JACC Cardiovasc Imaging. 2016; 9: 1007-1009https://doi.org/10.1016/j.jcmg.2016.04.003 Crossref PubMed Scopus (10) Google Scholar ]. Focal areas of low ESS lead to plaque development and progression [ [4] Samady H. Eshtehardi P. McDaniel M.C. et al. Coronary artery wall shear stress is associated with progression and transformation of atherosclerotic plaque and arterial remodeling in patients with coronary artery disease. Circulation. 2011; 124: 779-788https://doi.org/10.1161/CIRCULATIONAHA.111.021824 Crossref PubMed Scopus (456) Google Scholar , [5] Stone P.H. Saito S. Takahashi S. et al. Prediction of progression of coronary artery disease and clinical outcomes using vascular profiling of endothelial shear stress and arterial plaque characteristics: the PREDICTION Study. Circulation. 2012; 126: 172-181https://doi.org/10.1161/CIRCULATIONAHA.112.096438 Crossref PubMed Scopus (404) Google Scholar ], and contributes to plaque destabilization [ [6] Stone P.H. Maehara A. Coskun A.U. et al. Role of low endothelial shear stress and plaque characteristics in the prediction of nonculprit major adverse cardiac events: the PROSPECT study. JACC Cardiovasc Imaging. 2018; 11: 462-471https://doi.org/10.1016/j.jcmg.2017.01.031 Crossref PubMed Scopus (68) Google Scholar ]; focal areas of high ESS lead to features of plaque vulnerability and thrombus formation [ [7] Kumar A. Thompson E.W. Lefieux A. et al. High coronary shear stress in patients with coronary artery disease predicts myocardial infarction. J. Am. Coll. Cardiol. 2018; 72: 1926-1935https://doi.org/10.1016/j.jacc.2018.07.075 Crossref PubMed Scopus (66) Google Scholar , [8] McElroy M. Kim Y. Niccoli G. et al. Identification of the haemodynamic environment permissive for plaque erosion. Sci. Rep. 2021; 11: 7253https://doi.org/10.1038/s41598-021-86501-x Crossref PubMed Scopus (3) Google Scholar ], and physiologic values lead to plaque and arterial quiescence and stability.