Читать книгу Interventional Cardiology - Группа авторов - Страница 44

Despite the exposure of the entire coronary tree to the systemic risk factors and inflammation, spatial distribution of atherosclerotic plaques is often a focal phenomenon [224]. Vascular endothelium is subjected to complex mechanical stresses resulting from its 3‐D geometry, vessel curvatures and cardiac motion. These mechanical strains in combination with fluid frictional forces or shear stress gradients inside the arteries can lead to a number of structural and humoral changes in the endothelial cells [225, 226]. High wall shear stress (WSS) (>15 dyne/cm2) has been found to induce endothelial quiescence and an atheroprotective gene expression profile, whereas low shear stress (<4 dyne/cm2) stimulates an atherogenic phenotype [225]. It has been shown that the plaques and wall thickenings are localized mostly on the outer wall of one or both daughter vessels at bifurcations and along the inner wall of curved segments [224]. In the PREDICTION study, Stone et al. studied the natural history of plaques in 506 patients with ACS treated with percutaneous coronary intervention, and used reconstructed coronary models from angiography and IVUS. 74% patients had follow‐up studies at 6 to 10 months to relate the effects of local haemodynamic milieu on plaque changes. Authors reported that decrease in lumen area was independently predicted by baseline large plaque burden and low endothelial shear stress [227]. Other investigators have reported that high wall shear stress is associated with transformation of plaques into high risk phenotypes prone to instability and rupture [228,229].