Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease

Abstract

Intracranial atherosclerotic disease (ICAD) has been characterized by the degree of arterial stenosis and downstream hypoperfusion, yet microscopic derangements of endothelial shear stress at the luminal wall may be key determinants of plaque growth, vascular remodeling and thrombosis that culminate in recurrent stroke. Platelet interactions have similarly been a principal focus of treatment, however, the mechanistic basis of anti-platelet strategies is largely extrapolated rather than directly investigated in ICAD. Platelet FcγRIIa expression has been identified as a potent risk factor in cardiovascular disease, as elevated expression markedly increases the risk of recurrent events. Differential activation of the platelet FcγRIIa receptor may also explain the variable response of individual patients to anti-platelet medications. We review existing data on endothelial shear stress and potential interactions with the platelet FcγRIIa receptor that may alter the evolving impact of ICAD, based on local pathophysiology at the site of arterial stenosis. Current methods for quantification of endothelial shear stress and platelet activation are described, including tools that may be readily adapted to the clinical realm for further understanding of ICAD.

Remodeling of the brain angioarchitecture in experimental chronic neurodegeneration

“…The growth of atherosclerotic plaques can eventually lead to the narrowing of the vessel lumen, and hence, the formation of a zone of oscillatory shear stress with particularly turbulent blood flow [64,65]. This will further increase the risk of the intraluminal activation of platelets which could then lead to blood clotting [66]. High vessel tortuosity also changes the shear stress within the vessel lumen as follows: on the outer side of the vessel curvature, the shear stress becomes higher compared to that of a straight tube, while on the inner side, it becomes lower [67,68].…”

Hemodynamic changes for half cover Left subclavian artery ostium during thoracic endovascular aortic repair

“…Therefore, LSA revascularization in Z2 region after endovascular repair of thoracic aorta is very important. At present, there are many vascular reconstructions for LSA [20],…”

Effects of two different surgical methods for endovascular repair of the thoracic aorta on the hemodynamics of the left subclavian artery

“…Currently, there are many revascularizations described for the LSA [31], including surgical bypass, chimney, fenestration technology, single-branch stent technology, and others. Although the different revascularization of the LSA ensures good distal perfusion, it also changes its hemodynamics, as well as the occurrence and development of arteriosclerosis and thrombotic diseases (which are closely related to local hemodynamic changes) [32]. As such, we should be alert to the risk of acute thrombosis or long-term arteriosclerosis of the LSA.…”