[Research progress on cerebral hypoperfusion following revascularization for carotid artery stenotic disease]

In clinical practice, a subset of patients with severe carotid artery stenosis fails to achieve the expected improvement in cerebral perfusion despite successful carotid revascularization and restoration of arterial patency. In these patients, cerebral ischemic symptoms persist or even deteriorate, reflecting a mismatch between macrovascular recanalization and cerebral tissue perfusion. This phenomenon is referred to as cerebral hypoperfusion syndrome (CHypoS). The pathogenesis of CHypoS is likely multifactorial, involving unfavorable cerebrovascular anatomy, persistent hemodynamic impairment, cerebrovascular vasoconstriction, and microcirculatory dysfunction, all of which may increase the risk of recurrent ischemic stroke. Currently, there is no universally accepted diagnostic criterion for CHypoS, and high-quality evidence to guide its management remains lacking. Consequently, current treatment strategies rely largely on empirical hemodynamic optimization. Future studies should focus on elucidating the underlying pathophysiological mechanisms of CHypoS and shifting the therapeutic goal of carotid revascularization from achieving anatomical vessel patency to restoring effective cerebral perfusion and improving clinically meaningful outcomes, thereby enhancing stroke prevention and long-term prognosis.