Anemia and cerebrovascular disease: pathophysiological insights and clinical implications

Abstract

Anemia and cerebrovascular disease (CVD) are interconnected conditions that significantly impact global health, often coexisting to worsen clinical outcomes. Anemia-induced hypoxia increases the production of reactive oxygen species (ROS) via mitochondrial dysfunction and xanthine oxidase activity, amplifying oxidative stress. ROS directly harm endothelial cells by disrupting tight junctions, increasing vascular permeability, and compromising the integrity of the blood-brain barrier. This review delves into the pathophysiology of anemia in the context of CVD, emphasizing the impact of hypoxia, oxidative stress, and endothelial dysfunction. Clinically, anemia worsens CVD prognosis by elevating the risk of ischemic and hemorrhagic strokes, delaying recovery, and increasing mortality rates. If untreated, anemia exacerbates neuronal damage, promotes vascular remodeling, and perpetuates systemic inflammation, leading to poor functional outcomes. This review underscores the necessity of timely anemia diagnosis and targeted management in patients with cerebrovascular disease to mitigate these adverse outcomes.