COVID-19 and ischemic stroke

Abstract

Since the onset of the COVID-19 pandemic, a substantial proportion of COVID-19 patients had documented thrombotic complications and ischemic stroke. Several mechanisms related to immune-mediated thrombosis, the renin angiotensin system and the effect of SARS-CoV-2 in cardiac and brain tissue may contribute to the pathogenesis of ischemic stroke in patients with COVID-19. Simultaneously, significant strains on global healthcare delivery, including ischemic stroke management, have made treatment of stroke in the setting of COVID-19 particularly challenging. In this review, we summarize the current knowledge on epidemiology, clinical manifestation, and pathophysiology of ischemic stroke in patients with COVID-19 to bridge the gap from bench to bedside and clinical practice during the most challenging global health crisis of the last decades.

Keywords: COVID-19; SARS-CoV-2; ischemic stroke; pathophysiology.

FIGURE 1

Potential mechanisms of ischemic stroke in patients with COVID‐19. ACE2, angiotensin converting enzyme 2; AT₁R, angiotensin receptor type 1; AT₂R, angiotensin receptor type 2; BBB, blood–brain barrier; eNOS, endothelial nitric oxide synthase; ICAM‐1, intercellular adhesion molecule 1; IL‐1β, interleukin 1β; IL‐6, interleukin 6; IL‐8, interleukin 8; MasR, Mas receptor; MCP‐1, monocyte chemoattractant protein‐1; MIP‐1α, macrophage inflammatory protein 1α; NETs, neutrophil extracellular traps; RAS, renin angiotensin syndrome; TF, tissue factor; TLR, Toll‐like receptor; TNF, tumor necrosis factor; VCAM‐1, vascular cell adhesion molecule‐1