ABSTRACT
SARS-CoV-2 infects endothelial cells, induces a hypercoagulable state, and, in extreme cases, can provoke a “cytokine storm.” These etiopathological mechanisms, in addition to the hemodynamic and respiratory compromises characterizing severe COVID-19, can culminate in the emergence of various acute stroke phenotypes, such as arterial and venous thromboses, and hemorrhages. COVID-19-associated strokes have been encountered in younger patients with no cerebrovascular risk factors but the disease is also found to target older patients with comorbidities who are more likely to contract the more severe forms of the disease. Anticoagulation, antiplatelets, statins, thrombolysis and endovascular thrombectomy remain the cornerstone therapies for patients with ischemic strokes and COVID-19. An important aspect of secondary stroke prevention is blood pressure management recommendations which are currently being revisited as renin-angiotensin-aldosterone antagonists were initially thought to be detrimental to infected patients due to the interaction of the virions with ACE2 receptors. We also focus our attention on the reshaping of all aspects of stroke care during the pandemic, from the prehospital stage to telehealth. © 2021 Elsevier Inc. All rights reserved.