PMC:7534206 / 17069-18709 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7534206","sourcedb":"PMC","sourceid":"7534206","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7534206","text":"It is too early to determine the exact impact of COVID-19 on the incidence of acute cerebrovascular diseases. However, our reported observations provide an opportunity to anticipate and prepare for the challenges in stroke care. The pathophysiology of cerebrovascular disease in COVID-19 patients may be direct or indirect. Direct factors may be related to the SARS-CoV-2 ability to bind to angiotensin-converting enzyme 2 (ACE2) and reduce its downstream effect. The virus is neuroinvasive and neurovirulent, and has a tropism to endothelial cells and cardiomyocytes.13,14 Indirect factors are mainly due to a systemic process, including a hyperinflammatory response, hypercoagulable state, and coagulopathy (thromboembolic events and microangiopathy) (Figure 3).15–19 Additional factors include a prolonged intensive care unit (ICU) stay, which may be associated with hypotension and inadequate cerebral perfusion, stress cardiomyopathy and concomitant reduction in left ventricular ejection fraction, and atrial fibrillation.3,20\nFigure 3. (a) and (b) Access route for the SARS-CoV-2 to the CNS via the olfactory route and hematogenous route via direct access or via a Trojan. (c) The hyperinflammatory, hypercoagulable state induced by SARS-CoV-2. (d) The downregulation of ACE2 receptor at the endothelium level. This blocks the conversion of angiotensin I and II into their active metabolites. The decline in Angiotensin (1–7) levels leads to loss of neuroprotective effect and sympathetic hyperactivity. ACE2: angiotensin-converting enzyme 2; ANG (1–7): angiotensin (1–7); SARS-CoV-2: severe acute respiratory syndrome coronavirus 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