Pathophysiology of Cardiac Injury in COVID-19 Patients with Acute Ischaemic Stroke: What Do We Know So Far?-A Review of the Current Literature.

With the onset of the COVID-19 pandemic, it became apparent that, in addition to pulmonary infection, extrapulmonary manifestations such as cardiac injury and acute cerebrovascular events are frequent in patients infected with SARS-CoV-2, worsening clinical outcome. We reviewed the current literature on the pathophysiology of cardiac injury and its association with acute ischaemic stroke. Several hypotheses on heart and brain axis pathology in the context of stroke related to COVID-19 were identified. Taken together, a combination of disease-related coagulopathy and systemic inflammation might cause endothelial damage and microvascular thrombosis, which in turn leads to structural myocardial damage. Cardiac complications of this damage such as tachyarrhythmia, myocardial infarction or cardiomyopathy, together with changes in hemodynamics and the coagulation system, may play a causal role in the increased stroke risk observed in COVID-19 patients. These hypotheses are supported by a growing body of evidence, but further research is necessary to fully understand the underlying pathophysiology and allow for the design of cardioprotective and neuroprotective strategies in this at risk population.

The impact of SARS-CoV-2 infection on the outcome of acute ischemic stroke-A retrospective cohort study.

BACKGROUND: Acute ischemic stroke (AIS) is a common complication of severe acute respiratory syndrome coronavirus 2 (SARS­CoV­2) infection (COVID-19), but the prognosis of these patients is poorly understood. PURPOSE: To explore the impact of COVID-19 on neurological outcomes in AIS patients. METHODS: A comparative retrospective cohort study was conducted in 32 consecutive AIS patients with and 51 without COVID-19 between the 1st of March 2020 and 1st of May 2021. The evaluation was based on a detailed chart review for demographic data, medical history, stroke severity, cranial and vessel imaging results, laboratory parameters, COVID-19 severity, hospitalization time, in-hospital mortality, and functional deficits at discharge (modified Rankin Scale, mRS). RESULTS: COVID-19 AIS patients showed tendency to worse initial neurological deficit (NIHSS 9 (3-13) vs. 4 (2-10); p = 0.06), higher rate of large vessel occlusion (LVO; 13/32 vs. 14/51; p = 0.21), had prolonged hospitalization (19.4 ± 17.7 vs. 9.7 ± 7 days; p = 0.003), had lower chance of functional independence (mRS≤2) (12/32 vs. 32/51; p = 0.02) and showed higher in-hospital mortality (10/32 vs. 6/51; p = 0.02). In COVID-19 AIS patients, LVO was more common with COVID-19 pneumonia than without (55.6% vs. 23.1%; p = 0.139). CONCLUSION: COVID-19-related AIS carries a worse prognosis. COVID-19 with pneumonia seems to be associated with a higher rate of LVO.

Pathophysiology of Cardiac Injury in COVID-19 Patients with Acute Ischaemic Stroke: What Do We Know So Far?—A Review of the Current Literature

With the onset of the COVID-19 pandemic, it became apparent that, in addition to pulmonary infection, extrapulmonary manifestations such as cardiac injury and acute cerebrovascular events are frequent in patients infected with SARS-CoV-2, worsening clinical outcome. We reviewed the current literature on the pathophysiology of cardiac injury and its association with acute ischaemic stroke. Several hypotheses on heart and brain axis pathology in the context of stroke related to COVID-19 were identified. Taken together, a combination of disease-related coagulopathy and systemic inflammation might cause endothelial damage and microvascular thrombosis, which in turn leads to structural myocardial damage. Cardiac complications of this damage such as tachyarrhythmia, myocardial infarction or cardiomyopathy, together with changes in hemodynamics and the coagulation system, may play a causal role in the increased stroke risk observed in COVID-19 patients. These hypotheses are supported by a growing body of evidence, but further research is necessary to fully understand the underlying pathophysiology and allow for the design of cardioprotective and neuroprotective strategies in this at risk population.