Abstract
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.
Highlights
Acute ischemic stroke (AIS) is an emerging vascular complication in patients withCOVID-19 with reports on incidence ranging between 1 and 6% of hospitalized patients [1].Among pathophysiological causes of AIS in COVID-19, SARS-CoV-2 related cardiac injury, mediated by a thrombotic and inflammatory milieu, seems to play a major role
The systemic inflammatory virus disease COVID-19 is associated with impaired cardiac function and can subsequently lead to persistent structural myocardial damage [9]
An additional analysis of biomarkers of cardiac stress aside cardiac troponin B-type showed elevation of natriuretic peptide (BNP) in patients with cardiac injury hospitalized for COVID-19 [13]
Summary
Acute ischemic stroke (AIS) is an emerging vascular complication in patients with. COVID-19 with reports on incidence ranging between 1 and 6% of hospitalized patients [1]. In stage III, cardiac stress occurs due to respiratory failure and mechanisms of cardiac injury These mechanisms include viral infiltration into myocardial tissue as well as secondary reactions to hypoxemia and cardiac inflammation, subsequently leading to cardiac complications [7]. Biomarkers as indicators of (hyper-)inflammation include IL (interleukin)-6, IL-2, IL-7, TNF (tumor necrosis factor)-α, IFN (interferon)-γ IP (inducible protein)-10, MCP (monocyte chemoattractant protein)-1, MIP (macrophage inflammatory protein)-1α, G-CSF (granulocyte-colony stimulating factor), CRP (C-reactive protein), procalcitonin and ferritin. Elevations of these markers are associated with an increase in mortality [7]. We performed a narrative review of the current literature on the association of cardiac injury and acute ischemic stroke in patients with COVID-19 with a focus on pathophysiological mechanisms and potential biomarkers of cardiac involvement in this population at risk
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