Cardiovascular and Cerebrovascular Complications With COVID-19

Abstract

The coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 has affected the health of people across the globe. Cardiovascular diseases (CVDs) have a significant relationship with COVID-19, both as a risk factor and prognostic indicator, and as a complication of the disease itself. In addition to predisposing to CVD complications, the ongoing pandemic has severely affected the delivery of timely and appropriate care for cardiovascular conditions resulting in increased mortality. The etiology behind the cardiac injury associated with severe acute respiratory syndrome coronavirus-2 is likely varied, including coronary artery disease, microvascular thrombosis, myocarditis, and stress cardiomyopathy. Further large-scale investigations are needed to better determine the underlying mechanism of myocardial infarction and other cardiac injury in COVID-19 patients and to determine the incidence of each type of cardiac injury in this patient population. Telemedicine and remote monitoring technologies can play an important role in optimizing outcomes in patients with established CVD. In this article, we summarize the various impacts that COVID-19 has on the cardiovascular system, including myocardial infarction, myocarditis, stress cardiomyopathy, thrombosis, and stroke.

Pandemic-Related Impairment in the Monitoring of Patients With Hypertension and Diabetes and the Development of a Digital Solution for the Community Health Worker: Quasiexperimental and Implementation Study

“…Cardiovascular diseases have a significant relationship with COVID-19, both as risk factors and prognostic indicators and as complications [ 37 , 38 ]. Nevertheless, despite this, the pandemic forced a reorganization of health systems that compromised the provision of adequate and timely health services [ 39 , 40 ] and negatively affected mortality [ 41 ].…”

Reversible cerebral vasoconstriction syndrome in a patient with COVID-19

“…This may lead to the under-recognition of cerebrovascular complications such as RCVS. [11][12][13] COVID-19 encephalopathy may also present with headache and confusion. 14 Brain parenchymal imaging, CSF and EEG may then be abnormal.…”

“…11,12,[16][17][18][19] Among the cerebrovascular involvement is common. [11][12][13] They are ischemic stroke, intracerebral hemorrhage, and cerebral venous sinus thrombosis. The proposed mechanisms of cerebrovascular complications include thrombosis due to hypercoagulability, vessel wall damage due to local and systemic inflammation (cytokine stormmediated vasculitis), endothelial dysfunction due to angiotensin-converting enzyme 2 (ACE2) receptor dysregulation, cardio-embolism secondary to myocardial ischemia or arrhythmia, and intracranial bleeding due to coagulation abnormalities.…”

“…The proposed mechanisms of cerebrovascular complications include thrombosis due to hypercoagulability, vessel wall damage due to local and systemic inflammation (cytokine stormmediated vasculitis), endothelial dysfunction due to angiotensin-converting enzyme 2 (ACE2) receptor dysregulation, cardio-embolism secondary to myocardial ischemia or arrhythmia, and intracranial bleeding due to coagulation abnormalities. 2,[11][12][13]20,21 Patients with RCVS usually present with intense headache, sometimes associated with confusion, visual blurring, vomiting, focal neurological deficit, and seizures. 8,9,22 Although RCVS can occur spontaneously, predisposing factors such as drugs (vasoactive agents, cocaine, amphetamine, ecstasy, alcohol, intravenous immunoglobulin, and interferon), pregnancy, post-partum state, and a few medical conditions (HELLP syndrome, thrombotic thrombocytopenic purpura, and antiphospholipid syndrome) have been identified.…”

“…20,21 SARS-COV2 binds to ACE2 receptor for host cell entry and suppresses ACE2 expression through internalization, shedding, and downregulation. 12,13,20,21 Reduced ACE2 expression shifts the balance towards ACE1-angiotensin interaction leading to sympathetic overactivity, increased sodium/ water retention, vasoconstriction, endothelial dysfunction, and inflammation. The sympathetic overactivity and vasoconstriction secondary to ACE2 receptor downregulation thereby provide a possible mechanism of RCVS in COVID-19 infection.…”