Among patients with COVID-19 comorbidities like cerebrovascular event and atrial fibrillation have been reported in less than 2% of patients.1 Interestingly occurrences of new cerebrovascular events and atrial fibrillation have been also reported in patients with COVID-19. Irrespective of the onset, the presence of a cerebrovascular event has been reported to affect clinical outcome in COVID-19. Agarwal et al. had reviewed studies on the impact of prior CVD among patients with COVID-19. They reported an increase in severity of COVID-19 illness, among patients with CVD.2 In another review, we reviewed 2 studies reporting new-onset cerebrovascular events among patients with COVID-19 and reported that the presence of CVD as evident by neuroimaging predicted disease severity.3
Patients with severe COVID-19 illness can present with multiple patterns of cardiac injury including acute myocardial injury, cardiogenic shock, heart failure, cardiac arrhythmias, and myocarditis. Among these, only acute myocardial injuries, shock, and heart failure have been shown to predict the occurrence of stroke and disease severity.1
Aghamohammadi et al. have suggested that anticoagulants including enoxaparin and heparin have a mortality benefit in patients with COVID -19.4 The mechanisms that have been postulated to cause neurological injury, and cerebrovascular events in patients with severe COVID-19 are i) cytokine storm, ii) embolic event in the background of myocarditis, and arrhythmia, iii) hypoxia-induced ischemia and apoptosis, iv) thrombotic microangiopathy, v) coagulopathy and thrombocytopenia, vi) direct viral invasion.1
Among these mechanisms, instituting or continuing anticoagulation would be crucial in patients with prior history of atrial fibrillation, and the presence of embolism. Therapeutic anticoagulation has been tried among patients with severe COVID-19 with elevated D-dimers levels.5 Randomized clinical trials showing mortality benefit in these patients are still lacking. In the meantime, the clinician needs to be aware of the potential risks of the therapy. A recent study reported the occurrence of intracranial hemorrhage among 33 COVID-19 patients on therapeutic anticoagulation for elevated D-dimer levels. These patients were treated with unfractionated heparin, enoxaparin, and argatroban. Mortality was reported in 15.2% of these patients, which was attributed to the parenchymal hemorrhage causing mass-effect and herniation. Based on their findings, the authors recommended initial brain imaging, before the institution of anticoagulation in all patients with severe COVID-19.5
The newer oral anticoagulants have a proven advantage in terms of safety and efficacy when compared to warfarin in the general population. However, there is limited literature on the safety, efficacy, and interactions between most cardiac medications in patients with COVID-19. Multiple medications including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, steroids, hydroxychloroquine, antivirals, antibiotics have been proven to be noncontributory in COVID-19 related mortality.1 We believe the role of anticoagulation in patients with COVID-19 illness should be individualized. Future studies should compare outcomes among patients with non-severe and severe COVID-19.
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References
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