COVID-19 infection as a parameter in the CHA2DS2 vascular risk assessment tool
Editor – The study by Indurawa et al1 showing an increased prevalence of atrial fibrillation (AF) in hospitalised COVID-19 patients complements the findings of another study that also showed an increased risk of incident atrial fibrillation (AF) in hospitalised patients with COVID-19 infection. In that study 11,004 COVID-19-negative patients were matched with 3,090 COVID-19-positive patients, and 5,005 pre-pandemic patients were matched with 2,283 COVID-19-positive patients. After adjusting for demographic factors and comorbidities, COVID-19 positive patients had a 1.19 times odds (95% confidence interval (CI) 1.0–1.41) of developing AF compared to COVID-19 negative patients, and 1.56 times the odds (95% CI 1.23–1.41) of developing AF compared to pre-pandemic patients.2
Even in the post-hospital phase of COVID-19 infection, patients who have experienced a COVID-19 episode are at increased risk of incident arrhythmia (including AF).3 In this study, risk of arrhythmia was assessed at 6 months in mutually exclusive cohorts comprising non-hospitalised patients with COVID-19, people who were hospitalised for COVID-19, and people who were admitted to intensive care for COVID-19 during the acute phase (30 days) of the infection. All three categories were patients who had already been discharged from hospital at the time of evaluation. Beyond the first 30 days of illness, patients with COVID-19 who had been hospitalised for this infection had an increased risk of arrhythmia (hazard ratio 8.4, 95% CI 7.18–9.53).3 What is doubly disconcerting is that COVID-19 is also associated with a hypercoagulable state, as shown in the literature review by Abou-Ismail et al,4 thereby compounding the risk of cardiogenic thromboembolism. In that review the increased risk of thrombosis appeared to prevail despite anticoagulation. The proposed pathophysiology of COVID-19 coagulopathy is that it is initiated by the proinflammatory environment of COVID-19 infection. In that proinflammatory milieu participants in the aetiopathogenesis of hypercoagulability include cytokine release, localised intravascular coagulopathy, participation by monocytes and macrophages, neutrophil extracellular traps, complement-mediated microangiopathy and dysregulation of the renin-angiotensin system.4
For all these reasons history of COVID-19 infection deserves inclusion as one of the parameters in the CHAD2 vascular risk assessment tool.
- © Royal College of Physicians 2023. All rights reserved.
References
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- Indurawa I
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- Wollborn J
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