A relationship between COVID‐19 infection and an increasing incidence of atrial fibrillation has been observed. However, the underlying pathophysiology as a precipitant to AF has not been reviewed. This paper will consider the possible pathological and immunological AF mechanisms as a result, of COVID‐19 infection. We discuss the role myocardial microvascular pericytes expressing the ACE‐2 receptor and their potential for an organ‐specific cardiac involvement with COVID‐19. Dysfunctional microvascular support by pericytes or endothelial cells may increase the propensity for AF via increased myocardial inflammation, fibrosis, increased tissue edema, and interstitial hydrostatic pressure. All of these factors can lead to electrical perturbances at the tissue and cellular level. We also consider the contribution of Angiotensin, pulmonary hypertension, and regulatory T cells as additional contributors to AF during COVID‐19 infection. Finally, reference is given to two common drugs, corticosteroids and metformin, in COVID‐19 and how they might influence AF incidence.
Background
Prolonged electrocardiogram (ECG) QRS duration has been associated with increased cardiovascular risk. It is unclear whether the main predictor of cardiovascular risk, the Framingham risk score also predicts short-term changes in ECG QRS duration. Our aim is to determine whether baseline Framingham risk score is associated with baseline or changes in QRS duration.
Methods
A retrospective cross-sectional analysis was performed using observational data obtained from two hundred two participants. Framingham risk score was calculated using an online risk calculator. QRS duration was obtained using a 10 s trace from a Welch Allyn PC-based 12-lead ECG system.
Results
Average follow-up duration was 3.3 ± 1.1 years. Mean QRS change was 1.8 ± 11.4 ms. Specifically, among two hundred two participants, there are 104 subjects with a greater QRS duration at follow-up, while 98 subjects had the same or a shorter follow-up QRS duration. Baseline Framingham risk score did not significantly predict an increase in QRSd with an odds ratio of 1.04 (P = 0.230). Regression analysis of QRS duration at baseline and Framingham risk at baseline had a weak association (R2 = 0.020; P = 0.043). The Framingham risk score at follow-up was likewise has a weak association with follow-up QRS duration (R2 = 0.045; P = 0.002).
Conclusions
Our results do not demonstrate a statistically significant association between Framingham risk parameters and future QRS duration changes over longitudinal time. QRS duration had variable changes between baseline and follow-up. This might suggest that a longer period of follow-up is required to document more stable increases in QRS duration associated with ventricular pathology. A larger population study is needed to confirm our observations.
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