Our study found that bradycardia was not associated with mortality in COVID-19 patients. This result is contrary to the largest study on bradycardia and mortality by Kumar et al. that showed that bradycardia was predictive of mortality in COVID-19 patients.  The possible explanation for this is that Kumar et al. reported bradycardia being associated with mortality when bradycardic patients are compared to a subset of patients with normal heart rates. However, they excluded patients with tachycardia. Our study compared bradycardic patients with non-bradycardic patients, including patients with normal heart rates and tachycardic patients. Tachycardia has been associated with increased mortality in COVID-19 patients , and this might have explained why bradycardia was not associated with mortality in our study. Similarly, Olivia A et al. did not find any significant association between relative bradycardia, which is defined as heart rate < 90 bpm, and concomitant fever (temperature ≥ 38.3 °C) and mortality in COVID-19 patients. 
The average incidence of bradycardia in the three studies in our meta-analysis was 26%. The large variation in the incidence of bradycardia in the primary studies may be due to the difference in the study design. Kumar et al. and Chalkias et al. used continuous cardiac monitoring to determine bradycardia in all hospitalized COVID-19 patients and patients admitted to the ICU and reported a bradycardia incidence of 24.9% and 79%, respectively. [10, 16] Conversely, Antwi-Amoabeng et al. used ECG done after COVID-19 diagnosis to determine bradycardic patients and reported an incidence of seven percent . Thus, using an ECG done after the COVID-19 diagnosis will likely underestimate the incidence of sinus bradycardia in COVID-19 patients. Conversely, Chalkias et al. measured bradycardia in only ICU patients and will likely lead to over-estimation of bradycardia. 
The mechanism of bradycardia in COVID-19 appears to be multifactorial. It could be caused by the direct pathogenic effect of the virus on the myocardium, hypoxia, drug toxicity, severe downregulation of myocardial angiotensin-converting enzyme 2 (ACE2) pathways resulting in myocardial inflammation, or the effect of the inflammatory cytokines on the heart [10, 18, 19]. However, the direct pathogenic effect of the COVID-19 virus on pacemaker cells and the effect of the systemic inflammation on cardiac pacemaker cells are the two most commonly proposed mechanisms of bradycardia [18, 19]. Beta-blockers and hypoxia were not associated with bradycardia in both Kumar et al. and Chalkias et al. studies. [11, 16]
Similarly, relative bradycardia has been reported in COVID-19 patients [17, 20, 21]. Physiologically, the heart rate is expected to increase by about ten beats for each degree increase in temperature in degrees Fahrenheit. Thus, a temperature of 101 °F (38.3 °C) is expected to have a corresponding heart rate of about 110 . Relative bradycardia has been reported in infectious processes like typhoid and Q-fever and non-infectious processes like drug fever. The most common cause of relative bradycardia in patients with fever is the use of beta-blocker medications . However, beta-blockers have not been associated with bradycardia in COVID-19 and are unlikely to cause relative bradycardia seen in COVID-19 patients [11, 16]. The direct pathogenic effect of the COVID-19 virus on cardiac pacemaker cells and/or the effect of inflammatory cytokines on cardiac pacemaker cells has been proposed as possible causes of relative bradycardia. [20, 23]
Limitations of the study
One of the major limitations is the few studies combined in the meta-analysis due to the limited studies that reported bradycardia and its association with mortality in COVID-19 patients. Thus, the small number of studies and participants may make it difficult to detect an effect, even if one exists, so the results of this analysis should be interpreted with caution. Furthermore, two conference abstracts identified during the literature search were not included in the meta-analysis because of incomplete data, which could potentially bias our study's result. However, both conference abstracts did not find any statistically significant relationship between bradycardia and COVID-19 mortality, which is consistent with the findings of our meta-analysis. Additionally, the heterogeneity of the studies in the meta-analysis is considerable and could have affected the conclusion of our study. However, we mitigated the effect of the heterogeneity in our analysis by using a random-effects model for the meta-analysis, which assumes that the primary studies are heterogeneous and gives a more conservative estimate of effect. Finally, our study is a combination of observational studies, and there could have been unmeasured or unadjusted confounders that affected the study outcome in the primary studies.
Implications of the results for practice, policy, and future research
Our study showed that bradycardia was not significantly associated with mortality in COVID-19 patients. The implication for practice is that there might be no mortality benefit in aggressively treating asymptomatic sinus bradycardia in COVID-19 patients.
The opportunities for future research include more studies to investigate the relationship between bradycardia and mortality in COVID-19 patients. Some studies have suggested that bradycardia in COVID-19 patients might be harbingers of a more severe disease. Therefore, understanding that association may help clinicians prognostically triage the patients appropriately. Additionally, it may be interesting to see the effect of bradycardia in different sub-groups of COVID-19 patients, such as symptomatic vs. asymptomatic patients and younger vs. older patients.