A novel study on SARS-COV-2 virus associated bradycardia as a predictor of mortality-retrospective multicenter analysis.

BACKGROUND: SARS-CoV2 has affected more than 73.8 million individuals. While SARS-CoV2 is considered a predominantly respiratory virus, we report a trend of bradycardia among hospitalized patients, particularly in association with mortality. METHODOLOGY: The multi-center retrospective analysis consisted of 1053 COVID-19 positive patients from March to August 2020. A trend of bradycardia was noted in the study population. Absolute bradycardia and profound bradycardia was defined as a sustained heart rate < 60 BPM and < 50 BPM, respectively, on two separate occasions, a minimum of 4 h apart during hospitalization. Each bradycardic event was confirmed by two physicians and exclusion criteria included: less than 18 years old, end of life bradycardia, left AMA, or taking AV Nodal blockers. Data was fetched using a SQL program through the EMR and data was analyzed using SPSS 27.0. A logistic regression was done to study the effect of bradycardia, age, gender, and BMI on mortality in the study group. RESULTS: 24.9% patients had absolute bradycardia while 13.0% had profound bradycardia. Patients with absolute bradycardia had an odds ratio of 6.59 (95% CI [2.83-15.36]) for mortality compared with individuals with a normal HR response. The logistic regression model explained 19.6% (Nagelkerke R2 ) of variance in the mortality, correctly classified 88.6% of cases, and was statistically significant X2 (5)=47.10, p < .001. For each year of age > 18, the odds of dying increased 1.048 times (95% CI [1.25-5.27]). CONCLUSION: The incidence of absolute bradycardia was found in 24.9% of the study cohort and these individuals were found to have a significant increase in mortality.

Bradyarrhythmias in patients with COVID-19: Marker of poor prognosis?

BACKGROUND: Despite descriptions of various cardiovascular manifestations in patients with coronavirus disease 2019 (COVID-19), there is a paucity of reports of new onset bradyarrhythmias, and the clinical implications of these events are unknown. METHODS: Seven patients presented with or developed severe bradyarrhythmias requiring pacing support during the course of their COVID-19 illness over a 6-week period of peak COVID-19 incidence. A retrospective review of their presentations and clinical course was performed. RESULTS: Symptomatic high-degree heart block was present on initial presentation in three of seven patients (43%), and four patients developed sinus arrest or paroxysmal high-degree atrioventricular block. No patients in this series demonstrated left ventricular systolic dysfunction or acute cardiac injury, whereas all patients had elevated inflammatory markers. In some patients, bradyarrhythmias occurred prior to the onset of respiratory symptoms. Death from complications of COVID-19 infection occurred in 57% (4/7) patients during the initial hospitalization and in 71% (5/7) patients within 3 months of presentation. CONCLUSIONS: Despite management of bradycardia with temporary (3/7) or permanent leadless pacemakers (4/7), there was a high rate of short-term morbidity and death due to complications of COVID-19. The association between new-onset bradyarrhythmias and poor outcomes may influence management strategies for acutely ill patients with COVID-19.

It is time to drop hydroxychloroquine from our COVID-19 armamentarium.

Chloroquine (CQ) and hydroxychloroquine (HCQ) were among the first drugs repurposed for the treatment of SARS-CoV-2 infection. A few in vitro studies confirmed that both drugs exhibited dose dependent anti-SARS-CoV-2 activities. These observations and the encouraging results from early poorly conducted observational studies created a major hype about the therapeutic potential of these drugs in the treatment of COVID-19 disease. This was further catalyzed by media and political influences leading to a widespread use of these agents. Subsequent randomized trials revealed lack of efficacy of these agents in improving the outcomes of COVID-19 or in preventing infection in post-exposure prophylaxis studies. Nevertheless, many ongoing trials continue to actively recruit tens of thousands of patients to receive HCQ worldwide. In this perspective, we address the possible mechanisms behind the lack of efficacy and the increased risk of cardiac toxicity of HCQ in COVID-19 disease. For the lack of efficacy, we discuss the fundamental differences of treatment initiation between in vitro and in vivo studies, the pitfalls of the pharmacological calculations of effective blood drug concentrations and related dosing regimens, and the possible negative effect of HCQ on the antiviral type-I interferon response. Although it has been repeatedly claimed that HCQ has a longstanding safety track record for many decades in use, we present counterarguments for this contention due to disease-drug and drug-drug interactions. We discuss the molecular mechanisms and the cumulative epidemiological evidence of HCQ cardiac toxicity.