Background Coronavirus Disease 2019 (COVID-19) results in increased inflammatory markers previously associated with atrial arrhythmias. However, little is known about their incidence or specificity in COVID-19, or their association with outcomes. We determined the incidence, predictors and outcomes of atrial fibrillation or flutter (AF/AFL) in patients hospitalized with COVID-19, or hospitalized with Influenza. Methods This is a retrospective analysis of 3,970 patients admitted with PCR-positive COVID-19 between 2/4/2020-4/22/2020 with manual review performed of 1,110. The comparator arm included 1,420 patients with influenza hospitalized between 1/1/2017-1/1/2020. Results Among 3970 inpatients with COVID-19, the incidence of AF/AFL was 10% (N=375) and in patients without a history of atrial arrhythmias, 4% (N=146). Patients with new-onset AF/AFL were older with increased inflammatory markers including Interleukin-6 (93 vs 68 pg/ml, P<0.01), and more myocardial injury (Troponin-I: 0.2 vs 0.06ng/ml, P<0.01). AF/AFL were associated with increased mortality (46% vs 26%, P<0.01). Manual review captured a somewhat higher incidence of AF/AFL (13%, N=140). Compared to inpatients with COVID-19, patients with Influenza (N=1420) had similar rates of AF/AFL (12%, n=163) but lower mortality. The presence of AF/AFL correlated with similarly increased mortality in both COVID-19 (RR 1.77) and Influenza (RR 1.78). Conclusions AF/AFL occurs in a subset of patients hospitalized with either COVID-19 or Influenza, and is associated with inflammation and disease severity in both infections. The incidence and associated increase in mortality in both cohorts suggests that AF/AFL in not specific to COVID-19, but is rather a generalized response to the systemic inflammation of severe viral illnesses.

Background - Patients with coronavirus disease 2019 (COVID-19) who develop cardiac injury are reported to experience higher rates of malignant cardiac arrhythmias. However, little is known about these arrhythmias - their frequency, the underlying mechanisms, and their impact on mortality. Methods - We extracted data from a registry (NCT04358029) regarding consecutive inpatients with confirmed COVID-19, were receiving continuous telemetric ECG monitoring, and had a definitive disposition of hospital discharge or death. Between patients who died versus discharged, we compared a primary composite endpoint of cardiac arrest from ventricular tachycardia/fibrillation or bradyarrhythmias such as atrio-ventricular block. Results - Among 800 COVID-19 patients at Mount Sinai Hospital with definitive dispositions, 140 patients had telemetric monitoring and either died (52) or were discharged (88). The median (IQR) age was 61 years (48 - 74); 73% men; and ethnicity was Caucasian in 34%. Comorbidities included hypertension in 61%, coronary artery disease in 25%, ventricular arrhythmia history in 1.4%, and no significant comorbidities in 16%. Compared to discharged patients, those who died had elevated peak troponin I levels (0.27 vs 0.02 ng/mL), and more primary endpoint events (17% vs 4%, p = 0.01), a difference driven by tachyarrhythmias. Fatal tachyarrhythmias invariably occurred in the presence of severe metabolic imbalance, while atrioventricular block was largely an independent primary event. Conclusions - Hospitalized COVID-19 patients who die experience malignant cardiac arrhythmias more often than those surviving to discharge. However, these events represent a minority of cardiovascular deaths, and ventricular tachyarrhythmias are mainly associated with severe metabolic derangement.

Objectives: Because patients with hospital-acquired acute kidney injury (AKI) are at risk for subsequent development of heart failure (HF) and little is known about the relation between community-acquired AKI (CA-AKI) and HF, we sought to determine if CA-AKI is a risk factor for incident HF hospitalization. Methods: We utilized Baylor Scott & White Health databases at the primary care and inpatient hospitalization levels to identify adults without a prior history of HF who had 2 or more serum creatinine measurements within 13 months in the primary care setting. We defined CA-AKI as a serum creatinine increase ≥0.3 mg/dL or ≥1.5 times the baseline for consecutive values within a 13-month period. We created a flag for de novo HF hospitalization at 90, 180, and 365 days following CA-AKI evaluation. Results: In the analyses, 210,895 unique adults were included, of whom 5,358 (2.5%) had CA-AKI. Those with CA-AKI had higher rates of comorbidities, higher rate of males (48 vs. 42%, p < 0.001), and were older (61.5 [50.3, 73.1] vs. 54.1 [42.8, 64.7] years, p < 0.001) than those who did not have CA-AKI. In total, 607 (0.3%), 833 (0.4%), and 1,089 (0.5%) individuals had an incident HF hospitalization in the 90, 180, and 365 days following the CA-AKI evaluation, respectively. After adjusting for demographic and clinical characteristics, patients with CA-AKI had >2 times the risk of de novo HF hospitalization compared with patients who did not have CA-AKI (90 days: 2.35 [1.83–3.02], p < 0.001; 180 days: 2.52 [2.04–3.13], p < 0.001; 365 days: 2.16 [1.77–2.64], p < 0.001). These multivariable models yielded strong predictive abilities, with the areas under the receiver-operating characteristic curve >0.90. Conclusion: After controlling for baseline and clinical characteristics, patients with CA-AKI were at approximately twofold the risk of de novo HF hospitalization (within 90, 180, and 365 days) compared with those who did not have CA-AKI. Hence, detecting CA-AKI may provide an opportunity for early intervention at the primary care level to possibly delay HF development.