Results
The baseline characteristics of those with and without COVID-19 are shown in Table 1. The cohort had many features that put them at high risk for COVID-19 complications with a mean age of 60 ± 16 years, 180 (60%) were men, 170 (57%) were African-American, 109 (36%) were Caucasian, and there were high rates of underlying chronic metabolic, pulmonary, renal, and cardiovascular comorbidities that have been associated with poor outcome in other published COVID-19 cohorts.5, 14-16 Compared to those who were COVID- , COVID+participants were more likely to have a history of diabetes (47% vs. 34%, p=0.04), but less likely to have a systolic heart failure (9% vs 27%, p=0.001), diastolic dysfunction (17% vs 34%, p=0.001), paroxysmal atrial fibrillation (5% vs. 14%, p=0.004), chronic kidney disease (14% vs. 23%, p=0.05), chronic obstructive pulmonary disease (12% vs. 30%, p=0.0001), tobacco abuse (26% vs 50%, p=0.0001), and cirrhosis (1% vs. 9%, p=0.001). COVID+participants were less likely to be prescribed beta blockers in the outpatient setting (28% vs. 47%, p=0.001). COVID+ participants also had higher D-dimer (3542 ± 4664 ng/mL vs. 1861 ± 2290 ng/mL, p=0.02) and CRP levels (200 ± 113 mg/L vs. 93 ± 86 mg/L, p=0.0001) but lower brain natriuretic peptide (331 ± 566 pg/mL vs. 732 ± 812 pg/mL, p=0.0001) and high sensitivity troponin (549 ± 1599 ng/L vs. 1906 ± 7795 ng/L, p=0.03) levels. Individuals with COVID-19 were more likely to require vasopressor support (71% vs. 38%, p=0.0001) and mechanical ventilation (75% vs. 40%, p=0.0001) than those who were COVID- . COVID+ therapies included azithromycin in 150 participants, hydroxychloroquine in 7 participants, and remdesivir in 78 participants. An ATA was recorded by 12-lead ECG in 32 COVID+ participants (16%) and 19 COVID- participants (19%). ATAs included atrial fibrillation in 34 participants, atrial flutter in 14 participants, and atrial tachycardia in 3 participants.
In-hospital mortality by COVID status in those with and without ATA is shown in Table 2. Individuals who were COVID+ with new onset ATA had the highest in-hospital mortality (50%) of any group (p=0.01). When compared to those who were COVID-without new onset ATA, individuals who were COVID+with new onset ATA had higher in-hospital mortality in both unadjusted (OR 4.4 , 95% CI 1.8 to 10.7) and multivariable adjusted (OR 5.0, 95% CI 1.9 to 13.5) models. Individuals who were COVID-with new onset ATA also had increased in-hospital mortality when compared to those who were COVID- without new onset ATA after multivariable adjustment (OR 2.3, 95% CI 1.1 to 5.0). although the magnitude of this association was less than for those who were COVID+ with new onset ATA.
The demographic and clinical characteristics and inpatient therapies for individuals with ATAs are shown in Table 3. Those who were COVID+ and developed an ATA were more likely to require vasopressors (91% vs 47%, p=0.001), had a longer duration on vasopressors (9 ± 6 vs 2 ± 2 days, p=0.0001), were more likely to require mechanical ventilation (94% vs 42%, p=0.0001), had a longer duration of mechanical ventilation (18 ± 11 vs 4 ± 9 days, p=0.0001), had longer ICU lengths of stay (LOS) (23 ± 8 vs 12 ± 11 days, p=0.0001), and had longer hospital LOS (25 ± 6 vs 17 ± 9 days, p=0.0001) compared to those who were COVID- and developed an ATA.
HC occurred in 18 participants in the COVID+group and none in the COVID- group (p=0.0001). Among the 18 COVID+ individuals who experienced HC, 17 experienced an increasing NE Eq requirement and 1 required immediate direct current cardioversion for hemodynamic instability at ATA onset. In the 17 participants that had an increase in vasopressor requirement, the average change in NE Eq was 0.18 µg/kg/min. A graphical representation of NE Eq dosage changes can be found in Figure 2. ATA was treated with amiodarone in 29 (57%) participants, beta blockers in 38 (75%), calcium channel blocker in 5 (10%), and anticoagulation was felt to be safe in 31 (61%) participants.
Characteristics of participants with new onset ATA by hemodynamic status are shown in Table 4. When compared to the 14 COVID+ hemodynamically stable participants following ATA onset, the 18 COVID+participants who developed HC after ATA onset had similar comorbid conditions and baseline echocardiographic assessment with a lower mean arterial pressure (74 ± 16 vs 89 ± 10, p=0.004), higher serum potassium (4.5 ± 0.4 vs 4.2 ± 0.5, p=0.04), greater vasopressor use (83% vs 21%, p=0.0001), greater need for mechanical ventilation (100% vs 57%, P=0.002), higher positive end expiratory pressure (PEEP) requirements (10 ± 4 vs 5 ± 4, p=0.005), and increased in-hospital mortality (67% vs. 29%, p=0.03). In fact, of the 16 individuals with COVID-19 and a new onset ATA who subsequently died, 12 (75%) had HC immediately after developing the ATA.
When compared to the 19 COVID- participants who remained hemodynamically stable following ATA onset, the 18 COVID+ participants who developed HC after ATA onset had a decreased prevalence of past diastolic dysfunction (11% vs. 47%, p=0.02) and coronary artery disease (11% vs. 42%, p=0.03) but a higher serum potassium (4.5 ± 0.4 vs. 4.1 ± 0.6, p=0.02), greater need for vasopressor use (83% vs. 11%, p=0.0001), greater need for mechanical ventilation (100% vs. 16%, p=0.0001), higher PEEP (10 ± 4 vs. 1 ± 3 mm Hg, p=0.0001), higher fraction of inspired oxygen requirements (57 ± 17 vs. 29 ± 6, P=0.0001), and increased in-hospital mortality (67% vs. 29%, p=0.01).