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).