ABSTRACT
Amiodarone is a class III antiarrhythmic medication used to treat atrial and ventricular tachyarrhythmias. Pulmonary fibrosis from amiodarone use is a well-documented side effect. Pre-COVID-19 pandemic studies have shown that amiodarone-induced pulmonary fibrosis occurs in 1%-5% of patients and usually occurs between 12 to 60 months after initiation. The risk factors associated with amiodarone-induced pulmonary fibrosis include a high total cumulative dose (treatment longer than two months) and high maintenance dose (>400 mg/day). COVID-19 infection is also a known risk factor for developing pulmonary fibrosis and occurs in approximately 2%-6% of patients after a moderate illness. This study aims to assess the incidence of amiodarone in COVID-19 pulmonary fibrosis (ACPF). This is a retrospective cohort study with 420 patients with COVID-19 diagnoses between March 2020 and March 2022, comparing two populations, COVID-19 patients with exposure to amiodarone (N=210) and COVID-19 patients without amiodarone exposure (N=210). In our study, pulmonary fibrosis occurred in 12.9% of patients in the amiodarone exposure group compared to 10.5% of patients in the COVID-19 control group (p=0.543). In multivariate logistic analysis, which controlled for clinical covariates, amiodarone use in COVID-19 patients did not increase the odds of developing pulmonary fibrosis (odds ratio (OR): 1.02, 95% confidence interval (CI): 0.52-2.00). The clinical factors associated with the development of pulmonary fibrosis in both groups included a history of preexisting interstitial lung disease (ILD) (p=0.001), exposure to prior radiation therapy (p=0.021), and higher severity of COVID-19 illness (p<0.001). In conclusion, our study found no evidence that amiodarone use in COVID-19 patients increased the odds of developing pulmonary fibrosis at six-month follow-up. However, long-term amiodarone usage in the COVID-19 population should be based on the physician's discretion.
ABSTRACT
A 28-year-old G2P0010 woman with a history of COVID infection during her current pregnancy treated with monoclonal antibodies and benign gestational thrombocytopenia presented for routine prenatal care at 33 weeks' gestation. The patient was asymptomatic, but incidental tachycardia was noted on the physical exam with an irregular rhythm. An electrocardiogram (ECG) was performed and was consistent with multifocal atrial tachycardia at a rate of 144 beats per minute. The patient was started on labetalol 50 mg daily and was referred to cardiology for consultation. An echocardiogram was performed and showed dilated left ventricular cavity with a moderately reduced ejection fraction of 40%. No previous echocardiogram was available for comparison; the patient had no history of cardiac disease. The dose of labetalol was increased to 50 mg twice daily and she was admitted for digoxin loading and titration. Though fetal tolerance was excellent, her heart rate was not controlled. Digoxin was switched to flecainide and labetalol was switched to metoprolol which improved her heart rate and repeat echocardiogram showed an ejection fraction of 50%. The patient was admitted for induction of labor at 39 weeks of gestation and continued intrapartum flecainide. Metoprolol was continued intra and postpartum. Flecainide was resumed at three days postpartum due to the recurrence of atrial tachycardia and has been maintained. A repeat echocardiogram is scheduled six weeks postpartum to evaluate left ventricular function and wean off antiarrhythmics.