Money David B, Lee Dae Hyun, Hadar Ari, Doherty Justin, Malanga Christopher, Serino Alexa, Cohen Adam J
Department of Internal Medicine, University of South Florida, Tampa, USA.
Department of Cardiology, University of South Florida, Tampa, USA.
Cureus. 2023 Jan 23;15(1):e34109. doi: 10.7759/cureus.34109. eCollection 2023 Jan.
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.
胺碘酮是一种III类抗心律失常药物，用于治疗房性和室性快速心律失常。使用胺碘酮导致的肺纤维化是一种有充分文献记载的副作用。COVID-19大流行前的研究表明，胺碘酮所致肺纤维化在1%至5%的患者中发生，通常在开始用药后12至60个月出现。与胺碘酮所致肺纤维化相关的危险因素包括高累积总剂量（治疗超过两个月）和高维持剂量（>400毫克/天）。COVID-19感染也是已知的发生肺纤维化的危险因素，在中度疾病后约2%至6%的患者中出现。本研究旨在评估COVID-19肺纤维化（ACPF）中胺碘酮的发生率。这是一项回顾性队列研究，纳入了2020年3月至2022年3月期间确诊为COVID-19的420例患者，比较了两个群体，即接触胺碘酮的COVID-19患者（N=210）和未接触胺碘酮的COVID-19患者（N=210）。在我们的研究中，胺碘酮暴露组12.9%的患者发生了肺纤维化，而COVID-19对照组为10.5%的患者（p=0.543）。在控制了临床协变量的多因素逻辑分析中，COVID-19患者使用胺碘酮并未增加发生肺纤维化的几率（比值比（OR）：1.02，95%置信区间（CI）：0.52-2.00）。两组中与肺纤维化发生相关的临床因素包括既往存在间质性肺疾病（ILD）病史（p=0.001）、既往接受过放射治疗（p=0.021）以及COVID-19疾病的严重程度较高（p<0.001）。总之，我们的研究没有发现证据表明COVID-19患者使用胺碘酮会增加6个月随访时发生肺纤维化的几率。然而，COVID-19人群中长期使用胺碘酮应基于医生的判断。
