Why the study?
It was unclear whether idiopathic inflammatory myopathies exhibit distinct phenotypes in the context of COVID-19.
Does prior COVID-19 infection increase the risk of cardiac damage in patients with idiopathic inflammatory myopathies?
Does prior COVID-19 infection increase the risk of cardiac damage in patients with idiopathic inflammatory myopathies?
Prior COVID-19 infection in patients with idiopathic inflammatory myopathies is associated with increased cardiac involvement and myocardial damage, highlighting the need for long-term cardiovascular monitoring.
May warrant closer cardiac monitoring in IIM patients with prior COVID-19; hypothesis-generating and requires prospective validation.
The 2019 coronavirus disease (COVID-19) pandemic has changed the characteristics of many diseases. It remains unclear whether idiopathic inflammatory myopathies (IIMs) exhibit distinct phenotypes in the context of COVID-19. This retrospective study analyzed patients with IIMs admitted to West China Hospital from January 2022 to December 2023. Among them, 171 had a history of COVID-19 (prior COVID-19 [PC]), while 121 did not (no prior COVID-19 [NPC]). Medical histories, lab tests, and echocardiography data were compared. The PC group exhibited a greater incidence of cardiac damage, including a greater proportion of cardiac injury ( P = 0.016), clinical diagnosis of myocarditis ( P = 0.02), palpitation ( P = 0.031), and Myositis Activity Assessment Visual Analog Scale/Myositis Intention-to-Treat Activity Index cardiovascular involvement scores (all P < 0.001), and elevated levels of myoglobin ( P = 0.03), creatinine kinase MB ( P = 0.015), cardiac troponin T ( P = 0.011), N-terminal pro-B-type natriuretic peptide ( P = 0.028), lactate dehydrogenase ( P = 0.033), and hydroxybutyrate dehydrogenase ( P = 0.019). Echocardiographic analysis revealed a greater diameter of the left atrium ( P = 0.040), left ventricle ( P = 0.013), greater end-diastolic dimension ( P = 0.042), and greater end-diastolic volume ( P = 0.036) in the PC group than in the NPC group. Transcriptional data analysis based on public databases indicated that various mechanisms, including collagen matrix proliferation, calcium ion pathway regulation, oxidative stress, cell proliferation, and inflammatory molecules, collectively contribute to the pathogenesis of myocardial damage in patients with IIMs and COVID-19. The study serves as a crucial reminder for clinicians to remain vigilant regarding the enduring cardiovascular consequences associated with IIMs after COVID-19. IMPORTANCE This study systematically analyzed the clinical features, laboratory test results, and echocardiographic findings of patients with IIMs, comparing those with and without a history of COVID-19 infection. The analysis revealed significant alterations in the clinical manifestations of IIM patients after COVID-19, particularly in relation to cardiac involvement. Our findings highlight the crucial importance for clinicians to maintain vigilance concerning the potential long-term cardiovascular sequelae associated with IIMs in post-COVID-19 patients.
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Cheng et al. (2025) studied this question.
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