Investigating the Profile of Patients with Idiopathic Inflammatory Myopathies in the Post-COVID-19 Period: Emphasizing Myocardial Injury

Introduction : 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. Methods : This retrospective study included 171 IIMs patients with a history of COVID-19 (prior COVID-19, PC) and 121 without (no-prior COVID-19, NPC). Medical histories, lab tests, and echocardiography data were compared. Results : PC group exhibited a greater incidence of cardiac damage, including a greater proportion of clinical diagnosis of myocarditis (p=0.02), palpitation (p=0.031), and MYOACT/MITAX cardiovascular involvement scores (all p＜0.001), and elevated levels of myoglobin (MYO, p=0.03), creatinine kinase MB (CK-MB, p=0.015), cardiac troponin T (cTnT, p=0.011), N-terminal pro-B-type natriuretic peptide (NT-proBNP, p=0.028), lactate dehydrogenase (LDH, p=0.033), and hydroxybutyrate de-hydrogenase (HBDH, p=0.019). Echocardiographic analysis revealed greater diameter of left atrium (LA, p=0.040), left ventricle (LV, p=0.013), greater thicknesses of interventricular septum (IVS, p=0.043), and greater end-diastolic volume (EDV, 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. Conclusion : The study serves as a crucial reminder for clinicians to remain vigilant regarding the enduring cardiovascular consequences associated with IIMs subsequent to COVID-19.