Why the study?
It remained unclear whether patients with idiopathic inflammatory myopathies exhibit a predisposition to unique pathological damage and whether their clinical phenotypes are altered by COVID-19.
Does a prior history of COVID-19 infection increase cardiac impairment in patients with idiopathic inflammatory myopathies?
Does a prior history of COVID-19 infection increase cardiac impairment in patients with idiopathic inflammatory myopathies?
Patients with idiopathic inflammatory myopathies and a history of COVID-19 exhibit more pronounced myocardial damage and impaired diastolic function compared to those without prior COVID-19.
Prior COVID-19 was associated with heightened cardiac involvement in IIMs; leaves open whether screening or therapy adjustments are warranted pending prospective data.
Background As the COVID-19 pandemic progresses, there have been reports of a syndrome involving multisystem organ damage following the immune response to the virus. However, it remains unclear whether patients with specific autoimmune diseases, such as idiopathic inflammatory myopathies (IIMs), exhibit a predisposition to unique pathological damage and whether their clinical phenotypes are altered by COVID-19. Methods This study was a retrospective case‒control study that included 62 patients with IIMs who had a prior history of COVID-19 (prior COVID-19, PC) and 52 patients without such a history (no prior COVID-19, NPC). Medical histories, laboratory examinations, and echocardiography data were compared between the two groups. Additionally, we investigated the potential molecular mechanisms underlying the association between COVID-19 and post infection clinical phenotypes in IIMs using publicly available transcriptome databases. Results Compared to the NPC group, patients in the PC group exhibited a higher prevalence of cardiopulmonary symptoms, including palpitation and dyspnea, as well as elevated levels of pulmonary and cardiovascular myositis activity assessment visual analog scales (MYOACT)/myositis intention-to-treat activity index (MITAX), cardiac troponin T, and hydroxybutyrate dehydrogenase (HBDH). Echocardiographic analysis revealed larger left atrium (LA) dimensions, interventricular septum (IVS) thickness, and an increased ratio of peak velocity of left ventricular early-diastolic fast filling to the velocity of early diastolic myocardial movement at mitral ring (E/e’) in the PC group compared to the NPC group. Transcriptional data analysis based on public databases revealed that various mechanisms, including collagen matrix proliferation, regulation of the calcium ion pathway, oxidative stress, cell proliferation, and inflammatory molecules, collectively contribute to the pathogenesis of IIMs and COVID-19 infection. Conclusion Patients with IIMs exhibit more pronounced myocardial damage and impaired cardiac diastolic function following COVID-19, thereby offering valuable insights for the clinical management of IIMs patients and potential avenues for further investigation into the long-term consequences of COVID-19.
No takes yet. Share an insight, caveat, or question.
Cheng et al. (2023) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: