Cardiac Troponin in Autoimmune Rheumatic Diseases: Lights and Shadows

Cardiovascular involvement is a leading cause of morbidity and mortality in autoimmune rheumatic diseases (ARDs), arising through diverse mechanisms such as microvascular dysfunction, inflammation, fibrosis, in addition to traditional cardiovascular risk factors. Cardiac troponin (cTn), a sensitive and specific marker of myocardial injury, is increasingly investigated for its diagnostic and prognostic value. However, interpretation in ARDs is complex, as cTn elevations may reflect primary cardiac involvement, comorbidities or analytical interferences. This review explores the value of cTn as a biomarker of cardiac involvement in several ARDs, such as systemic sclerosis, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, and idiopathic inflammatory myopathies. Articles in the PubMed database (1969-november 2025) were selected using each ARD in combination with "troponin," "cardiovascular," "myocardial involvement," "cardiac involvement," and "biomarker", as keywords. High sensitivity cTn assays can identify both overt and subclinical myocardial injury, predict major adverse cardiovascular events, and correlate with imaging findings, such as myocardial fibrosis and inflammation. Also, cTn increase can result from renal impairment, infections, anemia, or pulmonary hypertension, which frequently complicate ARDs. Further challenges arise from analytical pitfalls, including heterophilic antibodies, rheumatoid factor interference, and macrocomplexes, which may generate false results in ARDs patients. Despite growing evidence, significant knowledge gaps persist regarding the differential value of cTn isoforms, optimal thresholds in ARDs populations, and their role in guiding treatment strategies. Overall, hs-cTn represents a promising, accessible tool to refine diagnosis, risk stratification, and monitoring in ARDs, provided results are interpreted carefully in the clinical and laboratory context.