Case Report: Discordant high-sensitivity cardiac troponin T elevation in polymyositis: a diagnostic pitfall
Background High-sensitivity cardiac troponin T (hs-cTnT) is widely used as a gold-standard marker of myocardial injury, yet non-ischemic elevations can occur in idiopathic inflammatory myopathies (IIM), creating a significant diagnostic pitfall. In contrast, high-sensitivity cardiac troponin I (hs-cTnI) generally retains strict cardiac specificity. Case report A 79-year-old female presented with progressive fatigue and elevated cardiac enzymes. Admission hs-cTnT was markedly elevated at 521 ng/L (reference 0–14 ng/L), and she was initially suspected of having a non-ST elevation myocardial infarction (NSTEMI) and underwent emergency coronary angiography, which revealed non-obstructive coronary artery disease. Polyethylene glycol (PEG) precipitation demonstrated a recovery rate exceeding 80%, excluding macromolecular complex interference, while follow-up hs-cTnT testing at an external hospital confirmed the elevation. However, hs-cTnI measured on both the Abbott and Yhlo platforms remained within normal limits. This hs-cTnT(+)/hs-cTnI(−) discrepancy, combined with electromyography (myogenic damage), muscle MRI, and a normal echocardiogram, established the final diagnosis of polymyositis (PM). Conclusion Regenerating skeletal muscle fibers can re-express embryonic cTnT isoforms, producing a true circulating cTnT elevation of skeletal muscle origin that mimics myocardial injury. PEG precipitation confirmed authentic monomeric cTnT antigen rather than an analytical artifact, redirecting the diagnostic focus. Concurrent hs-cTnI assessment is a critical strategy for distinguishing skeletal muscle-derived cTnT from true myocardial injury, thereby preventing misdiagnosis and unnecessary interventions in patients with inflammatory myopathies.