ArticleFrontiers in cardiovascular medicine2026
Case Report: Discordant high-sensitivity cardiac troponin T elevation in polymyositis: a diagnostic pitfall.
Article in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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