Key result
Statin cessation and rapid immunosuppression resolve severe anti-HMGCR myopathy mimicking acute myocardial injury.
Case Report (n=1)
Elevated high-sensitivity troponin T in inflammatory myopathies can complicate acute coronary syndrome evaluation, creating a management conflict between urgent revascularization and statin contraindication.
BACKGROUND: Anti-3-hydroxy-3-methylglutaryl coenzyme A reductase immune-mediated necrotizing myopathy causes progressive proximal weakness with marked creatine kinase elevation that persists after statin cessation. High-sensitivity troponin T may be elevated in inflammatory myopathies independent of myocardial ischemia, complicating acute coronary syndrome evaluation. CASE SUMMARY: A 69-year-old man presented after a fall with progressive proximal weakness. Rising high-sensitivity troponin T levels prompted non-ST-segment elevation myocardial infarction work-up; angiography revealed severe multivessel coronary artery disease including left main involvement. Concurrent creatine kinase of 4,356 U/L and transaminitis led to myopathy evaluation. Anti-3-hydroxy-3-methylglutaryl coenzyme A reductase antibody was strongly positive (459), and thigh magnetic resonance imaging confirmed diffuse myositis. Statins were discontinued; immunotherapy was escalated to pulse methylprednisolone, intravenous immunoglobulin, and methotrexate. DISCUSSION: This case highlights a management collision: urgent coronary revascularization planning vs absolute statin contraindication requiring rapid immunosuppression for immune-mediated necrotizing myopathy.
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Quasem et al. (2026) conducted a case report in Anti-HMGCR Myopathy and NSTEMI (n=1). Statin discontinuation and immunotherapy was evaluated. A 69-year-old man with severe coronary artery disease and rising troponin T was diagnosed with anti-HMGCR myopathy, requiring statin discontinuation and rapid immunosuppression.
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