Anti-HMGCR Myopathy During NSTEMI Evaluation: The Statin Paradox and Troponin Trap
Khaleel Quasem1, Michelle Carrasquel-Alvarez1, Haley Maser1
1Department of Internal Medicine, McLaren Greater Lansing, Lansing, Michigan, USA.
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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