JACC. Case reports · 2026
Anti-HMGCR Myopathy During NSTEMI Evaluation: The Statin Paradox and Troponin Trap.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Quasem Khaleel, Carrasquel-Alvarez Michelle, Maser Haley, Russell Claire, Barker Thomas, Thulluri Ramalakshmi, Felice Jordan, Nadipalli Vivek, Shah Ibrahim, Hong Charles
Аннотация
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.
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.