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Tyrosine Kinase Inhibitor-Induced Acute Myocarditis, Myositis, and Cardiogenic Shock
Author(s) -
Majid Asawaeer,
David Barton,
Stanley J. Radio,
Yiannis S. Chatzizisis
Publication year - 2018
Publication title -
methodist debakey cardiovascular journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.552
H-Index - 23
eISSN - 1947-6094
pISSN - 1947-6108
DOI - 10.14797/mdcj-14-3-e5
Subject(s) - medicine , cardiogenic shock , myocarditis , myositis , cardiology , acute myocarditis , shock (circulatory) , myocardial infarction
A 61-year-old female was admitted with acute dyspnea on exertion and diffuse muscle tenderness 1 month after initiation of sorafenib for renal cell carcinoma. On examination, she was tachycardic with elevated jugular venous pressure, ascites, and lower extremity edema. Initial laboratory testing revealed a troponin I of 13.1 ng/mL, elevated creatine kinase of 1,817 ng/mL, elevated aminotransferases, and B-natriuretic peptide of 534 pg/dL. Electrocardiogram showed acute ST segment elevation in the anteroseptal leads, which may suggest right ventricle (RV) myocardial damage more than left ventricle. Echocardiogram revealed a dilated and severely depressed right ventricle with global left ventricular systolic dysfunction (Figure 1 A). A lung ventilation/perfusion scan showed low probability for pulmonary embolism. Coronary angiogram showed normal coronary arteries (Figure 1 B). Right heart catheterization revealed a mean right atrial pressure of 20 mm Hg, a pulmonary capillary wedge pressure of 15 mm Hg, and a Fick cardiac output of 3.5 L/min, indexed to 1.7 L/min/m2. Endocardial biopsies (Figure 1 C, D) showed lymphohistiocytic active myocarditis with prominent endocardial plasma cells and eosinophilic infiltrate consistent with drug-mediated myocarditis. Reverse transcription polymerase chain reaction and staining were negative for viral or fungal etiologies.

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