Hypersensitivity myocarditis confirmed by cardiac magnetic resonance imaging and endomyocardial biopsy
A 68-year-old woman presented with constrictive chest pain lasting for 2 hours. She had a history of hypertension, transient cerebral ischemic attack, and osteoarthritis in both knees. Her blood pressure was 91/53 mmHg, pulse rate was 63 beats per minute, respiration rate was 20 breaths per minute, and body temperature was 37℃. Upon physical examination, heart sounds were normal without murmur. Pulmonary auscultation revealed coarse vesicular sounds with crackles on both lower lung fields. Multiple itchy erythematous lesions were present on the hands, buttocks, abdomen, and trunk ().\nThe results of laboratory examinations were as follows: white blood cell count, 9,140/mm3; eosinophil count, 1,380/mm3; hemoglobin, 10.3 g/dL; platelet count, 123,000/mm3; C-reactive protein level, 1.7 mg/dL; and erythrocyte sedimentation rate, 72 mm/sec. The levels of brain natriuretic peptide, creatine kinase-MB (CK-MB), and troponin-I were 944 pg/mL, 56.73 ng/mL, and 38.85 ng/mL, respectively.\nInitial electrocardiography showed ST segment elevation ≥ 1 mm in leads II, III, aVF, V5, and V6 (). Emergency coronary angiography was performed under the assumption of acute ST segment elevation myocardial infarction at the inferolateral wall, but coronary atherosclerosis was not evident. Echocardiography showed the "sparkling" appearance of the left ventricular (LV) myocardium, concentric LV hypertrophy, and mild hypokinesia on the anterior, anterolateral, and posterior walls from the mid-LV to the apex with 50% LV ejection fraction. Peripheral blood eosinophilia, skin rash, and a history of taking multiple medications suggested hypersensitivity myocarditis. The medications taken recently by the patient are shown in . Management of heart failure using aldosterone and furosemide was initiated promptly.\nOn the second day of hospital admission, however, dyspnea worsened, and newly developed bilateral pulmonary congestion was noted on chest radiography. The level of troponin I peaked at > 50.00 ng/mL. Therefore, CMR and EMB were carried out to confirm the diagnosis of hypersensitivity myocarditis. Prednisolone (60 mg, orally) treatment was initiated. Contrast-enhanced CMR (CE-CMR) showed high signal intensities in circular and nodular patterns mainly in the epicardium and septum of the left ventricle (). These patterns suggested infiltrative myocarditis, such as amyloidosis, sarcoidosis, or eosinophilic myocarditis. EMB obtained from the septum of the right ventricle revealed lymphocytic and eosinophilic infiltration in the interstitium and perivascular area, findings that were consistent with a diagnosis of hypersensitivity myocarditis ().\nThe dyspnea improved upon treatment with prednisolone and diuretics. Levels of CK-MB and troponin-I were normalized on days 6 and 9, respectively. The peripheral eosinophil count decreased from 1,380/mm3 to 620/mm3 on day 2 and was normalized (50/mm3) on day 4. The skin rash disappeared almost completely after use of 5 mg prednisolone, and the patient was discharged from the hospital on day 12. Echocardiography at the 6-month follow-up showed normalized regional wall motion abnormalities and improved LV systolic function from 50% to 70% of the ejection fraction. At the 6-month follow-up, CE-CMR showed that previously high signal intensities in circular patterns in the epicardium of the left ventricle had disappeared and the oval-shaped area of high signal intensity in the LV septum had decreased in size (). The patient remained asymptomatic without the need for prednisolone or diuretics.