Introduction: Eosinophilic myocarditis is a cardiac manifestation of hypereosinophilic syndrome. It is defined by eosinophilic infiltration of the myocardium causing progressive cardiac fibrosis with impaired relaxation associated with a high mortality rate.
 

Case presentation: We present the case of a 25-year-old female patient who was transferred to our hospital with a 3-day history of dyspnoea and left arm pain. She had a a history of chronic sinusitis and bronchial asthma. Initial echocardiography revealed a severely impaired left ventricular function and circular pericardial effusion. Chest X-ray showed pulmonary congestion. 

Upon transfer to our clinic, ECG showed sinus tachycardia with ubiquitously flattened T-wave with T-wave inversion in leads V3-V4. Laboratory workup revealed elevated troponin of 934 ng/dl (normal range: < 14 ng/dl) and C-reactive protein of 2,6 mg/dl (normal range: < 0,5 mg/dl). NT-proBNP peaked at 8135 pg/ml (normal range: <115 pg/ml). Leucocyte counts were normal (11,99*103/µl; normal range: 4,49-12,68 *103/µl). Venous oxygen was decreased to 29,4 mmHg. 

Transthoracic echocardiogram revealed a left ventricular ejection fraction of 25% with secondary mitral valve insufficiency and a circumferential pericardial effusion. Cardiac magnetic resonance (CMR) revealed a normal-sized left ventricle with diffuse inferoseptal and midventricular to apical inferior akinesia and hypokinesia of the residual wall segments. There were extensive inducible subendocardial perfusion defects e.g., throughout the septum, basal to midventricular septal and basal to midventricular anterolateral. Additionally, diffuse subendocardial to intramural enhancement basal to midventricular septal, inferior and lateral was apparent. On day 9, differential counts was pertinent for a peak absolute eosinophil count of 5,09*103/µl (normal range: 0,01-0,4*103/µl). Cardiac catheterization was performed, revealing reduced calibre of the left anterior descending artery with irregular wall contours consistent with vasculitis. Constellation of these findings were compatible with non-ischemic myocarditis, and in the setting of elevated eosinophils suggestive of eosinophilic myocarditis. Biopsies showed inflammation with an eosinophil rich infiltrate and small-caliber vessels confirming the diagnosis of eosinophilic myocarditis. Taking into account the history of bronchial asthma and chronic sinusitis with persistent bloody secretion, the initial diagnosis of eosinophilic granulomatosis with polyangiitis was confirmed. 

A heart failure therapy consisting of bisoprolol, enalapril, dapagliflozine, torasemide and ivabradine was initiated. The patient was treated with steroid therapy (initially 1 mg/kg body weight) and azathioprine with improved eosinophil count to 0,22*103/µl (normal range: 0,01-0,4*103/µl) and discharged home on prednisone 30 mg with a slow taper. 

Conclusion: Eosinophilic myocarditis should be added to the differential diagnoses in the setting of suspected myocarditis with signs and symptoms of hypersensitivity (asthma bronchiale, eosinophilia) especially in young patients with acute decompensated heart failure. Although CMR can be indicative of inflammatory myocarditis, endomyocardial biopsy remains the gold standard for diagnosis.