ABC | Volume 110, Nº6, June 2018

Case Report Eosinophilic Myocarditis: Clinical Case and Literature Review Paulo Dinis, Rogério Teixeira, Luís Puga, Carolina Lourenço, Maria Carmo Cachulo, Lino Gonçalves Centro Hospitalar e Universitário de Coimbra, Hospital Geral, Coimbra - Portugal Mailing Address: Paulo Dinis Rua Vila de Manteigas, nº 28, 2º Dto. Posta Code 6300-617, Guarda – Portugal E-mail: paulogdinis@gmail.com Manuscript received May 09, 2017, revised manuscript June 08, 2017, accepted June 13, 2017 Keywords Eosinophilia; Myocarditis; Hypereosinophilic Syndrome / mortality; Hypereosinophilic Syndrome / drug therapy; Magnetic Resonance Imaging. DOI: 10.5935/abc.20180089 Introduction Eosinophilic myocarditis is a rare and potentially lethal disease characterized by eosinophil infiltration of the myocardium. 1 The association between eosinophilia and myocardial injury is well established and may present several etiologies, from hypersensitivity and autoimmune diseases to neoplasias and infections. 1,2 In some cases the etiology remains unknown, and it is denominated idiopathic hypereosinophilic syndrome. Clinical manifestations present a wide spectrum, ranging from mild symptomatology to severe symptoms such as retrosternal pain, rhythm disturbances, and sudden death. 2,3 The definitive diagnosis is made through endomyocardial biopsy. 1 Cardiac magnetic resonance imaging is a valid alternative, identifying the main structural changes caused by myocarditis. 4 Treatment includes neurohumoral therapy, management of cardiac complications, and in cases selected, systemic corticosteroid therapy. 5 Next, we present the case of a patient with symptomatology suggestive of myocardial infarction, but who in the course of the investigation had the diagnosis of eosinophilic myocarditis. Case report Patient 79 years old, female, who came to the Emergency Department with complaints of epigastralgia with two weeks of evolution and aggravation last night. She denied another accompanying symptomatology. As personal background, she presented unmedicated dyslipidemia and intrinsic asthma with onset in adulthood. She was medicated with bronchodilators and an association of a B2-agonist with inhaled corticosteroids at low doses. The objective examination showed tachycardia, confirmed on electrocardiogramwith sinus rhythmof 125beats perminute. Analytically had leukocytosis (13.2 x 10 3 /uL) and eosinophilia (2.8 x 10 3 /uL or 23%), C-reactive protein (0.8 mg/dL) and elevation of markers of myocardial necrosis (troponin I of 7.6 ng/mL). Transthoracic echocardiography revealed severe left ventricular systolic dysfunction with an ejection fraction estimated at 30-35%, ventricular septal hypocontractility and an increase in the concentric thickness of the ventricular walls. Valvular disease was not evident. It was placed as a first hypothesis that it was an acute coronary syndrome, so anti-ischemic therapy with double platelet antiaggregation, enoxaparin, was started and the patient was assigned to an invasive strategy. Coronary angiography did not reveal epicardial coronary disease. After this, the diagnosis of eosinophilic myocarditis in a patient with a known atopic component was likely. She was admitted to hospital for treatment and study. Neuro-humoral, beta-blocker and diuretic therapy were initiated, maintaining aspirin. On the third day of hospitalization, cardiac magnetic resonance was performed which identified subepicardial foci of edema and late enhancement in the left ventricular myocardium (Figure 1); she also showed a small pericardial effusion in the free wall of the right ventricle. The ejection fraction was quantified by 33%. On the same day, she underwent an endomyocardial biopsy and collection of right ventricular infarct fragments, which confirmed the diagnosis of eosinophilic myocarditis (Figure 2). Systemic corticosteroid therapy was startedwith intravenous prednisolone (1mg/kg/day) with progressive improvement of general condition. On the 12th day of hospitalization, the echocardiogram showed a slight improvement in left ventricular global systolic function (ejection fraction estimated at 35-40%). She was discharged to home with prednisolone in weaning, and with follow-up consultation of cardiology and autoimmune diseases. The autoimmune serological study was negative. After seven months of corticotherapy, the echocardiogram showed a significant improvement (ejection fraction estimated at 45‑50%), and a decrease in concentric hypertrophy. Discussion In the case described, the patient had a history of asthma, which may have been the starting point for hypereosinophilia. She also presented an epigastric discomfort, which may be an atypical presentation of an acute coronary syndrome. 6 Electrocardiographic findings, sinus tachycardia, are neither specific nor sensitive. 1 Analytically, leukocytosis and eosinophilia with troponin I elevation were evident and explained by infiltration of eosinophils into the myocardium. This infiltration allows the release of toxic granules, cationic proteins, pro-inflammatory cytokines, and oxygen free radicals that will cause mitochondrial dysfunction, myocyte injury and necrosis. 7 Complementary diagnostic tests are important in the evaluation of this pathology. The echocardiogram allows excluding other causes, to monitor dimension of cavities, thickness of the ventricular walls, presence of pericardial effusion and to evaluate left ventricular systolic and diastolic function. Cardiac magnetic resonance provides a combination of safety, anatomical definition, and tissue characterization of the myocardium. 4 It allowed the identification of edema 597