ABC | Volume 110, Nº6, June 2018

Anatomopathological Correlation Case 3/2018 – A 60-year-old Female with Chagasic Heart Disease, Admitted Due to Heart Failure Decompensation, Cachexia and Pulmonary Infection Gustavo Alonso Arduine and Vera Demarchi Aiello Instituto do Coração (InCor) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HC-FMUSP), São Paulo, SP - Brazil Mailing Address: Vera Demarchi Aiello • Avenida Dr. Enéas de Carvalho Aguiar, 44, subsolo, bloco I, Cerqueira César. Postal Code 05403-000, São Paulo, SP – Brazil E-mail: demarchi@cardiol.br , vera.aiello@incor.usp.br Keywords Chagas Disease; Chagas Cardiomyopathy; Heart Failure; Cachexia; Pneumonia. Section editor: Alfredo José Mansur (ajmansur@incor.usp.br ) Associate editors: Desidério Favarato (dclfavarato@incor.usp.br ) Vera Demarchi Aiello (vera.aiello@incor.usp.br ) DOI: 10.5935/abc.20180100 The patient is a 60-year-old female with Chagas heart disease and cachexia, admitted due to heart failure decompensation attributed to bronchopneumonia. She eventually had a cardiac arrest with pulseless electrical activity after lung biopsy. The patient was being followed up at InCor since the age of 48 years, diagnosedwithChagas disease. She initially complained of palpitations, which subsided after amiodaronewas prescribed. In addition, she had systemic arterial hypertension. Her laboratory tests revealed: potassium, 5.2mEq/L; sodium, 144 mEq/L; creatinine, 0.8 mg/L; hemoglobin, 16.2 g/dL; hematocrit, 48%; glycemia, 87 mg/dL; cholesterol, 200 mg/dL; triglycerides, 53 mg/dL; TSH, 1.16 microIU/mL; free T4, 1.1 ng/dL; ALT, 8 IU/L; AST, 10 IU/L. At the time, the ECG revealed diffuse ventricular repolarization changes. The echocardiogram (August 2004) showed the following: aorta, 28 mm; left atrium, 52 mm; septal thickness, 11 mm; posterior wall, 7 mm; left ventricle (diast/syst), 71/62 mm; left ventricular ejection fraction (LVEF), 26%, with posterior (basal), inferior (basal) and lateral (basal) akinesia, and small apical aneurysm; right ventricle, 28 mm (dilated and hypokinetic); severe mitral regurgitation; and right ventricular systolic pressure, 65 mm Hg. The chest X-ray (2012) showed cardiomegaly (Figure 1). The Holter ECG at that time showed frequent ventricular extrasystoles and nonsustained ventricular tachycardia. The patient remained asymptomatic until 2013 (57 years of age) using hydrochlorothiazide (25 mg), spironolactone (25 mg), carvedilol (12.5 mg), enalapril (20 mg) and amiodarone (100 mg) daily. In April 2013, she had a resuscitated cardiac arrest, preceded by malaise and sustained ventricular tachycardia, receiving an implantable cardioverter defibrillator (ICD) with cardiac pacemaker programing for bradycardia episodes (ICD-T – ICD with antibradycardia and antitachycardia pacing and shock), being prescribed 600 mg of amiodarone daily. Five days before that episode, she had upper digestive bleeding with hematemesis, when endoscopy revealed gastric ulcer with no active bleeding, and clean base (Forrest III), with a lower risk for rebleeding. The patient experienced appropriate shock in May 2014. She was receiving an amiodarone dose lower than prescribed, thus the dose was increased, but the patient did not tolerate it because of dyspepsia. A cardiac electrophysiology study was indicated, aimed at the possible ablation of the sustained ventricular tachycardia pathways. The chest X-ray revealed pulmonary congestion and more severe cardiomegaly (Figure 2). The echocardiogram (August 4, 2014) revealed: aorta, 27mm; left atrium, 43 mm; ventricular septal thickness, 9 mm, posterior wall, 8 mm; left ventricular diameters, 68/57 mm; LVEF, 30%. The left ventricle showed eccentric hypertrophy and reduced systolic function due to an inferolateral wall aneurysm (mid and basal segments) and an apical aneurysm. The right ventricle was normal. There was moderate mitral valve regurgitation. The pulmonary artery pressure was 25 mm Hg. Her coronary tomography angiography (July 28, 2014) evidenced no coronary lesion. The cardiac electrophysiology study (July 31, 2014) identified poorly-tolerated sustained ventricular tachycardia triggered by extra-stimuli, which required electric cardioversion. The electroanatomic mapping revealed a scar associated with low and slow late potentials in the lateral (mid and basal segments), antero-lateral (mid and basal segments) and inferolateral (mid and basal segments) walls. Because of the proximity to the circumflex sub-branches, the radiofrequency pulses were not delivered through the epicardium, but through the endocardium. After the procedure, the new stimuli no longer triggered ventricular tachycardia similar to that initially observed. However, several poorly tolerated tachycardias of different morphologies were triggered, requiring cardioversion. On outpatient follow-up (November 2014), the patient complained of dyspnea on exertion and dizziness when changing from supine to orthostatic position. Her physical examination (November 11, 2014) revealed: weight, 70 kg; height, 1.7 m; arterial blood pressure, 102/80mmHg; heart rate, 68 bpm. The pulmonary auscultation was normal. On cardiac auscultation, her heart rhythm was regular with no abnormal heart sound, and a systolic heart murmur was heard over themitral area (++/4+). The abdominal examination was normal. There was no edema, and her pulses were palpable and symmetrical. Because of her complaints 588