ABC | Volume 113, Nº4, October 2019

Anatomopathological Correlation Case 5/2019 – 55-Year-Old Diabetic Man with Heart Failure After Non-ST Segment Elevation Myocardial Infarction Ana Vitória Vitoreti Martins, José Roberto de Oliveira da Silva, Paulo Sampaio Gutierrez Instituto do Coração (InCor) 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 , anpvera@incor.usp.br Keywords Diabetes Mellitus/complications; ST- Elevation Myocardial Infarction; Heart Failure; Cardiogenic Schock. Section editor: Alfredo José Mansur (ajmasur@incor usp.br) Associated editors: Desidério Favarato (dclfavarato@incor.usp.br ) Vera Demarchi Aiello (anpvera@incor.usp.br ) DOI: 10.5935/abc.20190225 A 55-year-old male patient which is insulin-dependent diabetes mellitus (DM) with visual complications and chronic kidney disease (CKD) was admitted a month ago (February 2017) after an episode of nocturnal dyspnea. A diagnosis of non-ST-segment elevation myocardial infarction (AMI) was identified. Admission examinations revealed elevatedmyocardial injury markers - CKMB of 70 ng/mL and 2 ng/mL troponin. The electrocardiogram (ECG) showed a ST-segment depression from V2 to V6 . The coronary angiography revealed a 30% lesion in the right and left coronary arteries did not present lesions (Figure 1). The echo revealed diffuse left ventricular hypokinesia and 36% ejection fraction. Creatinine was 1.8 mg/dL. After discharge, the patient developed orthopnea and lower limb edema and sought emergency care and was transferred to InCor two weeks after hospital discharge with a diagnosis of decompensated heart failure (March 22, 2017). During a physical examination, the patient had dyspnea, was hydrated, did not have a fever, had good peripheral perfusion, blood pressure was 100x70 mmHg, a 90 bpm heart rate and 92% oxygen saturation. There was jugular turgescence, bilateral and symmetrical vesicular murmur present, presence of crackles in both lung bases, normophonetic rhythmic sounds in two stages, without murmurs. There was no hepatomegaly or hepatojugular reflux. The patient's abdomen was flaccid, painless and had airborne noises present. The lower limbs presented a ++ / 4+ edema, the calves were free and there were symmetrical pedis pulses. The patient was using 100mg acetylsalicylic acid, 20 mg enalapril and NPH human insulin. The ECG (March 22, 2017) revealed sinus rhythm, low voltage of the QRS complex in the frontal plane and ST segment depression, 1 mm, horizontal fromV 2 to V5, and a reduction of the left ventricular potentials (Figure 2). Chest radiography (March 23, 2017) revealed massive bilateral pleural effusion and cardiomegaly (Figure 3), persistently identified on the radiograph on March 31, 2017. Laboratory tests revealed anemia and creatinine increases (Table 1). Echocardiography (March 23, 2017) revealed a 30 mm aortic diameter, 39mm left atrium, right ventricle in the basal portion, which was 44 mm and in the middle portion, which was 29 mm. The septum and posterior wall thickness were 7 mm, left ventricular diameters of 56 mm in diastole and 51 mm in systole, the area method ejection fraction (Simpson) was 22%. There was mild to moderate mitral regurgitation and pulmonary artery systolic pressure was 36 mmHg. The serologies for Chagas disease and cytomegalovirus were negative. With this history and the exam findings, the hypothesis of type 2 infarction or myocarditis was raised. Magnetic nuclear resonance showed marked biventricular systolic dysfunction - 11% left ventricular ejection fraction (LVEF) and slight dilatation (indexed final diastolic volume of 106 mL/m 2 and final systolic volume of 100 mL/m 2 ), with increased right ventricular dilation (final diastolic volume indexed was 137 mL/m 2 and final systolic volume of 122 mL/m², 6% ejection fraction). The right atrium had a normal volume while the left atrium was greatly enlarged (indexed volume 65 mL/m 2 ). The cardiac diameters were: aorta 2.5 mm, right ventricle in the longest axis 71 mm and shortest axis 40 mm; left ventricle diastole 57 mm, systole 56 mm; septum thickness 6 mm and 5mm lateral wall. There was a transmural, circumferential multifocal late enhancement, sparing the apical segments beyond the apex and compromising the papillary muscles, which all had subendocardium involvement (Figure 4). There was no pericardial effusion and there was massive bilateral pleural effusion. During hospitalization, thepatient hada fever and leukocytosis (Table 1), and was diagnosed with bronchopneumonia, treated with vancomycin and tazobactamwith a reduction in C-reactive protein and leukocytosis. Renal function worsened (Table 1) with oliguria and a shilley catheter was used in the femoral vein, but due to hemodynamic instability, hemodialysis was not possible. Since admission, the patient had severe dyspnea requiring long-term non-invasive ventilation and right hemithorax drainage due to respiratory discomfort with a serohematic discharge of about 3 liters during two days. The March 31 radiograph revealed massive bilateral pleural effusion prior to drainage. In the middle of the night on March 31st, 2017, the patient had cardiopulmonary arrest with pulseless electrical activity and was promptly resuscitated for 15 minutes with a return to spontaneous circulation. The patient received orotracheal intubation and required maximum doses of noradrenaline and dobutamine to maintain a mean blood 775