ABC | Volume 112, Nº6, June 2019

Anatomopathological Correlation Case 3/2019 – Young Male with Intense Dyspnea, Pulmonary Infiltrate, Normal Cardiac Area and Obliteration of the Apical Portion of the Left Ventricle Victor Sarli Iss a and Luiz Alberto Benvenut i 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 Youn g Adu l t ; He a r t Fa i l u r e / ph y s i opa t o l o g y ; Hypothyroidism; Cardiomyopathy, Hypertrophic Tobacco and Disorder; Hypercholesterolemia; Diagnostic Imaging; Inflammation; Pneumonia. Section Editor: Alfredo José Mansur (ajmansur@incor.usp.br) Associated Editors: Desidério Favarato (dclfavarato@incor.usp.br) Vera Demarchi Aiello (anpvera@incor.usp.br) DOI: 10.5935/abc.20190105 A 25-year-old male patient was hospitalized for severe dyspnea, even at rest, and with productive cough. The patient had been seen a week before with a complaint of back pain that irradiated to the precordial region triggered by exertion, such as climbing stairs and walking a block, which had started two weeks before. The patient was a smoker (8-pack-years) and reported having hypothyroidism after treatment with radioactive iodine. Previous examinations were carried out for him to be cleared for exercise practice. The electrocardiogram (ECG) (November 24, 2010) showed left atrial overload and a left ventricular strain pattern. There was an accentuation of ST-depression in the stress test. At admission (October 14, 2011), heart rate was 100 bpm, blood pressure was 100/70 mmHg, and the physical examination was normal. The ECG (October 14, 2011) revealed sinus tachycardia (101 bpm), PR interval of 144 ms, QRS duration 103 ms, QTc of 451 ms, left chamber overload and secondary alterations in ventricular repolarization (Figure 1). The chest X-ray (October 14, 2011) was normal. (Figure 2) The laboratory tests (October 14, 2011) showed: red blood cells, 4,600,000/mm³; hemoglobin; 14 g/dL, hematocrit; 39%, MCV 85 fL, RDW-CV 12.9%; leukocytes, 11,110/mm³ (72% neutrophils, 7% eosinophils, 17% lymphocytes and 4% monocytes); platelets, 185,000 / mm³; sodium, 138 mEq/L; potassium, 4.5 mEq/L; PT, (INR) 1; APTT (rel), 0.93; D-dimer, 485 ng/mL; CK-MB, 0.94 ng/mL; troponin I, 0.535 ng/mL; urea, 35 mg/dL; and creatinine, 0.94 mg/dL. On the following day, CK-MB was 0.71 ng/mL; troponin I, 0.511 ng/mL; total cholesterol, 219 mg/dL, HDL-c, 25 mg/dL; LDL-c, 171 mg/dL; triglycerides, 116 mg/dL; glucose, 92 mg/dL. The echocardiogram (October 17, 2011) disclosed diameters of the aorta 27 mm, of the left atrium 43 mm, septum thickness of 11 mm, posterior wall of 10 mm, normal right ventricular diameter, and left ventricular diameters (diastole/systole) of 54/34 mm, ejection fraction of 65%; marked hypertrophy in the mid-apical region, pseudonormal filling pattern. There was no left ventricular outflow tract obstruction or valve alterations. The coronary angiotomography (October 18, 2011) did not disclose coronary calcifications or lesions. However, left atrial dilation and obliteration of the apical portion of the left ventricle were observed. Diagnoses of hypertrophic cardiomyopathy and hypercholesterolemia were made. He was prescribed 50 mg of atenolol, 100 μg of levothyroxine and 20 mg of omeprazole and was referred for outpatient follow-up (October 18, 2011). Four days after hospital discharge (October 22, 2011), the patient sought emergency medical care for severe dyspnea, even at rest and in decubitus, in addition to productive cough. The physical examination (October 22, 2011) disclosed a heart rate of 101 bpm, blood pressure of 112/70 mmHg, pulmonary auscultation showing diffuse crackling rales, cardiac auscultation and abdomen without alterations, and mild edema of legs and feet, without any suggestive signs of deep venous thrombosis. The ECG (October 22, 2011) was similar to the previous one, with sinus tachycardia, left chamber overload and ST-segment depression with a superior concavity and accentuation of T-wave negativity in leads V 3 to V 6 . (Figure 3). A bilateral diffuse alveolar infiltrate was observed on the chest X-ray (October 23, 2011). (Figure 4) The laboratory tests (October 22, 2011) showed: erythrocytes, 3700000/mm³; hemoglobin, 11.6 g/dL; hematocrit, 31%; MCV, 84 fL; RDW-CV 13.2%; leukocytes, 4100/mm³ (18% band cells; 67% segmented; 2% eosinophils; 11% lymphocytes; and 2%monocytes), platelets, 207000/mm³; creatinine, 1.06 mg/dL; urea, 35 mg/dL; BNP, 1296 pg/mL; potassium, 4 mEq/L; sodium, 132 mEq / L; arterial lactate, 7 mg/dL; urine type I: density 1.009, ph = 5.5, proteins 0.5 g/L, leukocytes 2000/mL, erythrocytes 79000/mL and presence of severe hemoglobinuria. The pulmonary angiotomography (October 24, 2012) showed no alterations in vascular and mediastinal structures or signs of pulmonary thromboembolism; there was a confluent, diffuse, centrolobular micronodular infiltrate, in some areas with a tree-in-bud pattern, with a predominantly bronchocentric distribution, associated with areas of ground‑glass opacity attenuation, more evident in the apices and posterior basal segments. These findings were considered compatible with an inflammatory or infectious process. There was bilateral pleural effusion, moderate to the right and small to left. (Figure 5) The high-resolution chest tomography (November 1, 2011) disclosed lymphadenomegaly of para-aortic (2.7 x 1.3 cm) 793