The patient was a 47-year-old white single female referred for medical treatment to the Instituto do Coração, born and coming from the state of São Paulo, with four children, unemployed, but reporting having worked in coffee farming in inner Minas Gerais state.

At the time of her first medical consultation (September 25, 2015), she reported dyspnea on minimal exertion, orthopnea and anasarca, which had started 2 months earlier. She denied angina pectoris, previous myocardial infarction and syncope. She knew she had systemic arterial hypertension and diabetes mellitus, and was being treated at a basic health unit. She used to smoke (20 packs/year), but quit the habit 2 months before. She denied consuming alcoholic beverages and illicit drugs, as well as a family history of cardiovascular disease.

She was on metformin (2550 mg/day), furosemide (80 mg/day), carvedilol (12.5 mg/day), and losartan (50 mg/day).

On her first medical consultation, her physical exam showed regular general condition and dyspnea in the horizontal position. Her blood pressure was 100/70 mmHg, and heart rate, 102 bpm. Her pulmonary auscultation revealed no respiratory sound on the base of the right lung and no rales. Her cardiac auscultation showed regular gallop rhythm, due to the presence of the third heart sound, and no murmur. Her abdomen was globose, tense, painless, with signs of huge ascites. Her extremities were cold and edematous (++/4+), with symmetrical pulses.

The electrocardiogram on the medical consultation showed sinus rhythm, heart rate of 97 bpm, left atrial overload and indirect signs of right atrial overload (Peñaloza-Tranchesi sign), low voltage of the QRS complexes in the frontal plane and no progression of the R wave in V₁ to V₄ (probable electrically inactive area in the anterior wall), and diffuse changes of ventricular repolarization (Figure 1).

Figure 1

Her chest X-ray showed bilateral veiling of costophrenic sinus, with pleural effusion up to half of the right hemithorax, normal aorta and global heart enlargement (++++/4+) (Figure 2).

Figure 2

Her laboratory tests were as follows: hemoglobin 14.8 g/dL; hematocrit 46%; leukocytes 9950/mm³; creatinine 0.87 mg/dL; sodium 141 mg/dL; potassium 4.3 mg/dL; and negative serology for Chagas disease.

On that medical consultation, spironolactone 25 mg was added, and, due to gastrointestinal intolerance, metformin was replaced by glicazide 30 mg/day.

Returning to medical consultation at the outpatient clinic (December 16th, 2015), she reported marked improvement of the dyspnea, then triggered only by large exertion. Her physical exam revealed no pathological jugular venous distention, blood pressure of 100/70 mmHg, heart rate of 100 bpm. Her pulmonary auscultation showed no respiratory sound on the base of the right lung. Her cardiac auscultation evidenced the presence of the third heart sound and no murmur. Her abdomen was globose, tense, painless, with liver palpable 3 cm from the right costal margin. Her lower limbs had mild edema (+/4+). She had not undergone the tests requested on her first medical consultation. Her prescription was then changed: carvedilol to metoprolol 50 mg/day.

After missing her subsequent medical consultation, the patient was hospitalized on July 25, 2016, due to heart failure decompensation. She had mixed shock, with decreased level of awareness and increased levels of myocardial injury markers. She required dobutamine for hemodynamic control. Empiric antibiotic therapy was initiated with ceftriaxone and clarithromycin, being the patient later submitted to orotracheal intubation for respiratory support.

Bedside chest X-ray on that day evidenced bilateral veiling of costophrenic sinus, with reduced transparency of the lower third of the right hemithorax (pleural effusion), increased pulmonary vascular bed with Kerley’s B lines, and marked heart enlargement (Figure 3).

Figure 3

Her laboratory tests revealed: hemoglobin 14.1 g/dL; hematocrit 44%; leukocytes 15100/mm³ (band neutrophils 6%, segmented neutrophils 84%, lymphocytes 5%, and monocytes 5%); platelets 195000/mm³; CK-MB 9.7 ng/mL; troponin I 0.654 ng/mL; ALT 42 U/L; AST 80 U/L; urea 87 mg/dL; creatinine 1.18 mg/dL; sodium 132 mEq/L; potassium 3.5 mEq/L; International Normalized Ratio (INR) 2.3; ratio between activated thromboplastin times 1.06; magnesium 1.6 mEq/L; total bilirubin 3.14 mg/dL; direct bilirubin 2.19 mg/dL; C-reactive protein 156.50 mg/L; arterial lactate 22 mg/dL. Arterial blood gas analysis (with oxygen therapy) showed pH of 7.52, pCO₂ of 29.6 mmHg, pO₂ of 176 mmHg, oxygen saturation of 99.9%, bicarbonate of 24.1 mmol/L, and base excess of 2.2 mmol/L.

Bedside transthoracic echocardiography showed: left ventricular diffuse hypokinesia and ejection fraction of 20%; marked right ventricular hypokinesia; marked mitral and tricuspid regurgitation and poor leaflet coaptation; pulmonary valve with signs of pulmonary hypertension; mild pericardial effusion and presence of large heterogeneous mass in the left ventricle, measuring 30x28 mm, compatible with intracavitary thrombus. Estimated systolic pulmonary artery pressure of 65 mmHg.

Coronary angiography revealed coronary arteries without proximal lesions, but the anterior interventricular branch showed a 95% distal lesion, and the diagonal branch showed distal occlusion. Neither the circumflex artery nor the right coronary artery showed any sign of obstruction (Figures 4A, 4B, 4C, 4D).

Figure 4

The hypothesis of infarction of embolic cause was raised. The patient was referred to the intensive care unit, with progressive increase of vasoactive drugs and later introduction of noradrenaline and widening of the antimicrobial spectrum to meropenem and vancomycin. The patient had refractory shock and died on July 27, 2016, with multiple organ dysfunction.