ABC | Volume 111, Nº2, August 2018

Anatomopathological Session Favarato & Aiello A 59-year-old woman with rheumatic mitral valve disease with severe dyspnea, shock and pulmonary condensation. Arq Bras Cardiol. 2018; 111(2):215-222 Figure 6 – Right atrium open showing the mitral valve with fusion of commissures and multiple foci of calcification. blood cultures, skin complications (Osler spots, Janeway) or ophthalmic complications (Roth), peripheral abscesses (kidneys, spleen). 17 According to their frequency, the most common complications - heart failure > systemic embolization > stroke > intracardiac abscess. 18 However, endocarditis cannot be ruled out because in rheumatic valvular disease it can be difficult to diagnose the vegetation. Infection at any place can be responsible for the de‑compensation of heart failure in patients with severe valvopathy. In this case, pneumonia was suspected due to the presence of suggestive image at the right base (Figure 4) and leukocytosis, and antibiotic therapy was introduced; however, there was no change in the clinical situation compatible with the presence of pneumonia. As the last and most probable cause of the onset of the patient's final hemodynamic status there is pulmonary thromboembolism. The clinical situation is very non-specific and may be mixed up with acute coronary syndrome or pneumonia. Favoring it there is the image at the base of the right lung and dysfunction of the right ventricle. In the “International Cooperative Pulmonary Embolism Registry (ICOPER)” pulmonary thromboembolism is associated with the presence of heart failure (hazard ratio 2.4), right ventricle hypokinesia (2.0), systolic arterial hypotension < 90 mmHg (2.9), age > 70 years (1.6), cancer (2.3), chronic obstructive pulmonary disease (1.8). In the same sense, pulmonary thromboembolismwith right ventricle hypokinesia doubled the mortality within 3 months. 19 The exam deemed "gold standard" in the diagnosis of pulmonary thromboembolism is angiotomography, but failing that, or due to the patients’ hemodynamic instability, the finding of dilation and right ventricle dysfunction on the echocardiogram can be diagnostic alternatives. And as to hepatic alterations – elevation of transaminases and disorders in coagulation (elevation of TAP-INR- and relation of APTT times) – they are compatible with ischemic hepatitis with extensive liver necrosis due to low cardiac output in patients with high ventricular diastolic pressures. Its onset takes on average one week after the episode of low hepatic flow leading to centrilobular necrosis. 20 ( Dr. Desiderio Favarato) Diagnostic hypotheses: Rheumatic mitral valvopathy (double lesion), pulmonary thromboembolism, cardiogenic shock, multiple organ failure. (Dr. Desiderio Favarato) Necropsy The exam of the heart showed increased weight (470 g) as well as moderate to significant increase in volume of both atria. The mitral valve showed a lesion characterized by fusion of commissures and marked calcification of the cusps, compatible with rheumatic disease sequelae (Figures 6 and 7). The other valves suffered no significant morphological alterations. The left ventricle had its volume unchanged. There was hemothorax on the left (about 1000 ml). The lungs showed macroscopically thromboembolic vessels in hilar vessels, in addition to purplish-red areas with a firmer consistency in the lower lobes (Figure 8). Histological exam showed recent pulmonary infarctions, organized thrombi in pulmonary arteries, and signs of chronic passive congestion (Figure 9). The wall of the pulmonary veins had thickened, with intimal fibrosis (Figure 10) and hypertrophy of the tunica media of the arteries and arterioles (Figure 11). In the other organs there were signs compatible with shock, such as, for instance, recent centrilobular hepatic necrosis, acute renal tubular necrosis, and small sub-endocardial infarcts on ventricular walls. Anatomopathological diagnoses : rheumatic heart disease with mitral valve sequelae (calcified mitral stenosis); chronic passive pulmonary congestion with signs of passive pulmonary hypertension; hemothorax on the left without a defined causal factor. 219