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 4 – Chest X-ray. Pulmonary congestion, opacification at the right base, and cardiomegaly with double contour (enlargement of the left atrium), and abnormal enlargement or bulging at mid-arch of the aorta (enlargement of the right ventricle). 17840 mm/mm³ (93% neutrophils, 5% lymphocytes, 2% monocytes), platelets 148000/mm³, urea 104 mg/dL, creatinine 2.88 mg/dl (FG = 18 mL/min/1.73 m²), sodium 145 mEq/L, potassium 4.5 mEq/L, AST 1863 U/L, ALT 426 U/L, gammaGT 87 U/L, alkaline phosphatase 152 U/L, magnesium 1.9 mE L, total bilirubin 4.05 mg/dL, direct bilirubin 3.5 mg/dL, arterial lactate 173 mg/dL; arterial gasometry: pH 7, 16, pCO 2 32.7 mm Hg, pO 2 160 mm Hg, O 2 Saturation 99%, bicarbonate 11mEq/L, base excess (-) 16.2 mEq/L; TP (INR) 3.2; TTPA rel times 3.13. Tho r a x r a d i o g r a ph y ( 21 / S e p / 2011 ) s howe d hypotransparency in the right pulmonary base and an increase in the cardiac area (presence of double contour and abnormal enlargement or bulging at mid-arch of the aorta) (Figure 5). During hospitalization the patient developed hemodynamic instability, consumption coagulopathy, and presented cardiac arrest in pulseless electrical activity, with no response to resuscitation maneuvers, and she passed away (16h and 55min; 21/Sep/2011). Clinical aspects This is about a 59-year-old woman with double mitral lesions with pulmonary hypertension who, while awaiting surgery, had arterial hypotension, respiratory failure with hypotransparency in the right lung field. It evolved without improvement with vasoactive drugs, orotracheal intubation and antibiotic therapy, and she passed away in electrical activity without pulse. The etiology of this patient's valve disease should be attributed to rheumatic fever, although there is no description of an acute outbreak of that disease in the patient’s medical history. That is not unusual in a rheumatic disease scenario once using echocardiogram raises its frequency from 5 to 10 times when compared to a clinical diagnosis. 1-4 That difference in frequency between clinical diagnosis and echocardiography may be due to the autoimmune response triggered by molecular mimicry, 5 which may go ahead with predominance of humoral response mediated by Th2 lymphocytes, causing more symptoms and leading more easily to the use of secondary prophylaxis. Others show a predominance of cellular response, mediated by Th1 lymphocytes with milder forms of clinical manifestations, but those where cardiac involvement predominates. Thus, patients who would benefit the most from the use of that prophylaxis fail to do it and are subject to relapses that aggravate valve lesions. 6 Those subtypes of CD4 + (Th1 and Th2) lymphocytes produce different cytokines, those of Th1-type produce interleukin-2 and interferon-gamma cytokines, and those of Th2 subtype secrete Interleukins 4, 5 and 10. 7-9 The guidelines of the World Health Organization and the US National Institute of Health (NIH) have defined the diagnosis of rheumatic heart disease by the presence of cardiac murmur consistent with mitral or aortic insufficiency, and echocardiographic evidence of rheumatic valve damage, or history of acute rheumatic fever without echocardiogram done in the acute outbreak. 10 The predominant clinical onset of the heart rheumatic disease is dyspnea, which occurs between the third and fourth decade in life, mostly in women. 11 In this case, clinical manifestations happened later, but like in the rheumatic disease, they presented alterations in the mitral valve, the valve most frequently affected in the disease. Mitral regurgitation usually occurs earlier than stenosis, attributed to persistent or recurrent valvulitis. 12 Despite its earlier onset, mitral regurgitation generally has a longer asymptomatic period due to increased atrial compliance due to its progressive increase, maintenance of cardiac output by dilatation of the left ventricle, and decreased regurgitation fraction in exertions to decrease peripheral resistance in the exertion. Still on this case, the initial clinical scenario of de‑compensation due to the presence of tachycardia, once a shorter diastole is more detrimental to mitral stenosis, suggests 217