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 5 – Chest X-ray. More penetrated than the previous one. Presence of endotracheal cannula. 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 (right ventricle enlargement). its predominance. Additionally, the first echocardiogram (2010) was more compatible with the predominance of mitral stenosis with major hemodynamic repercussion, once the dimensions of the left ventricle were normal and there was an increase in the left atrium and in the pulmonary systolic pressure, as well as dilation of the right ventricle. Echocardiographic criteria for severe stenosis were present, although the valve area was not calculated, which would be less than 1.0 cm²/m² or < 1.5 cm², there was fusion of the cusps, in addition to the pressure gradient between the left atrium and the upper ventricle at 10 mmHg, and pulmonary arterial hypertension above 50 mmHg. 13,14 The indication for percutaneous and/or surgical treatment is basedon thepresence of symptoms or atrial fibrillation, or systemic embolism, in patients using anticoagulant andmoderate or severe mitral stenosis, and in asymptomatic patients with pulmonary systolic pressure ≥ 80 mmHg. Percutaneous valvuloplasty still requires the presence of favorable morphology - mobile thin cusps, free from calcification. In the second echocardiogram, one year after the accompaniment had started, the predominance of mitral insufficiency was not discarded because there was malfunction of the left ventricle. The right time of an indication for surgery in patients with severe mitral incompetence has always been controversial due to the symptoms’ late onset. Surgical treatment is indicated for the onset of symptoms, of dilatation (systolic diameter > 4.5 cm), or left ventricular dysfunction (ejection fraction < 60%). The guidelines define severe mitral regurgitation based on several parameters: valve morphology - ring dilation ≥ 3.5 cm; characteristics of the regurgitation jet - a rotating jet (multicolor) that reaches the posterior atrial wall, or lateral jet that fills at least 40% of the atrial surface; the vena contracta - width of the jet next to the valve ≥ 0.7 cm; effective regurgitation orifice ≥ 0.4 cm²; regurgitation volume ≥ 60 mL; regurgitation fraction ≥ 50%, ventricular filling pattern – ratio of the mitral valve’s velocity-time integral and the aortic valve above 1.3; wave velocity E ≥ 150 cm/s; pulmonary artery systolic pressure≥50mmHg; indexed atrial volume 60mL/m²; and left ventricle systolic diameter > 4.5 cm. 3,15 Thus, whichever was the predominance of valvular dysfunction, the patient already had indication for surgical treatment of the mitral valve because there was already severe hemodynamic repercussion and, as it usually happens in valvopathy with a rheumatic origin, there was a double lesion. Other ways in which the disease may appear are atrial arrhythmias, the most common being atrial fibrillation, embolic events, acute heart failure, or infective endocarditis. In this case there was de-compensation of heart failure due to nodal reentrant tachycardia, arrhythmia is usually not associated with mitral valvopathy. In mitral stenosis there is usually atrial fibrillation due to dilation and atrial fibrosis, in addition to an inflammatory process in the acute phase (Aschoff nodules). Atrial phenomena in mitral insufficiency are similar to those of stenosis as interstitial fribrosis and inflammation; however, there is no hypertrophy, myolysis and necrosis of atrial myocytes. 16 As to the patient's final condition, there are three possible causes: infectious endocarditis, pulmonary infection or pulmonary thromboembolism. For the diagnosis of endocarditis there would be only fever and de-compensation of heart failure, lacking worsened murmur and vegetation in the valves. In other words, the involvement of the endocardium in systemic infection has not been proven. Blood culture is not a diagnostic criterion. The clinical criteria of strong suspicion are: new valve injury (insufficiency), embolic events of unknown origin, sepsis of unknown origin, hematuria and fever in a patient who has a prosthesis, previous valvopathy and dental or endoscopic manipulation of the colons, new conduction disorders (atrioventricular blockage due to perivalvular abscess), first episode of cardiac de-compensation, positive 218