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  • Title: [Acute mitral valve insufficiency].
    Author: Acar J.
    Journal: Ann Cardiol Angeiol (Paris); 1995 Dec; 44(10):561-6. PubMed ID: 8787332.
    Abstract:
    This type of disease has benefited considerably, over recent decades, from progress in ultrasound technique and new methods of medical and surgical treatment. The aetiologies of mitral incompetence can be classified into 4 categories according to their mechanism: 1. Mutilating valve lesions, usually secondary to bacterial endocarditis, but sometimes secondary to trauma (percutaneous valvuloplasty). 2. Rupture of chordae tendineae, either spontaneous or bacterial, in a context of pre-existing valvular heart disease, usually degenerative. 3. Papillary muscle lesions, usually corresponding to rupture of a papillary muscle or the head of a papillary muscle, associated with myocardial infarction. 4. Biological or mechanical valve prosthesis dysfunction. The consequences of acute mitral incompetence depend on its aetiology and the presence or absence of previous mitral valve disease. Three factors determine the clinical presentation and prognosis: the volume of regurgitation, left ventricular function and left atrial compliance. In pure forms, such as those occurring after rupture of chordae tendineae, the haemodynamic profile consists of a marked elevation of left ventricular filling pressures, left atrial mean and systolic pressures (large V wave), and a reduction of the cardiac output. The left ventricular end-diastolic volume is moderately increased, while the end-systolic volume is normal or decreased and the ejection fraction is increased. The clinical picture is that of acute left ventricular failure with a systolic murmur of mitral regurgitation and a pulmonary hypertension syndrome. The absence of left ventricular hypertrophy on the electrocardiogram and the absence of left-sided dilatation on radiological examination indicate the recent nature of the haemodynamic disturbances. The diagnosis of acute IM is confirmed by Doppler ultrasound, which defines the mechanism and sometimes eliminates the need for an invasive investigation. The clinical course depends on the aetiology, the volume of regurgitation, left ventricular function and the treatment implemented. First-line treatment must include vasodilators. Sodium nitroprussate infusion decreases the left ventricular end-diastolic volume and the volume of regurgitation and increases the cardiac output. It allows a rapid reduction of pulmonary artery and capillary hypertension. When this treatment is not sufficient, intra-aortic counterpulsation may be useful. Emergency surgery is sometimes necessary, but usually after improvement of the haemodynamic state by vasodilators. Depending on the aetiology, surgery may consist of valve replacement or surgical repair, which can give excellent results even in the presence of active bacterial endocarditis. In other cases, following control of the acute phase by medical treatment, mitral incompetence will become chronic.
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