Acar J
Service de Cardiologie, Hôpital Tenon, Paris.
Ann Cardiol Angeiol (Paris). 1995 Dec;44(10):561-6.
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.
近几十年来,这类疾病在超声技术以及医学和外科治疗新方法方面取得的进展中受益匪浅。根据其机制,二尖瓣关闭不全的病因可分为4类:1. 瓣膜毁损性病变,通常继发于细菌性心内膜炎,但有时继发于创伤(经皮瓣膜成形术)。2. 腱索断裂,可为自发性或细菌性,发生于先前存在的瓣膜性心脏病背景下,通常为退行性病变。3. 乳头肌病变,通常对应于乳头肌或乳头肌头部的断裂,与心肌梗死相关。4. 生物或机械瓣膜假体功能障碍。急性二尖瓣关闭不全的后果取决于其病因以及先前是否存在二尖瓣疾病。三个因素决定临床表现和预后:反流容积、左心室功能和左心房顺应性。在单纯形式中,如腱索断裂后出现的情况,血流动力学特征包括左心室充盈压、左心房平均压和收缩压显著升高(大V波),以及心输出量降低。左心室舒张末期容积适度增加,而收缩末期容积正常或降低,射血分数增加。临床表现为急性左心室衰竭,伴有二尖瓣反流的收缩期杂音和肺动脉高压综合征。心电图上无左心室肥厚以及放射学检查无左侧扩张表明血流动力学紊乱为近期发生。急性二尖瓣关闭不全的诊断通过多普勒超声得以证实,其可确定机制,有时无需进行侵入性检查。临床病程取决于病因、反流容积、左心室功能以及所实施的治疗。一线治疗必须包括血管扩张剂。静脉输注硝普钠可减少左心室舒张末期容积和反流容积,并增加心输出量。它可使肺动脉和毛细血管高压迅速降低。当这种治疗不足时,主动脉内反搏可能有用。有时需要紧急手术,但通常在通过血管扩张剂改善血流动力学状态之后。根据病因,手术可能包括瓣膜置换或外科修复,即使在存在活动性细菌性心内膜炎的情况下也可取得良好效果。在其他情况下,通过药物治疗控制急性期后,二尖瓣关闭不全将变为慢性。