Prevalence and mechanisms of mitral regurgitation in the absence of intrinsic abnormalities of the mitral leaflets.
Prevalence and mechanisms of mitral regurgitation in the absence of intrinsic abnormalities of the mitral leaflets.
复制标题
在没有二尖瓣小叶内在异常的情况下，二尖瓣反流的患病率和机制。
DOI：
10.1016/0002-8703(89)90231-7
复制
发表时间：
1989
影响因子：
4.8
通讯作者：
Esquival,L
中科院分区：
文献类型：
--
作者：
Kaul,S;Pearlman,JD;Touchstone,DA;Esquival,L
分析了219例接受超声心动图检查的连续患者，以确定在二尖瓣瓣叶无内在异常的情况下二尖瓣返流（MR）的发生率。通过脉冲多普勒技术评估MR。无二尖瓣叶异常的二尖瓣返流发生率高于有二尖瓣叶异常的二尖瓣返流发生率（59%vs41%，p < 0.01）。二尖瓣返流最常见的原因是二尖瓣环钙化（MAC）和二尖瓣瓣叶关闭不全（IMLC）。MAC患者的钙化存款程度和IMLC收缩期患者二尖瓣瓣叶接合点至二尖瓣环平面的距离与多普勒技术显示的MR严重程度相关（rho分别为0.91和0.71）。为了确定这两种情况下二尖瓣返流的机制，29例MAC和28例IMLC患者被转诊至超声心动图实验室，并对10例年龄匹配的对照受试者进行前瞻性分析。与对照组相比，MAC患者在收缩期二尖瓣环的括约肌作用减少了50%。所有IMLC患者的左心室收缩功能均较差，大多数患者左心室、二尖瓣环和左心房扩张，只有8例患者局部室壁运动异常。判别函数分析显示，左室收缩功能差是IMLC患者与正常人的主要区别因素（F = 81.6，p < 0.0001）。我们的结论是：（1）成人二尖瓣返流最常见于二尖瓣叶无内在异常，主要由MAC和IMLC引起;（2）MAC患者的二尖瓣返流是由于二尖瓣环收缩期括约肌作用减弱所致;（3）IMLC是由于左心室收缩功能不良所致，与病因无关。
Two hundred nineteen consecutive patients referred for echocardiography were analyzed to determine the occurrence of mitral regurgitation (MR) in the absence of intrinsic abnormalities of the mitral leaflets. MR was assessed by means of the pulsed-Doppler technique. There was a higher incidence of MR associated with absence of mitral leaflet abnormalities compared to the presence of these abnormalities (59% vs 41%,p< 0.01). The most common causes of MR were mitral annular calcification (MAC) and incomplete mitral leaflet closure (IMLC). The extent of calcific deposit in patients with MAC and the distance from the mitral leaflet coaptation point to the mitral annular plane in systole patients with IMLC correlated well with the severity of MR by Doppler technique (rho = 0.91 and 0.71, respectively). To determine the mechanisms of MR in these two conditions, 29 consecutive patients with MAC and 28 with IMLC were referred to the echocardiography laboratory, and 10 age-matched control subjects were prospectively analyzed. Patients with MAC had a 50% reduction in the sphincteric action of the mitral anulus in systole compared to control subjects. All patients with IMLC had poor left ventricular systolic function; most had left ventricular, mitral annular, and left atrial dilation, and only eight had regional wall motion abnormalities. When discriminant function analysis was used, poor left ventricular systolic function was the principal variable that separated patients with IMLC from normal subjects (F = 81.6,p< 0.0001). We conclude that: (1) MR in adults occurs most commonly in the absence of intrinsic abnormalities of the mitral leaflets, primarily those resulting from MAC and IMLC; (2) MR in patients with MAC results from a reduced sphincteric action of the mitral anulus in systole; and (3) IMLC results from poor left ventricular systolic function, irrespective of the cause.