He S, Fontaine A A, Schwammenthal E, Yoganathan A P, Levine R A
Institute for Bioengineering and Bioscience, Chemical Engineering Department, Georgia Institute of Technology, Atlanta 30332-0100, USA.
Circulation. 1997 Sep 16;96(6):1826-34. doi: 10.1161/01.cir.96.6.1826.
Functional mitral regurgitation in patients with ischemic or dilated ventricles has been related to competing factors: altered tension on the leaflets due to displacement of their papillary muscle and annular attachments, which restricts leaflet closure, versus global ventricular dysfunction with reduced transmitral pressure to close the leaflets. In vivo, however, geometric changes accompany dysfunction, making it difficult to study these factors independently. Functional mitral regurgitation also paradoxically decreases in midsystole, despite peak transmitral driving pressure, suggesting a change in the force balance acting to create a regurgitant orifice, with rising transmitral pressure counteracting forces that restrict leaflet closure. In vivo, this mechanism cannot be tested independently of annular contraction that could also reduce midsystolic regurgitation.
An in vitro model was developed that allows independent variation of papillary muscle position, annular size, and transmitral pressure, with direct regurgitant flow rate measurement, to test the hypothesis that functional mitral regurgitation reflects an altered balance of forces acting on the leaflets. Hemodynamic and echocardiographic measurements of excised porcine valves were made under physiological pressures and flows. Apical and posterolateral papillary muscle displacement caused decreased leaflet mobility and apical leaflet tethering or tenting with regurgitation, as seen clinically. It reproduced the clinically observed midsystolic decrease in regurgitant flow and orifice area as transmitral pressure increased. Tethering delayed valve closure, increased the early systolic regurgitant volume before complete coaptation, and decreased the duration of coaptation. Annular dilatation increased regurgitation for any papillary muscle position, creating clinically important regurgitation; conversely, increased transmitral pressure decreased regurgitant orifice area for any geometric configuration.
The clinically observed tented-leaflet configuration and dynamic regurgitant orifice area variation can be reproduced in vitro by altering the three-dimensional relationship of the annular and papillary muscle attachments of the valve so as to increase leaflet tension. Increased transmitral pressure acting to close the leaflets decreases the regurgitant orifice area. These results are consistent with a mechanism in which an altered balance of tethering versus coapting forces acting on the leaflets creates the regurgitant orifice.
缺血性或扩张性心室患者的功能性二尖瓣反流与多种相互竞争的因素有关：乳头肌及其瓣环附着点移位导致瓣叶张力改变，从而限制瓣叶闭合，而整体心室功能障碍则使跨二尖瓣压力降低，进而影响瓣叶闭合。然而，在活体中，功能障碍伴随着几何形状的改变，使得难以独立研究这些因素。功能性二尖瓣反流在收缩中期也会反常地减少，尽管跨二尖瓣驱动压力达到峰值，这表明在形成反流口的力平衡发生了变化，跨二尖瓣压力升高抵消了限制瓣叶闭合的力。在活体中，这种机制无法独立于瓣环收缩进行测试，而瓣环收缩也可能减少收缩中期反流。
建立了一个体外模型，该模型允许乳头肌位置、瓣环大小和跨二尖瓣压力独立变化，并直接测量反流流速，以验证功能性二尖瓣反流反映作用于瓣叶的力平衡改变这一假设。在生理压力和血流条件下，对切除的猪瓣膜进行血流动力学和超声心动图测量。如临床所见，心尖和后外侧乳头肌移位导致瓣叶活动度降低，心尖瓣叶受牵拉或呈帐篷状并伴有反流。随着跨二尖瓣压力升高，该模型再现了临床上观察到的收缩中期反流和反流口面积的减少。瓣叶受牵拉延迟了瓣膜闭合，增加了完全贴合前的收缩早期反流容积，并缩短了贴合持续时间。对于任何乳头肌位置，瓣环扩张都会增加反流，产生具有临床意义的反流；相反，对于任何几何结构，跨二尖瓣压力升高都会减小反流口面积。
通过改变瓣膜瓣环与乳头肌附着的三维关系以增加瓣叶张力，可在体外再现临床观察到的瓣叶呈帐篷状的形态和动态反流口面积变化。作用于闭合瓣叶的跨二尖瓣压力升高会减小反流口面积。这些结果与一种机制相符，即作用于瓣叶的牵拉与贴合力平衡改变产生了反流口。
