Integrated mechanism for functional mitral regurgitation - Leaflet restriction versus coapting force: In vitro studies
Integrated mechanism for functional mitral regurgitation - Leaflet restriction versus coapting force: In vitro studies
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DOI：
10.1161/01.cir.96.6.1826
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发表时间：
1997-09-16
期刊：
影响因子：
37.8
通讯作者：
Levine, RA
中科院分区：
文献类型：
--
作者：
He, SQ;Fontaine, AA;Levine, RA
背景缺血性或扩张性心室患者的功能性二尖瓣返流与竞争因素有关：由于乳头肌和瓣环附件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伴二尖瓣压力降低，无法闭合瓣叶。然而，在体内，几何变化伴随着功能障碍，使得难以独立地研究这些因素。功能性二尖瓣返流在收缩中期也矛盾地减少，尽管峰值二尖瓣驱动压力，这表明力平衡的变化作用于创建顺应性瓣口，升高的二尖瓣压力抵消限制瓣叶闭合的力。在体内，这种机制不能独立测试的环形收缩，也可以减少收缩中期reflux.Methods和结果的体外模型的开发，允许独立的变化乳头肌的位置，环的大小，和transmartral压力，直接administant流速测量，测试的假设，功能性二尖瓣反流反映了改变平衡的力量作用于小叶。在生理压力和流量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和心尖瓣叶栓系或帐篷状伴返流。它再现了临床上观察到的收缩中期二尖瓣血流和瓣口面积随着二尖瓣压力增加而减少。栓系延迟了瓣膜关闭，增加了完全对合前的早期收缩压，缩短了对合时间。瓣环扩张会增加任何乳头肌位置的反流，造成临床上重要的反流;相反地，结论临床观察到的幕状瓣叶构型和动态瓣口面积变化可以通过改变三种构型在体外重现。瓣膜的瓣环和乳头肌附件的尺寸关系，以增加瓣叶张力。增大的二尖瓣压力作用于瓣叶闭合，减小了顺应性瓣口面积。这些结果与作用在瓣叶上的系留力与接合力的平衡改变产生顺应性瓣口的机制一致。
Background 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.Methods and Results 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.Conclusions 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.