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首页> 外文期刊>Circulation: An Official Journal of the American Heart Association >Paradoxic decrease in ischemic mitral regurgitation with papillary muscle dysfunction: insights from three-dimensional and contrast echocardiography with strain rate measurement.
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Paradoxic decrease in ischemic mitral regurgitation with papillary muscle dysfunction: insights from three-dimensional and contrast echocardiography with strain rate measurement.

机译:缺血性二尖瓣关闭不全与乳头状肌功能障碍的矛盾降低:三维超声心动图和应变率测量对比超声心动图。

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BACKGROUND: Ischemic mitral regurgitation (MR) was first ascribed to papillary muscle (PM) contractile dysfunction. Current theories include apical leaflet tethering caused by left ventricular (LV) distortion, but PM dysfunction is still postulated and commonly diagnosed. PM contraction, however, parallels apical tethering, suggesting the hypothesis that PM contractile dysfunction can actually diminish MR due to ischemic distortion of the inferior base alone. METHODS AND RESULTS: We therefore occluded the proximal circumflex circulation in 7 sheep while maintaining PM perfusion, confirmed by contrast echocardiography. By 3D echocardiography, we measured the tethering distance between the ischemic medial PM tip and anterior annulus and LV ejection volume to give MR (by subtracting flowmeter LV outflow). In 6 sheep without initial MR, inferior ischemia alone produced PM tip retraction with restricted leaflet closure and mild-to-moderate MR (regurgitant fraction, 25.2+/-2.8%). Adding PM ischemia consistently decreased MR and tethering distance (5.2+/-0.3 to 1.4+/-0.3 mL; +3.8+/-0.5 mm to -2.2+/-0.7 mm axially relative to baseline; P<0.001) as PM strain rate decreased from +0.78+/-0.07 per second (contraction) to -0.42+/-0.06 per second (elongation, P<0.001) and leaflet tenting decreased. In one sheep, prolapse and MR resolved with inferior ischemia and recurred with PM ischemia. CONCLUSIONS: PM contractile dysfunction can paradoxically decrease MR from inferobasal ischemia by reducing leaflet tethering to improve coaptation. This emphasizes the role of geometric factors in ischemic MR mechanism and potential therapy.
机译:背景:缺血性二尖瓣关闭不全(MR)首先归因于乳头肌(PM)收缩功能障碍。当前的理论包括由左心室(LV)畸变引起的根尖小叶系留,但仍假定并经常诊断PM功能障碍。然而,PM收缩与根部束缚相平行,提示这样的假说,即PM收缩功能障碍实际上可能会由于仅对下位碱基的缺血性扭曲而减少MR。方法和结果:因此,我们在保持PM灌注的同时阻塞了7只羊的近回旋支循环,这是通过对比超声心动图证实的。通过3D超声心动图,我们测量了缺血性内侧PM尖端与前瓣环之间的系留距离以及LV射血量,从而得出MR(通过减去流量计LV流出)。在6例没有初始MR的绵羊中,仅亚部缺血可导致PM尖端退缩,瓣叶闭合受限,MR轻度至中度(返流率,25.2 +/- 2.8%)。添加PM缺血会持续降低MR和束缚距离(相对于基线轴向5.2 +/- 0.3至1.4 +/- 0.3 mL;轴向相对于基线+3.8 +/- 0.5 mm至-2.2 +/- 0.7 mm; P <0.001)速率从每秒+0.78 +/- 0.07(收缩)降低到每秒-0.42 +/- 0.06(伸长,P <0.001),并且单张帐篷减少。在一只绵羊中,下肢缺血可导致脱垂和MR缓解,PM缺血可复发。结论:PM收缩功能障碍可通过减少小叶系留以改善适应性而反常降低下基底缺血引起的MR。这强调了几何因素在缺血性MR机制和潜在治疗中的作用。

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