Tibayan Frederick A, Rodriguez Filiberto, Zasio Mary K, Bailey Lynn, Liang David, Daughters George T, Langer Frank, Ingels Neil B, Miller D Craig
Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305-5247, USA.
Circulation. 2003 Sep 9;108 Suppl 1:II116-21. doi: 10.1161/01.cir.0000087940.17524.8a.
Better understanding of the precise 3-dimensional geometric changes of the mitral valvular-ventricular complex in chronic ischemic mitral regurgitation (CIMR) is needed in order to devise better surgical repair techniques. We hypothesized that changes after inferior myocardial infarction would be different in hearts that developed CIMR compared with those that did not.
Twenty-four sheep underwent coronary snare and marker placement (annulus, papillary muscles, and anterior and posterior leaflets). After 8 days, cinefluoroscopy provided 3-dimensional marker data, and snare occlusion of obtuse marginal branches created inferior myocardial infarction, including the posterior papillary muscle. After 7 weeks, the 16 surviving animals were studied again and grouped by mitral regurgitation grade (>or= 2+, n=10 versus <or= 1+, n=6). End-systolic mitral annulus dimensions, components of papillary muscle and leaflet displacement, were calculated. After inferior myocardial infarction, total displacement of the posterior papillary muscle from the midseptal annulus ("saddle horn") was greater in CIMR(+) animals: 6.5+/-3.2 versus 3.1+/-2.7 (P=0.02), with the posterior papillary muscle moving more laterally (6.8+/-3.4 versus 2.5+/-3.5 mm, P=0.01). Increase in mitral annular septal-lateral diameter was greater in animals with CIMR (4.9+/-2.7 versus 2.3+/-2.0, P=0.02), and apical displacement of the posterior leaflet (PL) margin was also greater in the CIMR(+) group (1.7+/-1.0 versus 0.3+/-0.5, P=0.01).
The CIMR(+) group had greater septal-lateral annular dilatation, lateral posterior papillary muscle displacement, and apical PL restriction, indicating that these associated geometric alterations may be important in the pathogenesis of CIMR. Treatment of CIMR should address both annular septal-lateral dilatation and lateral displacement of the posterior papillary muscle.
为了设计出更好的手术修复技术，需要更深入地了解慢性缺血性二尖瓣反流（CIMR）中二尖瓣 - 心室复合体精确的三维几何变化。我们假设，与未发生CIMR的心脏相比，下壁心肌梗死后发生CIMR的心脏变化会有所不同。
24只绵羊接受冠状动脉圈套器放置及标记物植入（瓣环、乳头肌以及前后叶）。8天后，通过荧光透视成像获取三维标记物数据，然后用圈套器闭塞钝缘支造成下壁心肌梗死，包括后乳头肌。7周后，对存活的16只动物再次进行研究，并根据二尖瓣反流程度分组（反流≥2 +，n = 10；反流≤1 +，n = 6）。计算收缩末期二尖瓣瓣环尺寸、乳头肌各组成部分及瓣叶移位情况。下壁心肌梗死后，CIMR（+）组动物后乳头肌从中隔瓣环（“鞍角”）的总移位更大：分别为6.5±3.2与3.1±2.7（P = 0.02），后乳头肌向外侧移位更多（分别为6.8±3.4与2.5±3.5 mm，P = 0.01）。CIMR组动物二尖瓣瓣环中隔 - 外侧直径增加更大（分别为4.9±2.7与2.3±2.0，P = 0.02），CIMR（+）组后叶（PL）边缘的心尖移位也更大（分别为1.7±1.0与0.3±0.5，P = 0.01）。
CIMR（+）组有更大的中隔 - 外侧瓣环扩张、后乳头肌向外侧移位以及后叶心尖受限，表明这些相关的几何改变可能在CIMR的发病机制中起重要作用。CIMR的治疗应同时解决瓣环中隔 - 外侧扩张和后乳头肌向外侧移位的问题。
