Gorman J H, Gorman R C, Plappert T, Jackson B M, Hiramatsu Y, St John-Sutton M G, Edmunds L H
Department of Surgery, School of Medicine, University of Pennsylvania, Philadelphia 19104, USA.
J Thorac Cardiovasc Surg. 1998 Mar;115(3):615-22. doi: 10.1016/S0022-5223(98)70326-5.
This study tests the hypothesis that neither small nor large myocardial infarctions that include the anterior papillary muscle produce mitral regurgitation in sheep.
Coronary arterial anatomy to the anterior left ventricle and papillary muscle was determined by dye injection in 41 sheep hearts and by triphenyl tetrazolium chloride in 13. Development of acute or chronic mitral regurgitation and changes in left ventricular dimensions were studied by use of transdiaphragmatic echocardiography in 21 sheep after infarction of 24% and 33% of the anterior left ventricular mass. These data were compared with previous data from large and small posterior left ventricular infarctions.
Ligation of two diagonal arteries infarcts 24% of the left ventricular mass and 82% of the anterior papillary muscle. Ligation of both diagonals and the first circumflex branch infarcts 33% of the left ventricle and all of the anterior papillary muscle. Neither infarction causes mitral regurgitation, although left ventricular cavity dimensions increase significantly at end systole. After the smaller infarction, the left ventricular cavity enlarges 150% over 8 weeks without mitral regurgitation.
In sheep small and large infarctions of the anterior wall that include the anterior papillary muscle do not produce either acute or chronic mitral regurgitation despite left ventricular dilatation. In contrast large posterior infarctions produce immediate mitral regurgitation owing to asymmetric annular dilatation and discoordination of papillary muscle relationships to the valve. After small posterior infarctions that include the posterior papillary muscle, mitral regurgitation develops because of annular and ventricular dilatation during remodeling.
本研究旨在验证以下假说:无论是累及前乳头肌的小面积还是大面积心肌梗死,均不会在绵羊中导致二尖瓣反流。
通过向41只绵羊心脏注射染料以及向13只绵羊心脏注射氯化三苯基四氮唑来确定左心室前壁和乳头肌的冠状动脉解剖结构。在21只绵羊的左心室前壁心肌梗死面积分别为24%和33%后,利用经膈超声心动图研究急性或慢性二尖瓣反流的发生情况以及左心室尺寸的变化。将这些数据与之前关于左心室后壁大面积和小面积梗死的数据进行比较。
结扎两条对角支动脉会使24%的左心室质量和82%的前乳头肌梗死。结扎两条对角支动脉和第一支回旋支会使33%的左心室和所有前乳头肌梗死。尽管收缩末期左心室腔尺寸显著增加,但这两种梗死均不会导致二尖瓣反流。在较小面积梗死之后,左心室腔在8周内扩大了150%,且未出现二尖瓣反流。
在绵羊中,累及前乳头肌的前壁小面积和大面积梗死,尽管左心室扩张,但不会产生急性或慢性二尖瓣反流。相比之下,大面积后壁梗死由于不对称的瓣环扩张以及乳头肌与瓣膜关系的不协调,会立即产生二尖瓣反流。在累及后乳头肌的小面积后壁梗死之后,二尖瓣反流是由于重塑过程中瓣环和心室的扩张而发展形成的。