Glasson J R, Komeda M, Daughters G T, Bolger A F, Karlsson M O, Foppiano L E, Hayase M, Oesterle S N, Ingels N B, Miller D C
Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Calif 94305-5247, USA.
J Thorac Cardiovasc Surg. 1998 Aug;116(2):193-205. doi: 10.1016/s0022-5223(98)70117-5.
The mechanism by which incomplete mitral leaflet coaptation develops during ischemic mitral regurgitation is debated, with recent studies suggesting that incomplete mitral leaflet coaptation may be due to apically displaced papillary muscle tips. Yet quantitative in vivo three-dimensional mitral leaflet motion during ischemic mitral regurgitation has never been described.
Radiopaque markers (sutured around the mitral anulus, to the central free mitral leaflet edges, and to both papillary muscle tips and bases) were imaged with the use of biplane videofluoroscopy in six closed-chest, sedated sheep before (control) and during induction of acute ischemic mitral regurgitation. Leaflet coaptation was defined as the minimum distance measured between edge markers during control conditions.
During control, leaflet coaptation occurred 23 +/- 7 msec (mean +/- standard error of the mean) after end-diastole, when left ventricular pressure was 27 +/- 6 mm Hg. During ischemic mitral regurgitation, coaptation was delayed to 115 +/- 19 msec after end-diastole (p < or = 0.01 vs control [n = 4]) when left ventricular pressure was 88 +/- 4 mm Hg. At end-diastole during ischemic mitral regurgitation, the mitral anulus area was 14% +/- 2% larger than control (7.4 +/- 0.3 cm2 vs 6.5 +/- 0.2 cm2, p < or = 0.005) as the result of the lengthening of muscular annular regions (76.0 +/- 2.5 mm vs 70.5 +/- 1.4 mm, p < or = 0.01). Mitral anulus shape (ratio of two diameters) at end-diastole was more circular during ischemic mitral regurgitation (0.79 +/- 0.01 vs 0.71 +/- 0.02, p < 0.01). At end-diastole during ischemic mitral regurgitation, the posterior papillary muscle tip was displaced 1.5 +/- 0.5 mm laterally and 2.0 +/- 0.6 mm posteriorly (p < or = 0.02 vs control), but there was no apical displacement of either papillary muscle tip.
Incomplete mitral leaflet coaptation during acute ischemic mitral regurgitation occurred early in systole, not at end-systole, and was due to "loitering" of the leaflets associated with posterior mitral anulus enlargement and circularization, as well as some posterolateral, but not apical, posterior papillary muscle tip displacement. These data suggest that early systolic mitral anulus dilatation and shape change and altered posterior papillary muscle motion are the primary mechanisms by which incomplete mitral leaflet coaptation occurs during acute ischemic mitral regurgitation.
缺血性二尖瓣反流时二尖瓣叶不完全对合的发生机制存在争议，近期研究表明二尖瓣叶不完全对合可能是由于乳头肌尖端向心尖移位所致。然而，缺血性二尖瓣反流时二尖瓣叶在体内的定量三维运动从未被描述过。
在6只开胸、镇静的绵羊身上，于急性缺血性二尖瓣反流诱导前（对照）和诱导期间，使用双平面视频荧光透视对不透X线的标记物（缝合在二尖瓣环周围、二尖瓣叶中央游离边缘、两个乳头肌尖端和基部）进行成像。瓣叶对合定义为对照条件下边缘标记物之间测量的最小距离。
在对照期间，舒张末期后23±7毫秒（平均值±平均值的标准误差）发生瓣叶对合，此时左心室压力为27±6毫米汞柱。在缺血性二尖瓣反流期间，对合延迟至舒张末期后115±19毫秒（与对照相比，p≤0.01[n = 4]），此时左心室压力为88±4毫米汞柱。在缺血性二尖瓣反流的舒张末期，二尖瓣环面积比对照大14%±2%（7.4±0.3平方厘米对6.5±0.2平方厘米，p≤0.005），这是由于肌性环区域延长（76.0±2.5毫米对70.5±1.4毫米，p≤0.01）。缺血性二尖瓣反流时舒张末期二尖瓣环形状（两个直径的比值）更接近圆形（0.79±0.01对0.71±0.02，p < 0.01）。在缺血性二尖瓣反流的舒张末期，后乳头肌尖端向外侧移位1.5±0.5毫米，向后移位2.0±0.6毫米（与对照相比，p≤0.02），但两个乳头肌尖端均无向心尖移位。
急性缺血性二尖瓣反流时二尖瓣叶不完全对合发生在收缩早期，而非收缩末期，是由于瓣叶“滞留”，与二尖瓣后环扩大和圆形化以及后乳头肌尖端的一些后外侧（而非心尖）移位有关。这些数据表明，收缩早期二尖瓣环扩张和形状改变以及后乳头肌运动改变是急性缺血性二尖瓣反流时二尖瓣叶不完全对合发生的主要机制。
