Tibayan Frederick A, Rodriguez Filiberto, Langer Frank, Liang David, Daughters George T, Ingels Neil B, Miller D Craig
Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford, CA, USA.
J Heart Valve Dis. 2004 May;13(3):414-20.
Papillary muscle displacement is an important element in the pathogenesis of ischemic mitral regurgitation (IMR). The effects of standard ring annuloplasty on subvalvular geometry are incompletely understood. The hypothesis was tested that annular reduction with a Panethtype suture annuloplasty would correct both annular and papillary muscle geometric abnormalities during acute left ventricular (LV) ischemia.
Eight adult sheep underwent insertion of an adjustable, double-suture Paneth-type mitral annuloplasty and radiopaque markers on the left ventricle, mitral annulus, leaflet edges, and anterior (APM) and posterior (PPM) papillary muscle tips. Immediately after surgey, 3-D marker coordinates were determined during Control conditions and during proximal left circumflex occlusion before and after tightening the annuloplasty suture.
Acute IMR (MR grade 0.3 +/- 0.3 to 2.1 +/- 0.4, Control versus Ischemia) was associated with end-systolic LV dilatation (+27 +/- 16 ml, change relative to Control), greater septal-lateral (+4.6 +/- 3.1 cm) and commissure-commissure (+3.3 +/- 1.6 cm) mitral annular diameters, longer anterior (+1.5 +/- 0.9 cm) and posterior (+0.6 +/- 0.9 cm) papillary muscle tethering distances, greater distance from the APM to the anterior commissure (+0.9 +/- 0.8 cm), and shorter distance from the PPM to the poslerior commissure (-1.3 +/- 1.5 cm). Suture annuloplasty corrected the annular and subvalvular changes, and IMR returned to Control levels (0.5 +/- 0.5); only LV end-systolic volume (ESV) was different from Control (+25 +/- 18 ml) (mean +/- SD, p < 0.05 versus Control by RMANOVA and Dunnett's test).
Suture annuloplasty corrected ischemia-induced end-systolic distortions of the entire valvular-ventricular complex (i.e. inter-leaflet separation, mitral annular dilatation in both axes, and papillary muscle displacements), and abolished acute IMR, independent of any change in ESV. A better understanding of the effects of annular reduction on papillary muscle geometry may lead to improved subvalvular mitral repair techniques.
乳头肌移位是缺血性二尖瓣反流(IMR)发病机制中的一个重要因素。标准瓣环成形术对瓣下结构几何形态的影响尚未完全明确。本研究检验了一个假设,即采用潘内特式缝线瓣环成形术进行瓣环缩小术可在急性左心室(LV)缺血期间纠正瓣环和乳头肌的几何形态异常。
八只成年绵羊接受了可调节的双缝线潘内特式二尖瓣瓣环成形术,并在左心室、二尖瓣瓣环、瓣叶边缘以及前(APM)后(PPM)乳头肌尖端植入了不透射线的标记物。手术后立即在对照状态下以及在收紧瓣环成形术缝线前后的左旋支近端闭塞期间确定三维标记物坐标。
急性IMR(反流程度从对照时的0.3±0.3级增加至缺血时的2.1±0.4级)与收缩末期左心室扩张(相对于对照增加27±16ml)、更大的室间隔-侧壁二尖瓣瓣环直径(增加4.6±3.1cm)和瓣连合-瓣连合二尖瓣瓣环直径(增加3.3±1.6cm)、更长的前乳头肌(增加1.5±0.9cm)和后乳头肌(增加0.6±0.9cm)腱索长度、前乳头肌到前瓣连合的距离增加(增加0.9±0.8cm)以及后乳头肌到后瓣连合的距离缩短(缩短1.3±1.5cm)相关。缝线瓣环成形术纠正了瓣环和瓣下结构的变化,IMR恢复到对照水平(0.5±0.5级);只有左心室收缩末期容积(ESV)与对照不同(增加25±18ml)(均值±标准差,重复测量方差分析和邓尼特检验显示与对照相比p<0.05)。
缝线瓣环成形术纠正了缺血引起的整个瓣膜-心室复合体的收缩末期变形(即瓣叶间分离、两个轴向上的二尖瓣瓣环扩张以及乳头肌移位),并消除了急性IMR,且与ESV的任何变化无关。更好地理解瓣环缩小对乳头肌几何形态的影响可能会带来改进的瓣下二尖瓣修复技术。