Gallagher K P, Gerren R A, Stirling M C, Choy M, Dysko R C, McManimon S P, Dunham W R
Circ Res. 1986 Apr;58(4):570-83. doi: 10.1161/01.res.58.4.570.
To evaluate the degree and lateral extent of dysfunction in nonischemic myocardium adjacent to ischemic muscle, we measured systolic wall thickening with sonomicrometers during circumflex coronary occlusion in 12 anesthetized, open-chest dogs. The locations of the wall thickness measurements relative to the perfusion boundary were determined with myocardial blood flow (microspheres) maps constructed from multiple, small tissue samples. Five minutes after circumflex occlusion, systolic wall thickening in the central ischemic zone decreased from 3.00 +/- 0.61 (mean +/- SD) mm to -0.61 +/- 0.36 mm (P less than 0.01). In nonischemic myocardium greater than 10 mm from the perfusion boundary, systolic wall thickening increased from 2.56 +/- 0.57 to 3.24 +/- 0.72 mm (P less than 0.01). In nonischemic myocardium within 10 mm of the perfusion boundary, systolic wall thickening was slightly but significantly reduced compared with control (2.72 +/- 0.80 to 2.44 +/- 0.79 mm, P less than 0.05), supporting the concept of regional dysfunction in nonischemic myocardium at the lateral borders of an ischemic area. Sigmoid curves were fitted to the data to model changes in wall thickening as a continuous function of distance from the perfusion boundary. This allowed estimation of the extent of dysfunction into nonischemic myocardium which averaged less than 8 mm (approximately 30 degrees of endocardial circumference) at one border. The level of functional impairment in this zone was relatively modest, and systolic wall thickening in the immediate border area was reduced more than 50% from control only in tissue characterized by a blood supply of mixed ischemic and nonischemic origin. We conclude that a functional border zone exists lateral to an acutely ischemic area, but measurement of regional function produces relatively small exaggeration of the size of the acutely ischemic zone if severe reduction in mechanical performance is used to define the extent of the ischemic area.
为了评估缺血心肌相邻的非缺血心肌功能障碍的程度和横向范围,我们在12只麻醉开胸犬的左旋冠状动脉闭塞期间,用超声微测仪测量了收缩期室壁增厚情况。通过由多个小组织样本构建的心肌血流(微球)图,确定了相对于灌注边界的室壁厚度测量位置。左旋冠状动脉闭塞5分钟后,中央缺血区的收缩期室壁增厚从3.00±0.61(均值±标准差)毫米降至-0.61±0.36毫米(P<0.01)。在距灌注边界大于10毫米的非缺血心肌中,收缩期室壁增厚从2.56±0.57毫米增加至3.24±0.72毫米(P<0.01)。在距灌注边界10毫米内的非缺血心肌中,与对照相比,收缩期室壁增厚略有但显著降低(从2.72±0.80毫米降至2.44±0.79毫米,P<0.05),支持了缺血区域外侧边界的非缺血心肌存在区域性功能障碍的概念。将S形曲线拟合到数据中,以模拟室壁增厚作为距灌注边界距离的连续函数的变化。这使得能够估计非缺血心肌功能障碍的范围,在一侧边界平均小于8毫米(约心内膜圆周的30度)。该区域的功能损害程度相对较轻,仅在具有缺血和非缺血混合血供特征的组织中,紧邻边界区域的收缩期室壁增厚比对照降低超过50%。我们得出结论,急性缺血区域外侧存在一个功能边界区,但如果用机械性能的严重降低来定义缺血区域的范围,区域功能测量会使急性缺血区大小的夸大相对较小。