Ehring T, Heusch G
Abteilung für Pathophysiologie, Universitätsklinikum Essen., FRG.
Am Heart J. 1990 Nov;120(5):1047-57. doi: 10.1016/0002-8703(90)90116-f.
There is a marked heterogeneity of myocardial wall thickening within the left ventricle and among different individuals. It is therefore difficult to detect regional myocardial dysfunction from absolute values of systolic wall thickening. We tested whether the extent of left ventricular asynchrony during ischemia and reperfusion can be used to quantify the severity of regional myocardial dysfunction when nonischemic baseline function is not known. In six anesthetized, open-chest dogs regional myocardial wall thickness was measured by means of sonomicrometry under control conditions, at three degrees of ischemic dysfunction (mild, moderate, and severe), and after release of a 15-minute occlusion of the left circumflex coronary artery, when degrees of moderate and mild reperfusion dysfunction similar to the preceding ischemic dysfunction were present. Two indexes of left ventricular asynchrony were calculated: (1) postejection thickening (PET) and (2) the phase difference of the first Fourier harmonic of posterior versus anterior myocardial wall motion (PD). Systolic myocardial wall thickening was decreased from 15.3 +/- 3.1 (standard deviation) % (control value) to 9.7 +/- 1.4% (mild ischemia), 4.2 +/- 1.6% (moderate ischemia), and -3.7 +/- 3.1% (severe ischemia). Conversely PET increased from 0.02 +/- 0.04 mm (control value) to 0.15 +/- 0.22 mm (mild ischemia), 0.19 +/- 0.15 mm (moderate ischemia), and 0.50 +/- 0.26 mm (severe ischemia). PD increased from 9 +/- 28 degrees (control value) to 22 +/- 19 degrees (mild ischemia), 54 +/- 18 degrees (moderate ischemia), and 107 +/- 21 degrees (severe ischemia). After release of the 15-minute left circumflex coronary artery occlusion, PET and PD recovered to 0.34 +/- 0.19 mm and 36 +/- 24 degrees (moderate dysfunction) and 0.25 +/- 0.31 mm and 29 +/- 8 degrees (mild dysfunction), respectively. There were inverse linear relationships between systolic wall thickening and PET (r = -0.86, p less than 0.001) and between systolic wall thickening and PD (r = -0.87, p less than 0.001). Inotropic stimulation by postextrasystolic potentiation increased regional systolic myocardial posterior and anterior wall thickening but did not alter the extent of left ventricular asynchrony. Thus, when normal baseline function is not known, the severity of regional myocardial dysfunction at a given inotropic state can be determined by analysis of left ventricular asynchrony. There was no significant correlation between the extent of PET and PD during ischemia and at early reperfusion and the recovery of contractile function at late reperfusion. Thus PET does not provide a prospective marker for the functional outcome of reperfusion.
左心室内以及不同个体之间的心肌壁增厚存在显著异质性。因此，很难从收缩期壁增厚的绝对值来检测局部心肌功能障碍。我们测试了在未知非缺血基线功能的情况下，缺血和再灌注期间左心室不同步的程度是否可用于量化局部心肌功能障碍的严重程度。在六只麻醉开胸犬中，通过超声微测法在对照条件下、三种缺血功能障碍程度（轻度、中度和重度）以及在左旋支冠状动脉闭塞释放15分钟后（此时存在与先前缺血功能障碍相似的中度和轻度再灌注功能障碍）测量局部心肌壁厚度。计算了两个左心室不同步指标：（1）射血后增厚（PET）和（2）后壁与前壁心肌壁运动的第一傅里叶谐波的相位差（PD）。收缩期心肌壁增厚从15.3±3.1（标准差）%（对照值）降至9.7±1.4%（轻度缺血）、4.2±1.6%（中度缺血）和-3.7±3.1%（重度缺血）。相反，PET从0.02±0.04mm（对照值）增加到0.15±0.22mm（轻度缺血）、0.19±0.15mm（中度缺血）和0.50±0.26mm（重度缺血）。PD从9±28度（对照值）增加到22±19度（轻度缺血）、54±18度（中度缺血）和107±21度（重度缺血）。在左旋支冠状动脉闭塞15分钟释放后，PET和PD分别恢复到0.34±0.19mm和36±24度（中度功能障碍）以及0.25±0.31mm和29±8度（轻度功能障碍）。收缩期壁增厚与PET之间（r = -0.86，p<0.001）以及收缩期壁增厚与PD之间（r = -0.87，p<0.001）存在负线性关系。早搏后增强的变力性刺激增加了局部收缩期心肌后壁和前壁增厚，但未改变左心室不同步的程度。因此，当未知正常基线功能时，在给定的变力状态下局部心肌功能障碍的严重程度可通过分析左心室不同步来确定。缺血期间和早期再灌注时PET和PD的程度与晚期再灌注时收缩功能的恢复之间无显著相关性。因此，PET不能为再灌注的功能结果提供前瞻性标志物。
