Roberts C S, Maclean D, Braunwald E, Maroko P R, Kloner R A
Am J Cardiol. 1983 Mar 1;51(5):872-6. doi: 10.1016/s0002-9149(83)80147-7.
The factors that determine the thickness of transmural myocardial infarcts are unknown. Therefore, the relation between the size and thickness of transmural infarcts in 67 rats 21 days after occlusion of the left main coronary artery was studied. On examination of histologic sections, infarct size was determined by planimetry and expressed as a percentage of the left ventricular (LV) area, and thickness was expressed as a percentage of noninfarcted ventricular septal wall thickness. The circumferential length of the infarcted ventricle was measured in millimeters, as well as the circumferential length of the noninfarcted ventricular septum. Septal wall thickness was similar in rats with transmural infarcts and in sham-operated rats. No significant correlation was observed between infarct size and thickness (r = 0.10) or between circumferential length of the infarct and infarct thickness (r = 0.17). However, large (greater than or equal to 20% of the left ventricle, n = 37) and small (less than 20% of the left ventricle, n = 30) infarcts which were similarly thin (37 +/- 1% and 34 +/- 2% of septal wall thickness, respectively) affected LV topography differently. Large infarcts resulted in a 23% greater loss of myocardium (p less than 0.001), greater expansion of the LV cavity (18 +/- 9 mm2 compared with 14 +/- 1 mm2 in small infarcts, p less than 0.005), and lengthening of the septal wall (7.2 +/- 1.1 mm and 6.7 +/- 1.0 mm in large and small infarcts, respectively [p less than 0.05], and 6.3 +/- 0.1 mm in shams). Increase in cavity area and septal length in infarcted ventricles suggested a volume overload hypertrophy, which at 3 weeks was nonetheless inadequate to provide as much normal muscle as was present in sham-operated rats. In an additional 9 rats with subendocardial infarctions (involving less than 75% of the LV wall from endocardium to epicardium), the LV walls were thicker (94 +/- 5% of septal wall thickness, compared with 35 +/- 1% for transmural infarcts, p less than 0.001) and an inverse correlation was observed between infarct size and thickness. In conclusion, neither the size of a transmural infarct in rat nor the circumferential length of infarction determines the thickness of the infarct; however, infarct size does affect LV topography by increasing LV cavity area and the length of the noninfarcted septal wall. Subendocardial infarcts result in less myocardial thinning than do transmural infarcts.
决定透壁性心肌梗死厚度的因素尚不清楚。因此，研究了67只大鼠在左主冠状动脉闭塞21天后透壁性梗死的大小与厚度之间的关系。在组织学切片检查中，梗死面积通过平面测量法确定，并表示为左心室（LV）面积的百分比，厚度表示为未梗死室间隔壁厚度的百分比。测量梗死心室的圆周长度（以毫米为单位）以及未梗死室间隔的圆周长度。透壁性梗死大鼠和假手术大鼠的室间隔壁厚度相似。未观察到梗死面积与厚度之间（r = 0.10）或梗死圆周长度与梗死厚度之间（r = 0.17）有显著相关性。然而，大面积（大于或等于左心室的20%，n = 37）和小面积（小于左心室的20%，n = 30）且厚度相似（分别为室间隔壁厚度的37±1%和34±2%）的梗死对左心室形态的影响不同。大面积梗死导致心肌损失多23%（p < 0.001），左心室腔扩张更大（大面积梗死为18±9 mm²，小面积梗死为14±1 mm²，p < 0.005），室间隔壁延长（大面积梗死和小面积梗死分别为7.2±1.1 mm和6.7±1.0 mm [p < 0.05]，假手术组为6.3±0.1 mm）。梗死心室腔面积和室间隔长度增加提示容量超负荷性肥大，然而在3周时，这种肥大仍不足以提供与假手术大鼠一样多的正常心肌。在另外9只患有心内膜下梗死（累及从心内膜到心外膜的左心室壁不到75%）的大鼠中，左心室壁更厚（为室间隔壁厚度的94±5%，而透壁性梗死为35±1%，p < 0.001），并且观察到梗死面积与厚度呈负相关。总之，大鼠透壁性梗死的大小和梗死的圆周长度均不能决定梗死的厚度；然而，梗死面积确实会通过增加左心室腔面积和未梗死室间隔壁的长度来影响左心室形态。心内膜下梗死导致的心肌变薄程度比透壁性梗死小。
