Department of Nephrology, University of Heidelberg, Heidelberg, Germany.
Am J Nephrol. 2010;32(1):13-22. doi: 10.1159/000313846. Epub 2010 May 19.
Renal failure is a well-established cardiovascular risk factor. We hypothesized that uremia negatively affects post-myocardial infarction (MI) remodeling and left ventricular (LV) function and examined the pathohistological correlations.
Subtotally nephrectomized rats (SNX) and controls with MI only (MIC) were examined 1, 4 and 8 weeks after MI. MI size, ejection fraction (EF), cardiac fibrosis, vascular density and cardiomyocyte density were studied.
The extension of MI was 0.08 +/- 0.02 in SNX versus 0.06 +/- 0.02 in MIC rats (p < 0.031). Prior to MI, EF was comparable in SNX and MIC (74 +/- 3 vs. 72 +/- 2%, n.s.). Despite a relatively small infarct size EF in SNX decreased to 58 +/- 4% 1 week after infarction and progressively worsened to 51 +/- 4% after 8 weeks. In MIC animals EF only slightly decreased 1 week after MI (70 +/- 3%) and remained unchanged at follow-up. In SNX animals LV end-diastolic diameter continuously increased following MI throughout the study period indicating accelerated remodeling. Furthermore, accelerated myocardial fibrosis was already notable 1 week after MI in SNX animals and the volume density of capillaries and cardiomyocytes was significantly lower in SNX rats.
MI in experimental uremia is associated with progressive impairment of LV function, LV dilatation and accelerated myocardial fibrosis.
肾衰竭是公认的心血管风险因素。我们假设尿毒症会对心肌梗死后（MI）的重构和左心室（LV）功能产生负面影响，并检查了组织病理学相关性。
部分肾切除术（SNX）大鼠和仅心肌梗死（MIC）大鼠在 MI 后 1、4 和 8 周进行检查。研究了 MI 大小、射血分数（EF）、心脏纤维化、血管密度和心肌细胞密度。
SNX 大鼠的 MI 扩展程度为 0.08 +/- 0.02，而 MIC 大鼠为 0.06 +/- 0.02（p < 0.031）。在 MI 之前，SNX 和 MIC 的 EF 相当（74 +/- 3% vs. 72 +/- 2%，无统计学意义）。尽管梗塞面积相对较小，但 SNX 大鼠的 EF 在 MI 后 1 周降至 58 +/- 4%，并逐渐恶化至 8 周时的 51 +/- 4%。在 MIC 动物中，EF 在 MI 后 1 周仅略有下降（70 +/- 3%），在随访期间保持不变。SNX 动物的 LV 舒张末期直径在整个研究期间随 MI 不断增加，表明重构加速。此外，在 SNX 动物中，心肌梗死后 1 周即可观察到加速性心肌纤维化，并且 SNX 大鼠的毛细血管和心肌细胞的体积密度明显降低。
实验性尿毒症中的 MI 与 LV 功能进行性受损、LV 扩张和加速性心肌纤维化有关。
