Dai Wangde, Wold Loren E, Dow Joan S, Kloner Robert A
The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California 90017, USA.
J Am Coll Cardiol. 2005 Aug 16;46(4):714-9. doi: 10.1016/j.jacc.2005.04.056.
We determined whether collagen implantation could thicken the infarcted left ventricular (LV) wall and improve LV function.
We hypothesized that thickening the infarcted wall by using collagen might result in some benefits that are similar to what previously had been reported when the infarcted wall was thickened with cells.
Fischer rats with one-week-old myocardial infarcts were injected with collagen or saline (100 microl) into the scar (n = 12 each group). Six weeks later, LV angiograms, hemodynamics, and regional myocardial blood flow were assessed. The hearts were processed for measurements of postmortem LV volume and histology.
Collagen injection significantly increased scar thickness (719 +/- 26 microm) compared with the saline-treated group (440 +/- 34 microm, p = 2.6 x 10(-6)). By LV angiography, stroke volume was significantly larger in the collagen-treated group (163 +/- 8 microl) than in the saline-treated group (129 +/- 6 microl, p = 0.005), and LV ejection fraction was also greater in the collagen-treated group (48.4 +/- 1.8%) than in the saline-treated group (40.7 +/- 1.0%, p = 0.002). Analysis of regional wall motion demonstrated paradoxical systolic bulging in 5 of 10 saline-treated rats that averaged 20.3 +/- 2.6% of the LV diastolic circumference, but in none of the 11 collagen-treated rats (p = 0.012). The LV end-diastolic and end-systolic volumes were 319 +/- 12 microl and 190 +/- 7 microl in the saline-treated group, respectively. There was a trend for larger LV end-diastolic volumes (343 +/- 23 microl), but smaller end-systolic volumes (180 +/- 16 microl) in the collagen-treated group.
This study shows that collagen injection thickens an infarct scar and improves LV stroke volume and ejection fraction, and prevents paradoxical systolic bulging after myocardial infarction.
我们确定胶原蛋白植入是否能增厚梗死的左心室(LV)壁并改善左心室功能。
我们假设通过使用胶原蛋白增厚梗死壁可能会带来一些益处,类似于之前用细胞增厚梗死壁时所报道的情况。
对患有一周龄心肌梗死的Fischer大鼠,在瘢痕处注射胶原蛋白或生理盐水(100微升)(每组n = 12)。六周后,评估左心室血管造影、血流动力学和局部心肌血流量。对心脏进行处理以测量死后左心室容积和组织学。
与生理盐水治疗组(440±34微米,p = 2.6×10⁻⁶)相比,胶原蛋白注射显著增加了瘢痕厚度(719±26微米)。通过左心室血管造影,胶原蛋白治疗组的每搏输出量(163±8微升)显著大于生理盐水治疗组(129±6微升,p = 0.005),胶原蛋白治疗组的左心室射血分数(48.4±1.8%)也高于生理盐水治疗组(40.7±1.0%,p = 0.002)。局部壁运动分析显示,10只生理盐水治疗的大鼠中有5只出现矛盾性收缩期膨出,平均为左心室舒张周长的20.3±2.6%,但11只胶原蛋白治疗的大鼠中均未出现(p = 0.012)。生理盐水治疗组的左心室舒张末期和收缩末期容积分别为319±12微升和1- 90±7微升。胶原蛋白治疗组有左心室舒张末期容积较大(343±23微升)但收缩末期容积较小(180±16微升)的趋势。
本研究表明,胶原蛋白注射可增厚梗死瘢痕,改善左心室每搏输出量和射血分数,并防止心肌梗死后出现矛盾性收缩期膨出。