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目的通过观察缬沙坦对风湿性心脏病房颤患者心房结构重构以及心房肌细胞凋亡指数(AI)影响,以探讨结构重构发生的分子生物学机制。方法选取51例风心病二尖瓣狭窄伴永久性房颤接受开胸换瓣手术者,共分为两组:对照组(常规药物治疗)23例;试验组(缬沙坦干预组)28例,所有患者在行外科手术前常规行超声心动图检查;以免疫印迹方法半定量检测心房肌中p38MAPK、AT1R及AT2R;以TUNEL法检测细胞凋亡,计算凋亡指数(AI)。结果与对照组相比,试验组左右心房均明显减小,尤以左心房明显,具有统计学差异(P<0.01)。试验组的p38MAPK含量及AT1R的含量减少(P<0.01);AT2R的含量则增加(P<0.01)。对照组患者凋亡指数明显高于试验组,具有统计学差异(P<0.01),而且与左房内径大小呈正相关(r=0.86,P<0.01)。结论风湿性心脏病房颤患者心房结构重构时心房肌细胞凋亡与p38MAPK通路相关,缬沙坦可以减缓心房肌细胞凋亡。
Objective To observe the effects of valsartan on atrial structural remodeling and atrial myocyte apoptosis index (AI) in rheumatic heart disease patients with atrial fibrillation, in order to explore the molecular biological mechanism of structural remodeling. Methods Fifty-one patients with rheumatic mitral stenosis and permanent atrial fibrillation underwent thoracotomy and valvuloplasty were divided into two groups: control group (conventional drug treatment), 23 cases; valsartan intervention group, 28 cases . All patients underwent routine echocardiography before surgery. P38MAPK, AT1R and AT2R in atrial myocardium were detected by Western blotting. Apoptosis was detected by TUNEL method and apoptosis index (AI) was calculated. Results Compared with the control group, the atria in the experimental group were significantly reduced, especially in the left atrium, with statistical significance (P <0.01). The p38MAPK content and AT1R content of the experimental group decreased (P <0.01), while the content of AT2R increased (P <0.01). The apoptotic index in the control group was significantly higher than that in the experimental group (P <0.01), and positively correlated with the size of the left atrium (r = 0.86, P <0.01). Conclusion Atrial myocyte apoptosis is associated with p38 MAPK pathway in atrial fibrillation patients with rheumatic heart disease. Valsartan can attenuate atrial myocyte apoptosis.