缬沙坦对老年心力衰竭患者N端脑钠肽前体及和肽素的影响

摘要

目的观察老年慢性心力衰竭（简称“心衰”）患者缬沙坦治疗前后血浆N端脑钠肽前体（NT-proBNP）及和肽素的变化，探讨缬沙坦抑制心室重构的作用机制。方法纳入2011年6月至2012年9月在湖南株洲凯德心血管病医院心内科就诊的老年慢性心衰患者99例，随机分为治疗组（常规治疗+缬沙坦，n＝50)和对照组(仅常规治疗，n＝49)，分别检测两组治疗前、治疗1个月、治疗6个月，血浆NT-proBNP、和肽素水平及心室结构功能的变化。结果两组患者治疗1个月与治疗前、治疗6个月与1个月比较，血浆NT-proBNP及和肽素水平均下降，差异均有统计学意义（P＜0.05或P＜0.01）；治疗组患者治疗1个月、6个月的血浆NT-proBNP、和肽素水平与同时间段对照组相比均下降，差异均有统计学意义（P＜0.05或P＜0.01）。治疗1个月，两组患者左室射血分数（LVEF）、左心室收缩末期内径（LVESD）及左心室舒张末期内径（LVEDD）与治疗前比较，以及两组间比较，差异均无统计学意义（P＞0.05）；治疗6个月，治疗组LVEF较对照组明显升高（P＜0.01），LVESD及LVEDD较对照组明显减小(均P＜0.01)。结论血管紧张素Ⅱ受体拮抗剂缬沙坦能够抑制老年慢性心衰患者血浆NT-proBNP、和肽素的分泌，抑制神经内分泌因子，抑制心室重构，改善心功能。%Objective To determine the effects of valsartan on the plasma levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and copeptin in the elderly patients with chronic heart failure (CHF), and to investigate the possible mechanism of valsartan to prevent ventricular remodeling. Methods A total of 99 CHF elderly patients aged from 60~81(68±12)years who were hospitalized in our department from June 2011 to September 2012 were recruited in this study. They were randomly divided into 2 groups:valsartan and conventional treatment group (valsartan group, n=50), and conventional treatment (control group, n=49). The plasma levels of NT-proBNP and copeptin, and the structural function of left ventricle were measured at the baseline, 1 and 6 months after valsartan treatment. Results The levels of NT-proBNP and copeptin were decreased in both groups at 1 month after treatment, and more significantly at 6 months (P<0.05 or 0.01). Their levels were significantly lower in the valsartan treatment group than in the control group at 1 and 6 months after treatment respectively (P<0.05 or 0.01). No significant difference was found in the left ventricular ejection fraction (LVEF), left ventricular end systolic diameter (LVESD) and left ventricular end diastolic diameter (LVEDD) in the 2 groups at 1 month after treatment, and between the 2 groups before and at 1 month after treatment (P>0.05). But at 6 months after treatment, the LVEF was significantly higher (P<0.01), while the LVESD and LVEDD were significantly lower in the valsartan treatment group than in the control group (P<0.01). Conclusion Angiotensin Ⅱ receptor antagonist valsartan could inhibit the secretion of NT-proBNP and copeptin in the plasma of elderly patients with CHF, and then suppresses neuroendocrine factors, prevents ventricular remodeling, and therefore improves the heart function.