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目的:观察急性冠脉综合征患者缬沙坦治疗前后血浆脑钠肽(BNP)及高敏C反应蛋白(hsCRP)的变化,探讨缬沙坦抑制心室重构的作用机制。方法:急性冠脉综合征患者66例(急性心肌梗死43例,不稳定性心绞痛23例),随机分为治疗组(n=32)和对照组(n=34),分别检测两组治疗前、治疗1个月、治疗6个月,血浆BNP、hsCRP水平及心室结构功能的变化。结果:治疗后治疗组、对照组的急性心肌梗死患者、不稳定性心绞痛患者血浆BNP和hsCRP水平均呈下降趋势,治疗组治疗1个月下降明显、治疗6个月降低速度减慢,治疗组治疗1个月、6个月与同时间段对照组相比下降,对照组、治疗组与同组前一时间段相比亦下降,差异均有统计学意义(P<0.05～0.01)。治疗1个月,两组患者左心室射血分数、左心室收缩末期内径及左心室舒张末期内径均无明显变化(P>0.05);治疗6个月,治疗组左心室射血分数较对照组明显升高(P<0.01),左心室收缩末期内径及心室舒张末期内径较对照组明显减小(P均<0.01),差异均有统计学意义。结论:血管紧张素Ⅱ受体拮抗剂缬沙坦能够抑制急性冠脉综合征患者血浆BNP及hsCRP的分泌,降低炎性反应,抑制心室重构,改善心功能。
Objective: To observe the changes of plasma brain natriuretic peptide (BNP) and high sensitive C-reactive protein (hsCRP) in patients with acute coronary syndrome before and after valsartan treatment and to explore the mechanism of valsartan in inhibiting ventricular remodeling. Methods: A total of 66 patients with acute coronary syndrome (Acute myocardial infarction in 43 cases, 23 cases of unstable angina pectoris) were randomly divided into treatment group (n = 32) and control group (n = 34) , Treatment for 1 month, treatment for 6 months, plasma BNP, hsCRP levels and changes in ventricular structural function. Results: After treatment, the levels of plasma BNP and hsCRP in patients with acute myocardial infarction in treatment group and control group showed a decreasing trend. The treatment group decreased significantly at 1 month and slowed down at 6 months. The treatment group Compared with the control group, the control group and the treatment group also decreased in the treatment group of 1 month and 6 months compared with that of the control group in the same time period. The differences were statistically significant (P <0.05-0.01). After treatment for one month, left ventricular ejection fraction, end-diastolic dimension and end-diastolic diameter of left ventricle did not change significantly in both groups (P> 0.05). After 6 months of treatment, the left ventricular ejection fraction in the treatment group was significantly higher than that in the control group (P <0.01). The diameter of the left ventricular end-systolic and the end-diastolic diameter of end-diastolic were significantly lower than those of the control group (all P <0.01). The differences were statistically significant. Conclusion: Angiotensin Ⅱ receptor antagonist valsartan can inhibit the secretion of plasma BNP and hsCRP in patients with acute coronary syndrome, reduce inflammatory reaction, inhibit ventricular remodeling and improve cardiac function.