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目的探讨急性心肌梗死后不同剂量的血管紧张素Ⅱ1型(AT1)受体拮抗剂早期干预对心功能和神经激素的影响。方法选择首次急性心肌梗死患者120例,所有病例在常规治疗基础上(包括硝酸酯类、β受体阻滞剂、阿司匹林、低分子肝素),随机分为卡托普利(C)组40例,口服卡托普利12.5～25mg,每日3次;缬沙坦(D1)组40例,口服缬沙坦80mg,每日1次;缬沙坦(D2)组40例,口服缬沙坦160mg,每日1次。分别于治疗1、6、12、18个月对所有患者的心功能有关指标进行检测,并同时检测血浆血管紧张素Ⅱ、醛固酮浓度。结果治疗12、18个月,缬沙坦D1、D2组与卡托普利组比较,心功能各项指标(除外缬沙坦D1组12个月左心室射血分数、左心室舒张末期容量)差异均有统计学意义(P<0.05,P<0.01);用药18个月缬沙坦不同剂量组间比较,D2组较D1组上述指标差异亦均有统计学意义(P<0.05)。缬沙坦两组和卡托普利组血浆血管紧张素Ⅱ(AngⅡ)水平治疗6、12、18个月均较治疗前升高,其中缬沙坦两组升高明显,差异有统计学意义(P<0.01);3组血浆醛固酮水平与治疗前相比,治疗1、6个月时开始降低,治疗12个月时卡托普利组逐渐升高,缬沙坦两组仍明显减低,差异有统计学意义(P<0.001)。结论AT1受体拮抗剂缬沙坦与血管紧张素转换酶抑制剂卡托普利一样,早期应用能有效改善急性心肌梗死后心室重构,保护心功能,其远期疗效可能优于卡托普利,且随着剂量增加疗效增强。
Objective To investigate the effects of early intervention with different doses of angiotensin Ⅱ type 1 (AT1) receptor antagonist on cardiac function and neurohormones after acute myocardial infarction. Methods A total of 120 patients with acute myocardial infarction (AMI) were enrolled in this study. All patients were randomly divided into captopril (C) group (n = 40), treated with nitrates, β blockers, aspirin and low molecular weight heparin , Oral captopril 12.5 ~ 25mg, 3 times a day; valsartan (D1) group of 40 patients, oral valsartan 80mg, once daily; valsartan (D2) group of 40 patients, oral valsartan 160mg, 1 times a day. The indexes of cardiac function were detected in all patients at 1, 6, 12, and 18 months after treatment, and plasma concentrations of angiotensin Ⅱ and aldosterone were measured simultaneously. Results At 12 and 18 months of treatment, valsartan D1, D2 group and captopril group, cardiac function indicators (except valsartan D1 group 12 months left ventricular ejection fraction, left ventricular end-diastolic volume) (P <0.05, P <0.01). Compared with the different dosages of valsartan for 18 months in the valsartan group, there were also significant differences between the D2 group and the D1 group (P <0.05). The levels of plasma angiotensin Ⅱ in valsartan group and captopril group were significantly higher than those before treatment at 6, 12, and 18 months, and valsartan increased significantly in both groups, with significant difference (P <0.01). The level of plasma aldosterone in the three groups began to decrease at 1 month and 6 months after treatment, and the level of captopril increased gradually at 12 months after treatment in both groups. The difference was statistically significant (P <0.001). Conclusions As the AT1 receptor antagonist valsartan, like angiotensin converting enzyme inhibitor captopril, its early application can effectively improve ventricular remodeling and protect cardiac function after acute myocardial infarction, and its long-term efficacy may be superior to that of captopril Lee, and with the dose increased efficacy.