目的研究辛伐他汀对高血压并发阵发性心房颤动患者房颤再发率和持续性房颤发生率的影响以及对肾素、血管紧张素Ⅱ(AngⅡ)水平的影响。方法将68例高血压并发阵发性房颤患者随机分为两组各34例:辛伐他汀组常规治疗的同时,予口服辛伐他汀20m/d;对照组仅给予常规治疗,跟踪24个月,观察2组治疗1年后阵发性房颤再发率和持续性房颤的发生率,并检测治疗前及治疗1年后肾素、AngⅡ的表达水平。结果辛伐他汀组房颤再次发作6例(17.6%)明显低于对照组12例(35.3%);辛伐他汀组转为持续性房颤2例(5.9%),亦明显低于对照组4例(11.8%);差异均有统计学意义(P<0.05)。辛伐他汀组治疗后血清肾素、AngⅡ的水平,与对照组比较均下降,差异均有统计学意义(P<0.01)。结论高血压并发阵发性房颤的患者应用辛伐他汀治疗,能够降低阵发性房颤的再发率,减少持续性房颤的发生率,而且降低血清肾素、AngⅡ的水平,后者可能与房颤的再发相关,提示肾素-血管紧张素-醛固酮系统的激活具有促进心房颤动的发生和持续的作用。 Objective To investigate the effect of simvastatin on the incidence of atrial fibrillation and the incidence of persistent atrial fibrillation in patients with hypertension complicated by paroxysmal atrial fibrillation and its effect on renin and angiotensin Ⅱ (AngⅡ) levels. Methods Sixty-eight patients with hypertension complicated with paroxysmal atrial fibrillation were randomly divided into two groups (n = 34): Simvastatin group was treated with simvastatin 20 m / d while conventional simvastatin group. The control group was given routine treatment only, followed by 24 Month. The incidence of paroxysmal atrial fibrillation and persistent atrial fibrillation after 1 year of treatment in both groups were observed. The levels of renin and angiotensin Ⅱ before and 1 year after treatment were measured. Results Six to seven (17.6%) cases of atrial fibrillation in simvastatin group were significantly lower than those in control group (35.3%), and two to 5.9% in simvastatin group, which was significantly lower than that in control group 4 cases (11.8%); the differences were statistically significant (P <0.05). The levels of serum renin and angiotensin Ⅱ in simvastatin group decreased compared with the control group, the difference was statistically significant (P <0.01). Conclusions Simvastatin treatment in patients with hypertension complicated with paroxysmal atrial fibrillation can reduce the recurrence rate of paroxysmal atrial fibrillation, reduce the incidence of persistent atrial fibrillation and decrease the levels of serum renin and AngⅡ. May be related to the recurrence of atrial fibrillation, suggesting that the activation of the renin-angiotensin-aldosterone system can promote the occurrence and sustained effect of atrial fibrillation.