阿托伐他汀对血脂正常的病窦综合征患者心房颤动复发的影响

Effect of atorvastatin on prevention of paroxysmal atrial fibrillation in patients with sick sinus syndrome and no dyslipidemia

目的探讨阿托伐他汀对血脂正常的病窦综合征(SSS)患者心房颤动(AF)复发的防治作用。方法选择62例SSS合并阵发性AF(PAF)未行心脏永久起搏器植入术且血脂正常的患者,随机分为对照组(常规治疗组)和治疗组(常规治疗基础上加阿托伐他汀20 mg/d),随访观察12个月,观察AF发作次数、AF持续时间及血浆C反应蛋白(CRP)水平、血脂水平的变化。结果治疗后治疗组AF的发作次数、AF持续时间虽没有明显降低但显著低于对照组(13.4±2.8次/年vs 16.2±3.6次/年,62.4±7.2小时/年vs 66.3±4.7小时/年),血CRP水平显著降低(7.95±0.87 mg/L vs 9.52±1.31 mg/L)且显著低于对照组(7.95±0.87 mg/L vs 10.02±1.37mg/L)。治疗组的血脂在治疗12个月时较治疗前明显改善(P<0.05),而对照组的上述指标则无明显改善。结论阿托伐他汀对血脂正常、未行心脏永久起搏器植入术的SSS患者AF的复发具有明显的防治作用。其机制可能与他汀类药物抑制炎症反应及调脂有关。

Objective To evaluate the effect of Atorvastatin on preventing paroxysmal atrial fibrillation （PAF） in patients with sick sinus syndrome（SSS） but without dyslipidemia. Methods Sixty-two patients with SSS suffering from PAF but without dyslipidemia and not accepting cardiac pacemaker implantation were randomized to the treatment group and the control group. The control group were given routine medication,while the treatment group were administrated with Atorvastatin,20 mg served everyday,in addition to routine medication. After 12 months of follow-up,the PAF times,AF duration,the serum level of C-reactive protein（CRP） and serum lipid levels were observed. Results At 12 months of follow-up, PAF times,AF duration in the treatment group were not lower than those before treatment but were significantly lower than that in the control group（P 〈0.05）, the serum level of CRP in the treatment group were significantly not only lower than those in the control group（P 〈0.06） ,but also lower than those before treatment. Furthermore the profih of serum lipid in the treatment group was ameliorated at the termination of treatment （P 〈 0. 05） compared with that before treatment, whereas it was not the case in the control group. Conclusions Atorvastatin can effectively inhibit the occurrence of PAF in patients with SSS suffering from PAF but without dyslipidemia and not accepting cardiac pacemaker implantation. The mechanism is probably associated with the effect of Atorvastatin to inhibit inflammatory reaction and to ameliorate serum lipid.