CAJ | 학술논문

目的观察阿托伐他汀对高血压患者超敏C反应蛋白(hs-CRP)、血管性假血友病因子(vWF)、P-选择素、低密度脂蛋白胆固醇(LDL-C)及颈动脉内膜-中层厚度(IMT)的影响.方法 151例高血压患者按治疗方法分为3组,50例用10 mg阿托伐他汀+氨氯地平+贝那普利治疗,61例用20mg阿托伐他汀+氨氯地平+贝那普利治疗,对照组40例采用氨氯地平+贝那普利治疗;每3个月检测患者hs-CRP、LDL-C、vWF及P-选择素等指标变化.共观察1年,并对结果进行统计学分析.结果 (1)10 mg和20 mg阿托伐他汀组hs-CRP、LDL-C、vWF、P-选择素及IMT均较对照组下降,差异有统计学意义(P＜0.05);(2)相关分析显示hs-CRP等指标变化与LDL-C下降之间无相关关系.结论阿托伐他汀能够延缓高血压患者动脉粥样硬化的发展,抗动脉硬化作用可能独立于调脂作用之外.
목적 관찰아탁벌타정대고혈압환자초민C반응단백(hs-CRP)、혈관성가혈우병인자(vWF)、P-선택소、저밀도지단백담고순(LDL-C)급경동맥내막-중층후도(IMT)적영향.방법 151례고혈압환자안치료방법분위3조,50례용10 mg아탁벌타정+안록지평+패나보리치료,61례용20mg아탁벌타정+안록지평+패나보리치료,대조조40례채용안록지평+패나보리치료;매3개월검측환자hs-CRP、LDL-C、vWF급P-선택소등지표변화.공관찰1년,병대결과진행통계학분석.결과 (1)10 mg화20 mg아탁벌타정조hs-CRP、LDL-C、vWF、P-선택소급IMT균교대조조하강,차이유통계학의의(P＜0.05);(2)상관분석현시hs-CRP등지표변화여LDL-C하강지간무상관관계.결론 아탁벌타정능구연완고혈압환자동맥죽양경화적발전,항동맥경화작용가능독립우조지작용지외.
Objective To identify the effects of atorvastatin on high-sensitivity C-reactive protein (hs-CRP), yon willebrand factor (vWF), P-selectin, low-density lipoprotein-cholesterol (LDL-C)and carotid intima-media thickness (IMT) of patients with essential hypertension. Methods One hundred and fifty-one patients with mild hypertension were randomly divided into 3 groups: 10 mg atorvastatin, amlodipine and benazepril were daily delivered to group A (n=50); 20 mg atorvastatin,amlodipine and benazepril were daily delivered to group B (n=61); and amlodipine and benazepril were daily delivered to control group (n=40). All patients were assessed for the levels of hs-CRP, vWF,P-selectin, LDL-C and IMT at the baseline and every 3 months. The observation period lasted for 1 y and statistical analysis was performed on these collected data. Results As compared with that in the control group, significant reduction was identified on the levels of hs-CRP, vWF, P-selectin, LDL-C and IMT in group A and group B (P＜0.05). Correlation analysis discovered that the changes of levels of hs-CRP, VWF, P-selectin and IMT did not correlate with the reduction of LDL-C. Conclusion The progression of atherosclerosis can be delayed by atorvastatin in patients with hypertension, which is probably independent from its lipid-lowering function.