不同他汀类药物标准剂量对稳定性斑块的影响

目的探讨不同他汀类药物标准剂量对稳定性斑块的影响。方法入选经冠状动脉造影和血管内超声检查确定为稳定性斑块的135例患者，分为3组：辛伐他汀20mg组47例，阿托伐他汀20mg组45例，瑞舒伐他汀10mg组43例。随访3-6个月，观察给予不同他汀类药物标准剂量的3组血清低密度脂蛋白-胆固醇（10wdensitvlipoprotein-cholesterol，LDL—C）、高密度脂蛋白-胆固醇（highdensitylipoprotein—cholesterol，HDL．C）、高敏C反应蛋白（high—sensitivityC．reactionprotein，hs—CRP）浓度变化及斑块坏死核所占百分比、斑块体积的动态变化。结果3组血清LDL—C、HDL—C、hs．CRP浓度及斑块坏死核所占百分比、斑块体积的基线资料比较，差异无统计学意义（P〉0．05）。随访3-6个月后，他汀类药物标准剂量治疗的3组血清LDL．C浓度与基线相比均有明显下降，均达标（P〈0．01），且瑞舒伐他汀最优，阿托伐他汀其次，辛伐他汀最后（P均〈0．01）。辛伐他汀组血清HDL-C浓度与基线比较。差异无统计学意义（P〉0．05），但阿托伐他汀组、瑞舒伐他汀组明显高于基线，差异有统计学意义（P=0．001．P=0．048），且两组间比较，差异无统计学意义（P=0．852）。辛伐他汀组血清hs—CRP浓度与基线比较，差异无统计学意义（P〉0．05），但阿托伐他汀组、瑞舒伐他汀组明显低于基线，差异有统计学意义（P=0．015，P=0．025）．且两组间比较，差异无统计学意义（P=0．411）。通过血管内超声虚拟组织成像技术（intravascularuhrasound—virtualhistology，IVUS—vH）检测，斑块坏死核所占百分比在辛伐他汀组明显高于基线，差异有统计学意义（16．33％-＋15．38％眦7．87％-＋1．04％，P〈0．01）；阿托伐汀组治疗后与基线相比，斑块坏死核所占百分比明显减少，差异有统计学意义（6．64％±3．25％帆7．91％±1．27％，P=0．007）；瑞舒伐他汀组斑块坏死核所占百分比与基线相比，差异无统计学意义（P=0．133）。斑块体积在辛伐他汀组治疗前、后比较，差异无统计学意义（P=O．286）；但阿托伐他汀组、瑞舒伐他汀组斑块体积明显低于基线，差异有统计学意义[（28．65±10．77）mm。vs．（33．31±10．75）mm3，P=0．041；（30．69_＋8．12）mm3ys．（36．337-＋12．15）mm。，P=0．013]，且治疗后两组体积比较，差异有统计学意义（P=0．322）。结论不同种类他汀类药物标准剂量对稳定性斑块疗效不同：对于LDL—C，辛伐他汀、阿托伐他汀、瑞舒伐他汀标准剂量治疗后均可达标；阿托伐他汀、瑞舒伐他汀能升高HDL—C，降低hs—CRP；辛伐他汀无遏制斑块向不稳定进展的作用，阿托伐他汀有促进斑块稳定，逆转斑块的作用，瑞舒伐他汀可阻止斑块进展及逆转斑块的作用。

Influence of different statins in standard dose on stable plaques

Objectives To investigate the effect of different statins in standard dose in patients with stable plaques. Methods Consecutive 135 patients who underwent coronary arteriography （CAG） and intravascular uhrasound （IVUS） were randomly assigned to receive simvastatin 20 mg/d, atorvastatin 20 mg/d and rosuvastatin l0 mg/d treatments respectively after being defined with stable plaques （simvastatin group, n=47; atorvastatin group, n=45; rosuvastatin group, n=43）. The endpoints including serum concentrations of low density lipoprotein-cholesterol （LDL-C）, high density lipoprotein-cholesterol （HDL-C）, high-sensitivity C-reactive protein （hs-CRP）, necrosis and plaque volumes were assessed after three to six months. Results Serum concentrations of LDL-C, HDL-C, hs-CRP and percentages of necrosis, plaque volumes had no significant differences at baseline in all the groups （P〉0.05）. After 3-6 months of follow up, serum concentrations of LDL-C in the three groups compared with baseline were obviously decreased（P〈0.01）, and rosuvastatin was the most optimal, atorvastatin was the second and simvastatin was the third （P〈0.01）.Serum concentrations of HDL-C in simvastatin group had no differences before and after treatment （P〉0.05）, but in atorvastatin group and rosuvastatin group, they were significantly higher than those of baseline （P=0.001,P=0.048）, and there was no significant difference between the two groups （P=0.852）. Hs-CRP levels in simvastatin group had no significant difference before and after treatment （P〉0.05） ; but in atorvastatin group and rosuvastatin group, they were significantly higher than those of baseline （P=0.015,P=0.025）, and there was no significant differences between the two groups （P= 0.411）. According to the results of intravascular ultrasound-virtual histology （IVUS-VH）, the percentage of necrosis in simvastatin group became significantly higher than that at baseline （16.33%±15.38% vs. 7.87%±1.04%,P〈0.01）. Percentage of necrosis in atorvastatin group became obviously less than that at baseline （6.64%±3.25% vs.7.91%±1.27%,P=0.007）, and that in rosuvastatin group compared with baseline had no significant difference （P=0.133）. Plaque volumes in simvastatin group before and after treatment had no statistical difference （P=0.286）. But plaque volumes in atorvastatin group and rosuvastatin group were significantly lower than those at baseline [ （28.65± 10.77） mm3 vs. （33.31±10.75） mm3, P=0.041; （30.69±8.12） mm3 vs. （36.337±12.15） mm3,p=0.0131, and there was no significant difference in the two groups after treatment （P=0.322）. Conclusions The influences of different kinds of statins in standard dose on the treatment efficacy of stable plaques are different. For LDL-C, simvastatin, atorvastatin, rosuvastatin in standard dose can achieve up to the standard. Atorvastatin and rosuvastatin can increase HDL-C and lower hs-CRP. Simvastatin cannot inhibit the plaques become unstable; atorvastatin can promote plaque stability and reverse the role of plaques ; rosuvastatin can prevent plaque progression and dwindle plaques.