薛 强,光雪峰,张伟华,戴海龙,鲁一兵,杨 栋,卢 静.急性冠脉综合征合并低密度脂蛋白胆固醇基线低水平患者短期中等强度阿托伐他汀治疗的冠脉斑块消退效应[J].现代生物医学进展英文版,2018,(18):3533-3537. |
急性冠脉综合征合并低密度脂蛋白胆固醇基线低水平患者短期中等强度阿托伐他汀治疗的冠脉斑块消退效应 |
Efficacy of Short-term Moderate-intensity Atorvastatin on Coronary Plaque Regression in Acute Coronary Syndrome patients with Low Baseline Low-density Lipoprotein Cholesterol Level |
Received:April 08, 2018 Revised:April 30, 2018 |
DOI:10.13241/j.cnki.pmb.2018.18.030 |
中文关键词: 急性冠脉综合征(ACS) 低密度脂蛋白胆固醇(LDL-C) 血管内超声导管(IVUS) 阿托伐他汀 斑块消退 |
英文关键词: Acute coronary syndrome Low-density lipoprotein cholesterol Intravascular ultrasound Atorvastatin Plaque regression |
基金项目:云南省自然科学基金项目(2017FE467(-199)) |
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中文摘要: |
摘要 目的:评估短期中等剂量序贯长期低剂量阿托伐他汀治疗急性冠脉综合征(Acute Coronary Syndrome,ACS)合并低密度脂蛋白胆固醇(Low-density Lipoprotein Cholesterol, LDL-C)基线低水平患者冠脉斑块消退效应,使用血管内超声(Intravascular Ultra- sound, IVUS)为斑块消退评估依据。方法:2014年1月至2016年12月在昆明医科大学附属延安医院接受IVUS指导下经皮冠脉介入治疗(Percutaneous Coronary Intervention,PCI)的ACS合并LDL-C基线低水平患者随机分组为中等剂量阿托伐他汀(20 mg/d)治疗3个月序贯低剂量阿托伐他汀(10 mg/d)治疗9月组与初始低剂量阿托伐他汀(10 mg/d)治疗12月组。分别测定基线、治疗后1、3、6、12月血脂,术后1年复查冠脉造影及IVUS,选取中度非罪犯冠脉斑块进行消退效应研究,并收集相关临床数据进行定量分析。结果:研究入选56例患者,51例患者完成研究。2组患者年龄、性别、LDL-C等基线资料无统计学差异。治疗1、3、6、12月,两组 (Total Cholesterol, TC)、LDL-C均有不同程度下降(P<0.05),(High Density Lipoprotein Cholesterol,HDL-C)不同程度升高(P<0.05),TC、HDL-C组间无差异,3月后序贯治疗组LDL-C水平明显低于单一治疗组(P<0.05)。序贯治疗组(Triglyc- eride,TG)治疗12月出现有统计学意义降低(P<0.05),单一治疗组TG降低无统计学差异。序贯治疗组冠脉斑块容积减少明显优于单一治疗组(P<0.05),斑块容积减少及斑块容积减少百分比分别为2.68±2.25&1.14±1.99(mm3)、34.60±30.37&11.73±20.71(%)。Logistic回归显示LDL-C降低与阿托伐他汀序贯治疗是斑块消退的重要决定因素。结论:短期中等强度序贯长期低强度阿托伐他汀治疗和长期低强度阿托伐他汀治疗均可导致ACS合并LDL-C低基线水平患者冠状动脉斑块消退,而前者效果优于后者。 |
英文摘要: |
ABSTRACT Objective: To detect effects of short-term moderate-intensity followed by long-term low-intensity atorvastatin on re- gression of coronary plaque using intravascular ultrasound (IVUS) in patients with acute coronary syndrome (ACS) and low baseline Low-density Lipoprotein Cholesterol (LDL-C) level. Methods: The ACS patients with low baseline LDL-C level who underwent percuta- neous coronary intervention(PCI) under IVUS guidance were randomized to receive moderate-intensity atorvastatin (20 mg/d) for 3 months followed by low-intensity atorvastatin (10 mg/d) for 9 months group or the initial low-intensity atorvastatin (10 mg/d) for 12 months group during the period from January 2014 to December 2016 in the Affiliated Yan'an Hospital of Kunming Medical University. Lipid levels were measured at baseline, 1, 3, 6, and 12 months after treatment, meanwhile coronary angiography and IVUS were per- formed again 1 year after PCI. The regression effect was conducted on the moderate non-culprit coronary plaques. The clinical data were entirely collected and quantitatively analyzed. Results: 56 patients were overall enrolled and randomly assigned to the sequential therapy group and the monotherapy group, 51 cases finally completed the study. None of statistical differences in baseline data such as age, sex, LDL-C, was found between the two groups. After treatment of 1, 3, 6, 12 months, total cholesterol (TC) and LDL-C differently decreased in both groups (P<0.05), high- density lipoprotein cholesterol(HDL-C) differently raised (P<0.05). No statistical difference existed in TC and HDL-C between two groups. The LDL-C level of the sequential therapy group was significantly lower than that of the monotherapy group 3 months later (P<0.05). The decrease of triglyceride in the sequential therapy group had statistical difference after 12 months of treatment (P<0.05), however that in the monotherapy group had no statistical difference. The reduction of plaque volume induced by the sequential therapy group was significantly larger than the monotherapy group (P<0.05). Mean change in plaque volume and mean per- centage change in plaque volume were 2.68±2.25&1.14±1.99(mm3), 34.60±30.37&11.73±20.71(%) in both groups respectively. Lo- gistic regression indicated that LDL-C reduction and atorvastatin sequential therapy were significant determinants of coronary regression. Conclusion: The sequential therapy of short-term moderate-intensity followed by long-term low-intensity atorvastatin and the monother- apy of long-term low-intensity atorvastatin can induce regression of coronary plaque in ACS patients with low baseline LDL-C level, whereas the former is superior to the latter. |
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