Interleukin-1B genotype modulates the improvement of coronary artery reactivity by lipid-lowering therapy with pravastatin: a placebo-controlled positron emission tomography study in young healthy men.
Interleukin-1B genotype modulates the improvement of coronary artery reactivity by lipid-lowering therapy with pravastatin: a placebo-controlled positron emission tomography study in young healthy men.
复制标题
Interleukin-1B 基因型通过普伐他汀降脂治疗调节冠状动脉反应性的改善：一项针对年轻健康男性的安慰剂对照正电子发射断层扫描研究。
DOI：
--
复制
发表时间：
2003
期刊：
影响因子：
--
通讯作者：
M. Hurme
中科院分区：
文献类型：
--
作者：
T. Lehtimäki;R. Laaksonen;T. Janatuinen;R. Vesalainen;P. Nuutila;K. Mattila;E. Ilveskoski;M. Luomala;P. Saikku;J. Knuuti;M. Hurme
白细胞介素1B(IL-1B)基因启动子-511位的多态性调节IL-1B水平、免疫和炎症反应以及可能的动脉粥样硬化形成。我们使用正电子发射断层扫描(PET)来研究冠脉反应性或其对普伐他汀的反应是否与IL-1B基因多态性有关。这项研究包括一项随机、双盲、安慰剂对照试验，包括两个治疗组：(I)普伐他汀(40毫克/天，n=14)和(Ii)安慰剂(n=20)，为期6个月(基线平均胆固醇5.5+/-0.8 mmol/L；年龄35+/-4岁)。用正电子发射计算机断层扫描(PET)测量静息状态和腺苷输注过程中的心肌血流量。在基线和治疗6个月后进行PET检查、血脂、IL-1β和C反应蛋白分析。采用聚合酶链式反应检测IL-1B基因分型。IL-1B等位基因2携带者(A2+)和非携带者(A2-)在基础心肌流量(ASMF)和腺苷刺激心肌流量(ASMF)方面无差异。关于ASMF和冠状动脉血流储备的变化，在随访期间，治疗组之间存在显著的IL-1B基因型交互作用(协方差分析，分别为P=0.028和P=0.002)。普伐他汀组IL-1B A2-组(n=7)ASMF增加18.0%，IL-1B A2+组ASMF降低2%(n=7)。与安慰剂接受者的基准值相比，没有明显的变化。治疗后，两组患者的血清总胆固醇和低密度脂蛋白胆固醇均有相似的下降(P<；均为0.0001)。总而言之，携带IL-1B A2-等位基因的受试者服用普伐他汀6个月后冠状动脉功能改善，但携带IL-1B A2+等位基因的受试者冠状动脉功能改善不明显。
A polymorphism at position -511 of interleukin-1B (IL-1B) gene promoter regulates IL-1B levels, immune and inflammatory responses and possible atherogenesis. We used positron emission tomography (PET) to study whether coronary reactivity or its response to pravastatin is related to this IL-1B polymorphism. The study comprised a randomized, double-blind, placebo-controlled trial with two treatment groups: (i) pravastatin (40 mg/day, n=14) and (ii) placebo (n=20) for 6 months (baseline mean cholesterol 5.5 +/- 0.8 mmol/l; age 35 +/- 4 years). Myocardial blood flow was measured by PET at rest and during adenosine infusion using 15O-labelled water. PET studies, lipid, IL-1beta and C-reactive protein analyses were performed at baseline and after 6 months of therapy. IL-1B genotype was determined by polymerase chain reaction. There were no differences between IL-1B allele 2 carriers (A2+) and non-carriers (A2-) in basal or adenosine-stimulated myocardial flow (ASMF), at baseline. Regarding the change in ASMF and coronary flow reserve, there was a significant IL-1B genotype-by-treatment group interaction (analysis of covariance, P=0.028 and P=0.002, respectively) during follow-up. In the pravastatin group, the ASMF increased by 18.0% in subjects with IL-1B A2- (n=7), but decreased by 2% in subjects with IL-1B A2+ (n=7). There were no significant changes from the baseline values in placebo recipients. After treatment, both genotype groups showed a similar decrease in serum total and low density lipoprotein cholesterol (P<0.0001 for both). In conclusion, coronary function improves after 6 months of pravastatin therapy in subjects with the IL-1B A2- allele but not in those with the IL-1B A2+ allele.
影响因子：
56.9
作者：
BROWN, MS;GOLDSTEIN, JL
通讯作者：
GOLDSTEIN, JL
影响因子：
158.5
作者：
TREASURE, CB;KLEIN, JL;ALEXANDER, RW
通讯作者：
ALEXANDER, RW