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首页> 外文期刊>PPAR research >PPARG2 Pro12Ala and TNFα -308GA Polymorphisms Are Not Associated with Heart Failure Development in Patients with Ischemic Heart Disease after Coronary Artery Bypass Grafting
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PPARG2 Pro12Ala and TNFα -308GA Polymorphisms Are Not Associated with Heart Failure Development in Patients with Ischemic Heart Disease after Coronary Artery Bypass Grafting

机译:PPARG2 Pro12Ala和TNFα-308g>多态性与冠状动脉旁路移植术后缺血性心脏病患者的心力衰竭发育无关

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摘要

TNFα and PPARγ are important modulators of metabolism, inflammation, and atherosclerosis. Coronary artery disease is the leading cause of heart failure (HF). The aim of the study was to assess whether polymorphisms of the TNFα (-308GA) and PPARG2 (Pro12Ala) genes are associated with the risk of developing HF by patients with ischemic heart disease. Methods. 122 patients without HF (aged 63 ± 8.8 years, 85% males) with confirmed coronary artery disease qualified for coronary bypass grafting were enrolled in the study. After the procedure, they were screened for cardiac parameters. Those with elevated NT-proBNP or diminished left ventricular ejection fraction during follow-up were assigned to the HF group (n=78), and the remaining ones to the non-HF group (n=44). The TNFα -308GA and PPARG2 Pro12Ala polymorphisms were detected using the TaqMan method. Results. The distributions of TNFα -308GA and PPARG2 Pro12Ala did not differ between the HF and non-HF groups (-308GA: 16% vs. 11.4% of alleles; Pro12Ala: 23.9% vs. 20.5% of alleles, respectively). IL-6 concentration in the plasma of TNFα A-allele carriers at months 1 and 12 after CABG was higher in the HF group compared to the non-HF group (1 month after CABG: 5.3 ± 3.4 vs. 3.1 ± 2.9, p0.05; 12 months after CABG: 4.2 ± 3,9 vs. 1.4 ± 1.2, p0.01, respectively). Both polymorphisms were not related to changes in the plasma TNFα concentration or other parameters related to HF. Conclusions. Our study did not reveal any correlation between the PPARG2 Pro12Ala and TNFα -308GA polymorphisms and development of HF in patients with ischemic heart disease after coronary bypass grafting.
机译:TNFα和PPARγ是新陈代谢,炎症和动脉粥样硬化的重要调节剂。冠状动脉疾病是心力衰竭(HF)的主要原因。该研究的目的是评估TNFα(-308g> A)和PPARG2(PRO12ALA)基因的多态性是否与缺血性心脏病患者发育HF的风险有关。方法。 122例没有HF(63±8.8岁,85%雄性)具有证实冠状动脉疾病的冠状动脉疾病的患者纳入该研究。过程后,它们被筛选用于心脏参数。在随访期间,具有升高的NT-proPnP或左心室喷射部分减少的那些,将其剩余的N = 78)分配给非HF组(n = 44)。使用Taqman方法检测TNFα-308g> A和PPARG2 Pro12Ala多态性。结果。 HF和非HF基团的TNFα-308g> A和PPARG2 Pro12A1的分布在-1M和非HF基团之间没有区别(-308g> A:16%与11.4%的等位基因; Pro12Ala分别:23.9%与20.5%的等位基因) 。与非HF组相比,HF组在HF组中的TNFαa-等位基因载体血浆中的IL-6浓度在HF组中较高(CABG后1个月:5.3±3.4与3.1±2.9,P < 0.05; CABG后12个月:4.2±3,9 vs.分别为1.4±1.2,P <0.01)。两种多态性与血浆TNFα浓度或与HF相关的其他参数的变化无关。结论。我们的研究未揭示PPARG2 Pro12Ala和TNFα-308g之间的任何相关性,冠状动脉旁路嫁接后缺血性心脏病患者的HF多态性和发育。

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