Wojtkowska Izabela, Bonda Tomasz A, Tysarowski Andrzej, Seliga Katarzyna, Siedlecki Janusz A, Winnicka Maria M, Stępińska Janina
Institute of Cardiology, Intensive Cardiac Therapy Clinic, Alpejska St., 04-628 Warsaw, Poland.
Medical University of Bialystok, Department of General and Experimental Pathology, Mickiewicza 2c, 15-222 Bialystok, Poland.
PPAR Res. 2019 Jun 2;2019:1932036. doi: 10.1155/2019/1932036. eCollection 2019.
TNF and PPAR 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 (-308G>A) and (Pro12Ala) genes are associated with the risk of developing HF by patients with ischemic heart disease. . 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 -308G>A and 2 Pro12Ala polymorphisms were detected using the TaqMan method. . The distributions of -308G>A and 2 Pro12Ala did not differ between the HF and non-HF groups (-308G>A: 16% vs. 11.4% of alleles; Pro12Ala: 23.9% vs. 20.5% of alleles, respectively). IL-6 concentration in the plasma of 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, p<0.05; 12 months after CABG: 4.2 ± 3,9 vs. 1.4 ± 1.2, p<0.01, respectively). Both polymorphisms were not related to changes in the plasma TNF concentration or other parameters related to HF. . Our study did not reveal any correlation between the Pro12Ala and -308G>A polymorphisms and development of HF in patients with ischemic heart disease after coronary bypass grafting.
肿瘤坏死因子（TNF）和过氧化物酶体增殖物激活受体（PPAR）是代谢、炎症和动脉粥样硬化的重要调节因子。冠状动脉疾病是心力衰竭（HF）的主要原因。本研究的目的是评估TNF（-308G>A）和PPAR（Pro12Ala）基因多态性是否与缺血性心脏病患者发生HF的风险相关。122例确诊为冠状动脉疾病且符合冠状动脉搭桥手术条件的无HF患者（年龄63±8.8岁，85%为男性）纳入本研究。手术后，对他们进行心脏参数筛查。随访期间NT-proBNP升高或左心室射血分数降低的患者被分配到HF组（n=78），其余患者被分配到非HF组（n=44）。采用TaqMan方法检测TNF -308G>A和PPAR 2 Pro12Ala多态性。TNF -308G>A和PPAR 2 Pro12Ala在HF组和非HF组之间的分布无差异（-308G>A：等位基因分别为16%和11.4%；Pro12Ala：等位基因分别为23.9%和20.5%）。与非HF组相比，HF组冠状动脉搭桥术后1个月和12个月时A等位基因携带者血浆中白细胞介素-6（IL-6）浓度更高（冠状动脉搭桥术后1个月：5.3±3.4 vs. 3.1±2.9，p<0.05；冠状动脉搭桥术后12个月：4.2±3.9 vs. 1.4±1.2，p<0.01）。两种多态性均与血浆TNF浓度变化或其他与HF相关的参数无关。我们的研究未发现PPAR Pro12Ala和TNF -308G>A多态性与冠状动脉搭桥术后缺血性心脏病患者HF发生之间存在任何相关性。
