Abstract

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 (-308G>A) 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 -308G>A and PPARG2 Pro12Ala polymorphisms were detected using the TaqMan method. Results. The distributions of TNFα -308G>A and PPARG2 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 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, 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 TNFα concentration or other parameters related to HF. Conclusions. Our study did not reveal any correlation between the PPARG2 Pro12Ala and TNFα -308G>A polymorphisms and development of HF in patients with ischemic heart disease after coronary bypass grafting.

Highlights

  • Coronary heart disease (CHD) plays a critical role in the development of heart failure (HF)

  • The plasma levels of tumor necrosis factor α (TNFα) and IL-6 were not related to the PPARG or TNF polymorphisms before coronary artery bypass surgery (CABG) and during follow-up

  • Plasma IL-6 concentration was higher before CABG, subsequently decreased one month after the procedure, and remained at a stable level in both the HF and non-HF groups irrespective of the TNFα and PPARG genotype (p

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Summary

Introduction

Coronary heart disease (CHD) plays a critical role in the development of heart failure (HF). Progression of atherosclerosis is the main reason for development of CHD and is influenced by numerous factors such as high plasma LDL cholesterol concentration, blood glucose level, inflammation, and oxidative stress [1]. There has been a growing interest in the link between PPAR gene polymorphisms, including PPARA intron 7G/C, PPARD +294T/C, PPARG Pro12Ala and C161T, and CHD risk [3,4,5,6,7,8], but data from these single studies have not provided consistent results. Meta-analyses including large populations have not provided any clear evidence for association between PPAR polymorphisms and coronary artery disease [9,10,11].

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