@article{3173054,
    title = "The-174 G > C Interleukin-6 Gene Polymorphism is Associated with
Angiographic Progression of Coronary Artery Disease over a 4-Year Period",
    author = "Toutouzas, Konstantinos and Klettas, Dimitrios and and Anousakis-Vlachochristou, Nikolaos and Melidis, Konstantinos and and Azilazian, Zeta and Asimomiti, Maria and Karanasos, Antonios and Spanos, and Anastasios and Tsiamis, Eleftherios and Nihoyannopoulos, Petros and and Tousoulis, Dimitris",
    journal = "Ελληνική καρδιολογική επιθεώρηση",
    year = "2017",
    volume = "58",
    number = "1",
    pages = "80-86",
    publisher = "HELLENIC CARDIOLOGICAL SOC",
    issn = "1011-7970",
    doi = "10.1016/j.hjc.2017.02.002",
    keywords = "Coronary artery disease; inflammation; progression; interleukin-6; gene
polymorphisms; SNP",
    abstract = "Background: Inflammation is a key process underlying the clinical course
of coronary artery disease (CAD). C-reactive protein (CRP) and
interleukin-6 (IL-6) contribute to its pathophysiology and act as
biomarkers. We sought to examine whether known single nucleotide
polymorphisms (SNPs) impact CAD progression, reflecting increased
inflammation.
Methods: We retrospectively evaluated coronary angiographies of patients
with established CAD who were re-investigated for stable/unstable angina
after a time interval of > 12 months. We defined progression of CAD as
the emergence of a new plaque or a >= 20 % increase of a formerly
non-significant lesion. We genotyped patients for the 1846 C > T CRP and
-174 G > C IL-6 SNPs. The probability of CAD progression among the
Mendelian randomization groups was evaluated using the Kaplane-Meier
method. Data were analyzed using a Cox model that included relevant
clinical factors.
Results: A total of 157 patients were included. The serum levels of CRP
and IL-6 differed significantly between genotypes. The genotype
frequencies of IL-6 were consistent with Hardy -Weinberg equilibrium,
whereas those for CRP were excluded from our conclusions. At 48 months,
83 patients (52.9 %) with the IL-6 C allele versus 74 (47.1 %) with
the G allele exhibited CAD progression. Patients with the IL-6 C allele
had a 52.8 % probability for progression versus 13.3 % for those with
the G allele (p=0.005). The results were confirmed by multivariate
analysis; dyslipidemia, family history, and IL-6 SNP emerged as
significant factors.
Conclusion: Patients with established CAD who carried the -174 C allele
of the IL-6 gene demonstrated an increased risk for the progression of
coronary plaques over a four-year period. Further studies will be needed
to validate these findings. (c) 2017 Hellenic Society of Cardiology.
Publishing services by Elsevier B. V."
}