Abstract 11870: The -174 G>C Interleukin-6 Gene Polymorphism is Associated With Angiographic Progression of Non-culprit Coronary Plaques in a Mid-term Period
Hypothesis: Inflammation is the key process underlying the course of CAD. Interleukin-6 (IL-6) is an upstream key regulator of inflammation. Single nucleotide polymorphisms (SNPs) of inflammatory genes, reportedly influence the outcomes of CAD patients. We sought to evaluate the impact of -174 G>C IL-6 SNP in patients with established CAD.
Methods: We examined previous angiographies of patients with a PCI history, who were prospectively re-investigated for stable/unstable angina after >12 months. We defined progression of CAD by qCA as the emergence of a new culprit lesion. We genotyped patients to their Mendelian randomization group of -174 G>C IL-6 SNP (rs1800795). The probability for CAD progression was evaluated with the Kaplan-Meier and Cox model analysis including age, hypertension, family history, dyslipidemia and diabetes.
Results: A total of 157 patients were included with a median follow-up time of 48 months. Genotype distribution was: GG: 30, CC: 55, GC: 72, C variant: 58%, frequencies were in Hardy-Weinberg equilibrium: χ2=0.54, p=0.46. Baseline characteristics were evenly distributed. Serum levels of IL-6 differed significantly: CC 5.58±2.52, GG 2.73±1.08, GC 4.04±1.86 mg/L, p<0.001. At 48 months, carriers of IL-6 C allele had 52.8% cumulative probability for progression vs 13.3% G allele, p=0.005. Results were confirmed in multivariate analysis: C allele HR: 5.09, 95% CI (1.55, 16.7), p=0.007, family history HR: 2.46, 95% CI (1.43, 4.23), p=0.001, dyslipidemia HR: 1.47, 95% CI (1.02, 2.11), p=0.041.
Conclusions: Patients with established CAD, carrying the -174 C allele of IL-6 gene, had increased risk for progression of non-culprit plaques in a 4-year period. C allele significantly contributed to CAD progression along with family history and dyslipidemia.
Author Disclosures: N. Anousakis-Vlachochristou: None. D. Klettas: None. K. Melidis: None. Z. Azilazian: None. M. Asimomiti: None. A. Karanasos: None. A. Spanos: None. E. Tsiamis: None. K. Toutouzas: None. P. Nihoyannopoulos: None. D. Tousoulis: None.
- © 2016 by American Heart Association, Inc.