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Effect of interleukin-6 genetic variability on the pathophysiology of atherosclerosis and the risk for coronary artery disease and myocardial infarction

Session Poster session 2

Speaker Evangelos Oikonomou

Event : ESC Congress 2014

  • Topic : coronary artery disease, acute coronary syndromes, acute cardiac care
  • Sub-topic : Coronary Artery Disease (Chronic)
  • Session type : Poster Session

Authors : G Hatzis (Athens,GR), D Tousoulis (Athens,GR), N Papageorgiou (Athens,GR), A Antonopoulos (Athens,GR), A Miliou (Athens,GR), C Antoniades (Athens,GR), S Brili (Athens,GR), A Synetos (Athens,GR), E Oikonomou (Athens,GR), C Stefanadis (Athens,GR)

G. Hatzis1 , D. Tousoulis1 , N. Papageorgiou1 , A. Antonopoulos1 , A. Miliou1 , C. Antoniades1 , S. Brili1 , A. Synetos1 , E. Oikonomou1 , C. Stefanadis1 , 1University of Athens Medical School, 1st Cardiology Department, “Hippokration” Hospital - Athens - Greece ,

European Heart Journal ( 2014 ) 35 ( Abstract Supplement ), 315

Purpose: Interleukin-6 (IL-6) is an early marker of inflammatory activation, strongly related to the pathophysiology of coronary artery disease (CAD). The exact role of IL-6 gene on mechanisms of atherosclerosis remains unclear. In the present study we examined the impact of the G174C (rs1800795) genetic polymorphism of IL-6 gene promoter on inflammatory and thrombotic process, as well as on the extent of CAD in patients with stable angina pectoris.

Methods: We enrolled 405 patients with angiographically documented CAD and 295 healthy controls. Rs1800795 was estimated by PCR and digestion with SFA NI restriction enzyme. The endothelial function was determined with flow mediated dilation (FMD). High sensitivity C-reactive protein (hsCRP) (mg/l) and D-dimers (pg/l) were determined with immunonephelometry, while fibrinogen (fib) (mg/dl) with the Clauss method. IL-6 (pg/ml), TNF-a (pg/ml) and sCD40L (pg/ml) were assessed by ELISA.

Results: We have found that the C carriers compared to GG homozygotes had significantly higher levels of inflammatory markers not only in CAD (IL-6: 3.26±1.13 vs 2.01±0.87, TNF-a: 6.37±0.32 vs 4.80±0.53, hsCRP: 1.93±0.64 vs. 1.17±0.49, p<0.001 for all), but also in controls (IL-6: 1.69±0.4 vs. 0.94±0.31, TNF-a: 2.17±0.26 vs. 1.32±0.27, hsCRP: 1.17±0.49 vs. 0.79±0.39, p<0.001 for all). On the contrary, no significant effect was observed on coagulation markers in CAD patients (fibrinogen: 440.7±129.2 vs. 452.9±141.4, sCD40L: 1.61±1.90 vs. 2.29±1.71, D-dimers: 412.6±215.1 vs. 319.4±328.3, p=NS for all). In controls, although there was a marginally positive effect on fibrinogen levels (fibrinogen: 394.4±106.1 vs. 365.3±93.5, p=0.047) there was no effect in the rest of coagulation markers (sCD40L: 1.04±2.23 vs. 1.09±2.31, D-dimers: 284.9±195.3 vs. 288.1±214.6, p=NS for all). Moreover, the C allele demonstrated a detrimental effect on endothelial function compared to GG homozygotes in CAD patients (3.56±2.68% vs. 4.11±2.38%, p=0.003) and in controls (5.8±2.94% vs. 6.91±2.37%, p=0.02). Although rs1800795 did not affect either the risk for CAD [O.R=1.09, 95%C.I.(0.79-1.50), p=NS] or the risk for MI [O.R=1.07, 95%C.I.(0.71-1.64), p=NS), the C allele carriers were associated with significantly more extensive CAD, as assessed by the presence of 2 or 3 vessels diseased versus one compared to GG homozygotes [OR=2.03, 95%CI (1.3-3.34), p=0.03].

Conclusions: Our data suggest that the C allele of rs1800795 on IL-6 gene promoter significantly induces inflammatory processes and endothelial dysfunction, accelerating thus the atherosclerotic mechanisms in patients with already established CAD.

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