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Disease Markers
Volume 2015 (2015), Article ID 232048, 7 pages
Research Article

The Relation between eNOS −786 C/T, 4 a/b, MMP-13 rs640198 G/T, Eotaxin 426 C/T, −384 A/G, and 67 G/A Polymorphisms and Long-Term Outcome in Patients with Coronary Artery Disease

1Department of Internal Medicine/Cardioangiology and ICRC, St. Anne’s University Hospital, Faculty of Medicine, Masaryk University, Pekařská 53, 656 91 Brno, Czech Republic
2Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, 625 00 Brno, Czech Republic

Received 17 March 2015; Revised 3 July 2015; Accepted 13 September 2015

Academic Editor: Mariann Harangi

Copyright © 2015 Vladimír Kincl et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aim. The purpose of this study is to determine the association between eotaxin 426 C/T, −384 A/G, 67 G/A, eNOS −786 T/C, 4 a/b, and MMP-13 rs640198 G/T and prognosis of patients with known CAD. Methods. From total of 1161 patients referred to coronary angiography, 532 patients with angiographically confirmed CAD were selected. Their long-term outcome was followed up using hospital database. Subsequent events were assessed in this study: death or combined endpoint-myocardial infarction, unstable angina pectoris, revascularization, heart failure hospitalization, and cardioverter-defibrillator implantation. Results. The multivariate Cox regression model identified age, smoking, and 3-vessel disease as significant predictors of all-cause death. Further analysis showed that eotaxin 67 G/A (GA + AA versus GG) and eotaxin −384 A/G (GG versus GA + AA) were significant independent prognostic factors when added into the model: HR (95% CI) 2.81 (1.35–5.85), ; HR (95% CI) 2.63 (1.19–5.83), ; eotaxin −384 A/G was significantly associated with the event-free survival, but it did not provide the prognostic information above the effect of two- or three-vessel disease. Conclusion. The A allele in eotaxin 67 G/A polymorphism is associated with worse survival in CAD patients.