Combined Endpoint Myocardial Infarction Research Articles

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), p = 0.006; HR (95% CI) 2.63 (1.19–5.83), p = 0.017; 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.