Abstract 3560: 8-hydroxy-2′-deoxyguanosine Predicts Adverse Clinical Outcomes in Patients With Heart Failure
Background: Oxidative stress due to reactive oxygen species (ROS) is thought to be a factor exacerbating heart failure. DNA in the nucleus is one of the major targets of ROS and oxidative DNA damage has been implicated in the pathogenesis of chronic heart failure. 8-hydroxy-2′-deoxyguanosine (8-OHdG) is produced from deoxyguanosine in DNA by hydroxyl free radicals. The purpose of this present study was to examine the clinical significance of serum 8-OHdG levels in patients with heart failure.
Methods: Serum 8-OHdG levels were measured in 247 patients who were hospitalized for congestive heart failure (CHF) and 40 control subjects without CHF. They were followed-up for 591±451 days with the end points of cardiac death and re-hospitalization due to progressive heart failure.
Results: Serum 8-OHdG levels increased with advancing New York Heart Association (NYHA) functional class (NYHA I: 0.32±0.14, II: 0.39±0.19, III: 0.37±0.17, IV: 0.59±0.42 ng/ml, P<0.0001). Normal upper limit of 8-OHdG level was determined as mean + 2SD value from 40 control subjects (0.35 ng/ml). Abnormally high serum 8-OHdG levels (>0.35 ng/ml) were observed in 29.8%, 44.3%, 39.7%, and 66.7% through NYHA I to IV (P<0.001). The serum 8-OHdG level was higher in the cardiac event group than event free group (0.47±0.34 vs. 0.36±0.19 ng/ml, P=0.0022). Kaplan-Meier survival curves demonstrated that the cardiac event rate was higher in the high serum 8-OHdG group than in the normal serum 8-OHdG level group (42.2% vs. 24.6%, P=0.0426).
Conclusion: Elevation of serum 8-OHdG level predicts adverse clinical outcomes in patients with CHF.