A total of 503 CHD patients (457 nonhypoxemic and 46 hypoxemic) and 772 control patients fulfilled inclusion criteria. Demographic, clinical, and analytical data [serum
uric acid and 24h urine
uric acid levels, N-terminal pro-
B-type natriuretic peptide (NT-pro-BNP), and
C-reactive-protein (CRP) concentrations] were studied. Survivals curves to determine
cardiac death and arterial
thrombosis in CHD patients were also examined.
RESULTS: Noncyanotic and cyanotic CHD patients had significant higher serum
uric acid concentration (5.2 ± 1.5 vs 4.9 ± 1.3mg/dL, P = .007 and 6.7 ± 2.1 vs 4.9 ± 1.3mg/dL, P < .001, respectively) and
gout (1% vs 0%, P = .003 and 4% vs 0%, P < .01, respectively) than the control population. Among CHD patients, hyperuricemic patients were significant older and with
overweight, used more
diuretics, were more cyanotic and had higher serum
creatinine, NT-pro-BNP and CRP concentrations than nonhyperuricemic. In the multivariable analysis, the body mass index (BMI) (OR 1.09; 95% CI 1.01-1.18),
cyanosis (OR 6.2; 95 CI 1.5-24.6), serum
creatinine concentration (OR 49; 95% CI 44-538), and being under
diuretic treatment (OR 4.5; 95% CI 1.4-14.5) proved to be risk factors for
hyperuricemia in CHD patients. The Kaplan-Meier events free survival curves, during a 5.2 ± 2.7 years follow-up of up time, showed that hyperuricemic CHD patients had significant higher cardiovascular death (P = .002). However, after applying the Cox regression analysis
uric acid levels lost its statistical significance. No significant differences were seen in relation to thrombotic events between CHD patients with and without
hyperuricemia.
CONCLUSIONS: