OBJECTIVE: Uric acid (UA) levels are frequently increased in patients with heart failure (HF), and may be an indicator of a poor prognosis and an innovative target for treatment. We evaluated the effect of UA and allopurinol use on clinical outcome in patients with HF. METHODS AND RESULTS: We evaluated patients with a diagnosis of HF at a Health Maintenance Organization (n = 6204). Patients were followed for cardiac-related hospitalizations and death. Mean UA levels were 6.5 ± 1.9 mg/dL. Median follow-up was 498 days. We divided patients into quartiles of serum UA; 22.6% (n = 1,568) were in the highest UA level quartile (>7.7 mg/dL). Cox regression analysis after adjustment for significant predictors including age, sex, ischemic heart disease, hypertension, atrial fibrillation, body mass index, hemoglobin, sodium, estimated glomerular filtration rate, urea levels, standard HF drug therapies, and allopurinol demonstrated that high UA levels (>7.7 mg/dL) were a predictor of increased mortality (hazard ratio [HR] 1.37, 95% confidence interval [CI] 1.17-1.60; P < .0001) and increased cardiac hospitalizations (HR 1.10, 95% CI 1.01-1.22; P < .05). An increase in UA levels during follow-up was also an independent predictor of mortality (HR 1.46, 95% CI 1.25-1.71; P < .00001) and cardiac hospitalizations (HR 1.15, 95% CI 1.06-1.23; P < .00001). Treatment with allopurinol was independently associated with improved survival (HR 0.79, 95% CI 0.64-0.98; P < .05). Echocardiographic data demonstrated a significant correlation between UA levels and E/A ratio, a marker of diastolic dysfunction. CONCLUSIONS: Increased UA levels and an increase in UA during follow-up were independent predictors of increased morbidity and mortality. Treatment with allopurinol was associated with improved survival.
OBJECTIVE:Uric acid (UA) levels are frequently increased in patients with heart failure (HF), and may be an indicator of a poor prognosis and an innovative target for treatment. We evaluated the effect of UA and allopurinol use on clinical outcome in patients with HF. METHODS AND RESULTS: We evaluated patients with a diagnosis of HF at a Health Maintenance Organization (n = 6204). Patients were followed for cardiac-related hospitalizations and death. Mean UA levels were 6.5 ± 1.9 mg/dL. Median follow-up was 498 days. We divided patients into quartiles of serum UA; 22.6% (n = 1,568) were in the highest UA level quartile (>7.7 mg/dL). Cox regression analysis after adjustment for significant predictors including age, sex, ischemic heart disease, hypertension, atrial fibrillation, body mass index, hemoglobin, sodium, estimated glomerular filtration rate, urea levels, standard HF drug therapies, and allopurinol demonstrated that high UA levels (>7.7 mg/dL) were a predictor of increased mortality (hazard ratio [HR] 1.37, 95% confidence interval [CI] 1.17-1.60; P < .0001) and increased cardiac hospitalizations (HR 1.10, 95% CI 1.01-1.22; P < .05). An increase in UA levels during follow-up was also an independent predictor of mortality (HR 1.46, 95% CI 1.25-1.71; P < .00001) and cardiac hospitalizations (HR 1.15, 95% CI 1.06-1.23; P < .00001). Treatment with allopurinol was independently associated with improved survival (HR 0.79, 95% CI 0.64-0.98; P < .05). Echocardiographic data demonstrated a significant correlation between UA levels and E/A ratio, a marker of diastolic dysfunction. CONCLUSIONS: Increased UA levels and an increase in UA during follow-up were independent predictors of increased morbidity and mortality. Treatment with allopurinol was associated with improved survival.
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