Impact of Oxypurinol in Patients With Symptomatic Heart FailureResults of the OPT-CHF Study
Joshua M. Hare, MD*,*,
Brian Mangal, MSc ,
Joanne Brown, BSc,
Charles Fisher, Jr, MD,
Ronald Freudenberger, MD ,
Wilson S. Colucci, MD ,
Douglas L. Mann, MD||,
Peter Liu, MD¶,
Michael M. Givertz, MD#,
Richard P. Schwarz, PhD* for the OPT-CHF Investigators
* The University of Miami Miller School of Medicine, Miami, Florida
Cardiome Pharma Corporation, Vancouver, British Columbia, Canada
Robert Wood Johnson University Hospital, New Brunswick, New Jersey
Boston University, Boston, Massachusetts
|| Baylor Heart Clinic, Houston, Texas
¶ Toronto General Hospital, Toronto, Ontario, Canada
# Brigham & Women's Hospital, Boston, Massachusetts.
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Figure 1 Impact of Oxypurinol on the CCE
As depicted, randomization to oxypurinol failed to increase the proportion of patients improving according to the composite categorization. CCE = composite clinical end point.
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Figure 2 Impact of Oxypurinol on SUA
Serum uric acid (SUA) was measured at monthly intervals throughout the 6-month follow-up period. As depicted, oxypurinol effectively lowered SUA by approximately 2 mg/dl, and this effect was evident within 1 month of therapy. *Indicates p < 0.0001 versus placebo and is based on a repeated measures mixed model with baseline as a covariate and change from baseline as the dependent variable.
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Figure 3 Impact of Oxypurinol on the CCE in High and Low SUA Subgroups
p = 0.02 for interaction between high and low serum uric acid (SUA) groups. CCE = composite clinical end point.
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Figure 4 Scatterplot of Baseline SUA to Final SUA by Outcome
Overall, the oxypurinol-treated group had improved final serum uric acid (SUA) compared with their baseline SUA levels when evaluated against the placebo group.
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Figure 5 Degree of SUA Reduction in Patients With Low and High SUA
As depicted, the degree of serum uric acid (SUA) reduction was greatest in treated patients classified as improved or unchanged with high baseline SUA. *p < 0.05 versus worsened group.
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