Uric acid in chronic heart failure.
The pathophysiologic understanding of chronic heart failure (CHF) has shifted from a mere hemodynamic disorder to a much more complex approach including changes and imbalances in neurohormonal, immune, and metabolic functions. Among metabolic abnormalities, hyperuricemia is a constant finding in CHF. The xanthine oxidase metabolic pathway increasingly is appreciated as an important contributor to both symptoms of CHF as well as progression of the disease. Recent data suggest hyperuricemia to be an independent marker of impaired prognosis in CHF. In this article, the significance of the xanthine oxidase metabolic pathway in CHF is discussed. Data on xanthine oxidase inhibition are reviewed, which suggest a beneficial effect of therapeutically targeting this enzymatic pathway.
Doehner
Wolfram
W
Division of Applied Cachexia Research, Department of Cardiology, Charite Medical School, Humboldt University, D-13353 Berlin, Germany. w.doehner@imperial.ac.uk
Anker
Stefan D
SD
D000493:Allopurinol / Q000627:therapeutic use; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001783:Blood Flow Velocity / Q000502:physiology; D001808:Blood Vessels / Q000378:metabolism / Q000503:physiopathology; D002908:Chronic Disease; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D006333:Heart Failure / Q000097:blood / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D033461:Hyperuricemia / Q000097:blood / Q000150:complications / Q000503:physiopathology; D011379:Prognosis; D014527:Uric Acid / Q000097:blood*; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors / Q000097:blood
D015415:Biomarkers; D004791:Enzyme Inhibitors; D014527:Uric Acid; D000493:Allopurinol; D014969:Xanthine Oxidase