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Allopurinol as a cardiovascular drug.
Cardiol Rev. 2011 Nov-Dec; 19(6):265-71.CR

Abstract

Cardiovascular disease (CVD) remains the leading cause of death in the United States. There is evidence that shows a direct relationship between an elevated uric acid level and an increased risk of cardiovascular (CV) events, which has set the foundation for the investigation of uric acid-lowering drugs for the treatment of CVD. Although traditionally the cornerstone therapy for gout, allopurinol's ability to be a competitive inhibitor of the key enzyme, xanthine oxidase, needed for uric acid formation, has prompted recent clinical research evaluating allopurinol as a CV drug. Epidemiologic and biochemical studies on uric acid formation have shown that it is not only uric acid itself that leads to worsening prognosis and increased CV events, but also the free radicals and superoxides formed during xanthine oxidase activity. The combination of uric acid formation and formed free radicals could ultimately lead to coronary endothelial dysfunction and worsening of myocardial oxidative stress. Along with preventing uric acid formation, allopurinol also has the ability to behave as a free radical scavenger of the superoxide anions and free radicals released during uric acid formation.Clinical studies have shown that allopurinol improves endothelial dysfunction and subsequently improves the exercise capacity in patients diagnosed with angina pectoris. Allopurinol has also been shown to decrease oxidative stress and ameliorate the morbidity and mortality of congestive heart failure patients by possibly improving mechanoenergetic uncoupling, with the enhancement of myocardial contractility and the left ventricular ejection fraction. This review presents the pharmacologic action of allopurinol on the CV system and describes the effectiveness of allopurinol as a potential drug to treat 2 CVD morbidities: ischemic heart disease and congestive heart failure.

Authors+Show Affiliations

Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

21983313

Citation

Kelkar, Anita, et al. "Allopurinol as a Cardiovascular Drug." Cardiology in Review, vol. 19, no. 6, 2011, pp. 265-71.
Kelkar A, Kuo A, Frishman WH. Allopurinol as a cardiovascular drug. Cardiol Rev. 2011;19(6):265-71.
Kelkar, A., Kuo, A., & Frishman, W. H. (2011). Allopurinol as a cardiovascular drug. Cardiology in Review, 19(6), 265-71. https://doi.org/10.1097/CRD.0b013e318229a908
Kelkar A, Kuo A, Frishman WH. Allopurinol as a Cardiovascular Drug. Cardiol Rev. 2011 Nov-Dec;19(6):265-71. PubMed PMID: 21983313.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Allopurinol as a cardiovascular drug. AU - Kelkar,Anita, AU - Kuo,Allen, AU - Frishman,William H, PY - 2011/10/11/entrez PY - 2011/10/11/pubmed PY - 2012/2/9/medline SP - 265 EP - 71 JF - Cardiology in review JO - Cardiol Rev VL - 19 IS - 6 N2 - Cardiovascular disease (CVD) remains the leading cause of death in the United States. There is evidence that shows a direct relationship between an elevated uric acid level and an increased risk of cardiovascular (CV) events, which has set the foundation for the investigation of uric acid-lowering drugs for the treatment of CVD. Although traditionally the cornerstone therapy for gout, allopurinol's ability to be a competitive inhibitor of the key enzyme, xanthine oxidase, needed for uric acid formation, has prompted recent clinical research evaluating allopurinol as a CV drug. Epidemiologic and biochemical studies on uric acid formation have shown that it is not only uric acid itself that leads to worsening prognosis and increased CV events, but also the free radicals and superoxides formed during xanthine oxidase activity. The combination of uric acid formation and formed free radicals could ultimately lead to coronary endothelial dysfunction and worsening of myocardial oxidative stress. Along with preventing uric acid formation, allopurinol also has the ability to behave as a free radical scavenger of the superoxide anions and free radicals released during uric acid formation.Clinical studies have shown that allopurinol improves endothelial dysfunction and subsequently improves the exercise capacity in patients diagnosed with angina pectoris. Allopurinol has also been shown to decrease oxidative stress and ameliorate the morbidity and mortality of congestive heart failure patients by possibly improving mechanoenergetic uncoupling, with the enhancement of myocardial contractility and the left ventricular ejection fraction. This review presents the pharmacologic action of allopurinol on the CV system and describes the effectiveness of allopurinol as a potential drug to treat 2 CVD morbidities: ischemic heart disease and congestive heart failure. SN - 1538-4683 UR - https://www.unboundmedicine.com/medline/citation/21983313/Allopurinol_as_a_cardiovascular_drug_ L2 - https://doi.org/10.1097/CRD.0b013e318229a908 DB - PRIME DP - Unbound Medicine ER -