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The Oxidative Stress Hypothesis of Congestive Heart Failure*: Radical Thoughts

Susanna Mak, MD; Gary E. Newton, MD
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*From Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada.

Correspondence to: Gary E. Newton, MD, Division of Cardiology, Mount Sinai Hospital, 600 University Ave, Room 1604, Toronto, Ontario, M5G 1X5, Canada; e-mail: gary.newton@utoronto.ca



Chest. 2001;120(6):2035-2046. doi:10.1378/chest.120.6.2035
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There is extensive experimental evidence from in vitro and animal experiments that congestive heart failure (CHF) is a state of oxidative stress. Moreover, in animal models, the development of CHF is accompanied by changes in the antioxidant defense mechanisms of the myocardium as well as evidence of oxidative myocardial injury. This has led to the hypothesis that oxidative stress may be a mechanism of disease progression in CHF. Indeed, many patients consume antioxidant supplements making the assumption that no harm will result and, possibly, that this therapy will yield some clinical benefits. The focus of this review is to examine the oxidative stress hypothesis of CHF as it pertains to humans. To date, human studies that have sought evidence for a role of oxidative stress in patients with CHF have fallen short of providing strong support for this hypothesis. Studies that have demonstrated an association between oxidant stress and CHF are small and are hindered by methodologic limitations that diminish the impact of their conclusions. Randomized trials of antioxidant supplementation for CHF are scarce, and to our knowledge no study yet convincingly demonstrates any benefit from consuming antioxidant supplements. Therefore, the available evidence is insufficient to support or negate the oxidative stress hypothesis of CHF and the use of antioxidants cannot be recommended as a specific therapy for this condition.

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