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A Rationale for Antioxidant Use in Cardiovascular Disease

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Antioxidants and Cardiovascular Disease

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 233))

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Abstract

Free radicals contribute to the pathogenesis of both acute (ischemia-reperfusion injury) and chronic (atherosclerosis) cardiovascular diseases. Prospective epidemiological studies have demonstrated a strong inverse relationship between serum antioxidant levels and the number of adverse events associated with coronary artery disease. The mechanistic rationale for this antioxidant benefit can be attributed to the “oxidative-modification hypothesis”, a model that proposes that certain inflammatory processes associated with atherogenesis are triggered by free radical-induced modification of lipids associated with low density lipoproteins and vascular cell membranes. Oxidative stress is also an important feature of heart failure; increasing levels of serum malondialdehyde, a product of lipid peroxidation, can be correlated with severity of disease. In this review, the basic mechanisms by which free radicals effect cell injury and the potential role for compounds with antioxidant activity to intervene in these disease processes will be discussed.

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Mason, R.P. (2000). A Rationale for Antioxidant Use in Cardiovascular Disease. In: Tardif, JC., Bourassa, M.G. (eds) Antioxidants and Cardiovascular Disease. Developments in Cardiovascular Medicine, vol 233. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4375-2_10

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  • DOI: https://doi.org/10.1007/978-94-011-4375-2_10

  • Publisher Name: Springer, Dordrecht

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