Heart failure is a common, costly, and debilitating syndrome that is associated with a highly complex drug regimen, a large number of comorbidities, and a large and often disparate number of healthcare providers. All of these factors conspire to increase the risk of heart failure exacerbation by direct myocardial toxicity, drug-drug interactions, or both. This scientific statement is designed to serve as a comprehensive and accessible source of drugs that may cause or exacerbate heart failure to assist healthcare providers in improving the quality of care for these patients.

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arious studies have evaluated the antioxidant effects of vitamin E in the prevention or treatment of coronary artery disease (CAD). In vitro data suggest that vitamin E protects against oxidation of low-density lipoprotein and decreases the deposition of atherogenic oxidized low-density lipoprotein in arterial walls. Various observational and epidemiological studies also suggest a relationship between vitamin E serum concentrations or intake and CAD. One prospective, randomized trial suggested that low-dosage vitamin E supplementation (50 IU/d) decreases the risk of angina in patients without previously diagnosed CAD. Another study, using high-dosage vitamin E supplementation (400 or 800 IU/d), demonstrated a decrease in the combined end point of nonfatal myocardial infarction and cardiovascular death in patients with established CAD. Discordant data, however, have been published that imply no cardiovascular benefit of low-dosage vitamin E supplementation (50 IU/d) and detrimental effects if vitamin E is combined with beta carotene. At this point, clinicians should emphasize a low-fat diet with high intake of fruits and vegetable sources containing vitamin E. Supplemental vitamin E may be considered in patients at high risk for CAD or with documented CAD, but the potential beneficial effects should be weighed against possible long-term adverse effects. If vitamin E supplementation is initiated, the literature suggests dosages of 100 to 400 IU/d, with the higher dosage considered in patients with documented CAD. Additional investigation is warranted to further define the role of vitamin E supplementation in CAD and to critically evaluate the optimal dosage, duration of use, and method of consumption (dietary vs supplemental).

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