Various studies have evaluated the antioxidant effects of vitamin E in the
prevention or treatment of coronary artery disease (CAD). In vitro data sug
gest that vitamin E protects against oxidation of low-density lipoprotein a
nd 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 suppl
ementation (400 or 800 IU/d), demonstrated a decrease in the combined end p
oint of nonfatal myocardial infarction and cardiovascular death in patients
with established CAD. Discordant data, however, have been published that i
mply 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 l
ong-term adverse effects. If vitamin E supplementation is initiated, the li
terature suggests dosages of 100 to 400 IU/d, with the higher dosage consid
ered in patients with documented CAD. Additional investigation is warranted
to further define the role of vitamin E supplementation in CAD and to crit
ically evaluate the optimal dosage, duration of use, and method of consumpt
ion (dietary vs supplemental).