Background Observational and experimental studies suggest thatthe amount of vitamin E ingested in food and in supplementsis associated with a lower risk of coronary heart disease andatherosclerosis.
Methods We enrolled a total of 2545 women and 6996 men 55 yearsof age or older who were at high risk for cardiovascular eventsbecause they had cardiovascular disease or diabetes in additionto one other risk factor. These patients were randomly assignedaccording to a two-by-two factorial design to receive either400 IU of vitamin E daily from natural sources or matching placeboand either an angiotensin-converting–enzyme inhibitor(ramipril) or matching placebo for a mean of 4.5 years (theresults of the comparison of ramipril and placebo are reportedin a companion article). The primary outcome was a compositeof myocardial infarction, stroke, and death from cardiovascularcauses. The secondary outcomes included unstable angina, congestiveheart failure, revascularization or amputation, death from anycause, complications of diabetes, and cancer.
Results A total of 772 of the 4761 patients assigned to vitaminE (16.2 percent) and 739 of the 4780 assigned to placebo (15.5percent) had a primary outcome event (relative risk, 1.05; 95percent confidence interval, 0.95 to 1.16; P=0.33). There wereno significant differences in the numbers of deaths from cardiovascularcauses (342 of those assigned to vitamin E vs. 328 of thoseassigned to placebo; relative risk, 1.05; 95 percent confidenceinterval, 0.90 to 1.22), myocardial infarction (532 vs. 524;relative risk, 1.02; 95 percent confidence interval, 0.90 to1.15), or stroke (209 vs. 180; relative risk, 1.17; 95 percentconfidence interval, 0.95 to 1.42). There were also no significantdifferences in the incidence of secondary cardiovascular outcomesor in death from any cause. There were no significant adverseeffects of vitamin E.
Conclusions In patients at high risk for cardiovascular events,treatment with vitamin E for a mean of 4.5 years has no apparenteffect on cardiovascular outcomes.
Oxidative modification of low-density lipoprotein is an importantstep in the development and progression of atherosclerosis inexperimental studies,1,2 and antioxidants such as vitamin Ehave been shown to slow atherosclerosis.3,4,5 An inverse relationhas been observed between coronary heart disease and the consumptionof fruits, vegetables, and other foods containing vitamins,particularly vitamin E.6,7,8,9 Observational studies have indicatedthat persons who consume more than 100 IU of vitamin E a dayfor more than two years have lower rates of coronary events10,11and lower rates of progression of coronary artery lesions.12However, observational studies cannot distinguish whether thelower risk of coronary heart disease associated with higherlevels of vitamin E consumption is due to the vitamin or toother associated lifestyle factors such as increased exerciseand other aspects of diet. There have been four randomized,controlled trials of the relation between vitamin E and coronaryheart disease,13,14,15,16 but their results are conflicting,perhaps because of the low doses of vita-min E used in somestudies,13,14 the small numbers of events,15 or the limitedduration of treatment.15,16
We evaluated a high dose (400 IU per day) of vitamin E fromnatural sources, which has high bioavailability, in a large,five-year, prospective study of patients at high risk for cardiovascularevents. The primary outcome was a composite of myocardial infarction,stroke, and death from cardiovascular causes. The secondaryoutcomes included death from any cause, hospitalization forunstable angina or congestive heart failure, revascularizationor limb amputation, complications of diabetes, and cancer. Thetrial was also designed to evaluate the effects of an angiotensin-converting–enzymeinhibitor, ramipril, on the incidence of cardiovascular events.After nearly 4.5 years of follow-up, the collection of dataon cardiovascular disease was stopped in April 1999 on the basisof a finding by the independent data and safety monitoring boardthat the trial had conclusively demonstrated the benefits oframipril and a lack of effect of vitamin E on cardiovascularevents. This report presents our findings relating to the effectsof vitamin E on the primary and secondary cardiovascular outcomes.The study has been continued in the majority of centers to evaluatethe effects of vitamin E on the incidence of cancer.
Methods
Study Design
The Heart Outcomes Prevention Evaluation (HOPE) Study is a double-blind,randomized trial with a two-by-two factorial design, conductedto evaluate the effects of ramipril and vitamin E in 9541 patientsat high risk for cardiovascular events. The results of the comparisonof ramipril with placebo are reported in a companion article.17Details of the methods are given in that article17 and in apreviously published article.18 Briefly, eligible patients athigh risk were randomly assigned to receive either 400 IU ofvitamin E from natural sources or an equivalent placebo dailyfor 4 to 6 years (mean, 4.5) and in addition to receive either10 mg of ramipril or an equivalent placebo daily. Patients wereevaluated every six months for a variety of outcomes.
Outcomes
The primary outcome was a composite of myocardial infarction,stroke, and death from cardiovascular causes. Deaths classifiedas due to cardiovascular causes were unexpected deaths presumedto be due to ischemic cardiovascular disease and occurring within24 hours after the onset of symptoms without clinical or postmortemevidence of another cause; deaths from myocardial infarctionor stroke that occurred within seven days after the myocardialinfarction or stroke; and deaths from congestive heart failure,dysrhythmia, pulmonary embolism, or ruptured abdominal aorticaneurysm. Deaths for which the cause was uncertain were presumedto be due to cardiovascular disease. Myocardial infarction wasdiagnosed when two of the following three criteria were met:typical symptoms, increased cardiac enzyme levels (at leasttwice the upper limit of normal), and diagnostic electrocardiographicchanges. Stroke was defined as a neurologic deficit lastingmore than 24 hours. A computed tomographic or magnetic resonanceimaging examination was recommended to define the type of stroke.
Secondary and other outcomes were death from any cause; unstableangina, defined as worsening angina or angina at rest requiringhospitalization; hospitalization for heart failure with clinicaland radiologic signs of congestion; revascularization or limbamputation; the development of overt nephropathy or the needfor dialysis or laser therapy among patients with diabetes;and the development of heart failure or new or worsening anginaregardless of the need for hospitalization.
Results
Characteristics of the Patients
The characteristics of the 9541 patients are shown in Table 1.The rate of compliance with the assigned regimen was highthroughout the study. The percentages of patients who were takingvitamin E in the vitamin E and placebo groups, respectively,were 94.2 percent and 1.0 percent at one year, 93.3 percentand 1.7 percent at two years, 91.3 percent and 2.0 percent atthree years, 90.2 percent and 2.7 percent at four years, and89.2 percent and 3.4 percent at the final visit.
Table 1. Base-Line Characteristics of the Patients.
Primary Cardiovascular Outcomes and Deaths from Any Cause
A total of 772 of the 4761 patients who were assigned to receivevitamin E (16.2 percent) and 739 of the 4780 who were assignedto placebo (15.5 percent) had a primary cardiovascular event(relative risk, 1.05; 95 percent confidence interval, 0.95 to1.16; P=0.33) (Table 2 and Figure 1). There were no significantdifferences between the groups in the numbers of deaths fromcardiovascular causes (342 in the vitamin E group vs. 328 inthe placebo group; relative risk, 1.05), myocardial infarctions(532 vs. 524; relative risk, 1.02), deaths from coronary heartdisease (287 vs. 277; relative risk, 1.06), or strokes (209vs. 180; relative risk, 1.17) (Figure 2 and Figure 3). The totalnumbers of deaths were similar in the two groups (535 vs. 537;relative risk, 1.00). Vitamin E had no signifi-cant effect onthe primary outcome either among patients who were receivingramipril (338 events among those who were receiving vitaminE and 313 events among those who were receiving placebo; relativerisk, 1.08) or among patients who were not receiving ramipril(421 and 405 events, respectively; relative risk, 1.05).
Figure 1. Kaplan–Meier Estimates of the Effect of Vitamin E on the Composite Outcome of Nonfatal Myocardial Infarction, Stroke, or Death from Cardiovascular Causes.
The relative risk of the composite outcome in the vitamin E group as compared with the placebo group was 1.05 (95 percent confidence interval, 0.95 to 1.16; P=0.33).
Figure 2. Kaplan–Meier Estimates of the Effect of Vitamin E on the Incidence of Myocardial Infarction (Panel A) and Stroke (Panel B).
The relative risk of myocardial infarction in the vitamin E group as compared with the placebo group was 1.02 (95 percent confidence interval, 0.90 to 1.15; P=0.74), and the relative risk of stroke was 1.17 (95 percent confidence interval, 0.95 to 1.42; P=0.13).
Figure 3. Kaplan–Meier Estimates of the Effect of Vitamin E on the Incidence of Death from Any Cause.
The relative risk in the vitamin E group as compared with the placebo group was 1.00 (95 percent confidence interval, 0.89 to 1.13; P=0.99).
Secondary Cardiovascular and Combined Outcomes
There were no differences between patients assigned to vitaminE and those assigned to placebo in the number of hospitalizationsfor unstable angina (586 vs. 569; relative risk, 1.04), hospitalizationsfor heart failure (160 vs. 144; relative risk, 1.12), or revascularizationsor limb amputations (848 vs. 787; relative risk, 1.09) (Table 3).There were no significant differences in the number of patientswith angina of new onset (278 vs. 245; relative risk, 1.15)or microvascular complications of diabetes (340 vs. 325; relativerisk, 1.06). A combined analysis of the proportion of patientswho had any primary or secondary event found a nonsignificantlyhigher rate among those assigned to vitamin E (1630 vs. 1576;relative risk, 1.05; 95 percent confidence interval, 0.98 to1.13; P=0.14).
Table 3. Incidence of Secondary and Other Outcomes.
Subgroup Analyses
There was no heterogeneity of results among subgroups definedaccording to sex, age, previous cardiovascular disease, or useof other drugs with respect to the primary or secondary outcomes(data not shown). Specifically, there was no significant differencein the incidence of the primary outcome among patients withdiabetes (325 of those assigned to vitamin E vs. 313 of thoseassigned to placebo; relative risk, 1.04) or among smokers (135vs. 139; relative risk, 1.02).
Adverse Effects
There was no significant difference between groups in the incidenceof adverse effects or in the number of patients who stoppedtaking the study medication. There was no increase in hemorrhagicstroke associated with vitamin E use (17 of those assigned tovitamin E had hemorrhagic stroke, as compared with 13 of thoseassigned to placebo) or among those who were also taking anantiplatelet agent (11 vs. 8).
Discussion
In our study, vitamin E did not reduce the incidence of cardiovascularevents, as compared with the incidence among patients assignedto placebo, during a follow-up period of four to six years.Given the large number of events and the consistent lack ofdifference in all secondary cardiovascular outcomes, it is veryunlikely that vitamin E had any clinically worthwhile beneficialeffect on cardiovascular disease during four or five years oftreatment.
Results have been reported from four randomized trials of theeffects of vitamin E on cardiovascular events. In a Chinesestudy, 29,584 adults from Linxian Province, who did not havecardiovascular disease at entry, were randomly assigned to receivedaily vitamin E (30 mg), beta carotene, and selenium supplementsor to receive placebo.13 During the 5.2 years of follow-up,there was a 9 percent decrease in deaths from any cause withoutany significant reduction in cardiovascular events. The doseof vitamin E in this study was small, the nutritional statusand cardiovascular risk of this population were very differentfrom those of Western populations, and the beneficial effectson overall mortality cannot be attributed only to vitamin E.
The second trial was the Alpha-Tocopherol, Beta Carotene CancerPrevention Study, involving 29,133 male smokers who were 50to 69 years of age.14 Daily treatment with 50 mg of vitaminE for five to eight years had no effect on the risk of deathfrom coronary heart disease. In a subgroup of 1862 men witha previous myocardial infarction at entry, there was a nonsignificantincrease in the risk of death from coronary heart disease (relativerisk, 1.33; 95 percent confidence interval, 0.86 to 2.05; P=0.20).However, a reduction in the risk of nonfatal myocardial infarctionwas documented among men assigned to vitamin E only (40 vs.55; relative risk, 0.62; 95 percent confidence interval, 0.41to 0.96), but not among those receiving the combination of vitaminE and beta carotene, in comparison with those receiving placeboonly.19 In this subgroup, the number of events was small. Inthe remaining patients in this study, there was no significanteffect of vitamin E on nonfatal or fatal myocardial infarction,despite large numbers of events (1204 and 907, respectively).20Thus, in this well-conducted trial, vitamin E had no effecton coronary heart disease. Although the trial used a low doseof synthetic vitamin E (50 mg per day), the median level ofalpha-tocopherol increased significantly, from 28.5 µmolper liter at base line to 42.5 µmol per liter at threemonths.
The third trial was the Cambridge Heart Antioxidant Study, whichrandomly assigned 2002 patients with coronary atherosclerosisto receive either vitamin E or placebo.15 The mean alpha-tocopherollevels increased from 34.2 to 51.1 µmol per liter in patientsreceiving 400 IU of vitamin E per day and to 64.5 µmolper liter in patients receiving 800 IU per day. The majorityof the patients received 400 IU per day. After a median follow-upof 1.4 years, a large reduction in the number of patients withnonfatal myocardial infarction was observed (14 in the vitaminE group vs. 41 in the placebo group; relative risk, 0.53; 95percent confidence interval, 0.11 to 0.47; P= 0.005), but therewas no difference in deaths due to cardiovascular causes (27vs. 23; relative risk, 1.18; 95 percent confidence interval,0.62 to 2.27; P=0.61). In this trial, the number of events wassmall and there were imbalances in several base-line characteristicsthat call into question whether randomization resulted in trulycomparable groups.
Furthermore, the very large reduction in nonfatal myocardialinfarction within a relatively short time (median, 1.4 years)is inconsistent with the results of other interventions, suchas lipid-lowering agents or antihypertensive medications, thatreduce cardiovascular events. It is therefore likely that theresults of the Cambridge Heart Antioxidant Study may have beendue to chance. This possibility is supported by the resultsof a recent Italian trial,16 in which 11,000 patients who hadhad myocardial infarctions were randomly assigned to receive300 IU of vitamin E per day or placebo for a median of 3.5 years.The number of patients with nonfatal myocardial infarction wasslightly higher in the vitamin E group than the placebo group(295 vs. 284; relative risk, 1.02; 95 percent confidence interval,0.87 to 1.21), and the number of deaths from coronary heartdisease was slightly smaller (227 vs. 249; relative risk, 0.92;95 percent confidence interval, 0.77 to 1.11). Neither differencewas statistically significant.16
Our study used a high dose of vitamin E (400 IU per day), hadhigh rates of compliance, and involved high-risk patients. Thestudy had a large number of primary outcomes and therefore hadhigh statistical power (more than 90 percent power to detecta 13 percent relative reduction in the risk of the primary outcome).Furthermore, a large number of secondary outcomes (e.g., revascularizationor limb amputation, unstable angina, worsening angina, and heartfailure) were examined. Such data are not available from mosttrials. Combining the data from all trials of vitamin E indicatesthat such treatment has little effect on the risk of death orcardiovascular events (Table 4), at least over a four-to-six-yearperiod.
Table 4. Meta-Analysis of the Effects of Vitamin E on Myocardial Infarction, Stroke, or Death from Cardiovascular Causes in Large Trials.
Steinberg has hypothesized that unlike agents that lower cholesterolor blood pressure, antioxidants may have to be used for morethan five years to have a demonstrable benefit, since the primarymechanism of these agents may be the prevention of new lesions.22Therefore, in a population like the one we studied, it may takelonger than five years to detect an effect on clinical outcomes.However, the Physicians' Health Study did not find a benefitof beta carotene (another antioxidant with a different action)after 12 years.23 Similar data are not available for vitaminE, but observational studies that demonstrated a lower rateof coronary heart disease with vitamin E supplementation suggestedthat a lower risk should be evident after two years.10,11 Ina nested substudy, we are examining whether the thickness ofthe carotid intima and media (an indication of the risk of earlyatherosclerosis) can be favorably altered by vitamin E.24 Ifso, Steinberg's hypothesis may be worth exploring with moreprolonged follow-up or treatment to assess whether such changesin the development of atherosclerosis would translate into abenefit in terms of clinical outcomes.
Although the moderate duration of vitamin E supplementation(four to six years) and the characteristics of the populationmay explain our finding of a lack of benefit of vitamin E, anotherreason may be our use of vitamin E alone, without other antioxidants.In the epidemiologic studies that found an association betweenhigher dietary intake of vitamin E and lower rates of coronaryheart disease, higher vitamin E consumption was also associatedwith higher intake of a number of other antioxidants and micronutrients.6,7,8,9It is possible that vitamin E supplementation requires thesecofactors to have a beneficial effect.25 Although the existenceof interactions between vitamin E and other vitamins,10 betacarotene,6,14 or selenium13 is not supported by the findingsof prospective observational studies or randomized trials, thishypothesis can be tested only in trials in which combinationsof vitamins are given; some such trials are now in progress.26,27,28
In conclusion, 400 IU of vitamin E administered daily for fourto six years had no beneficial effects on cardiovascular outcomesin a high-risk population of patients who were 55 years of ageor older. Vita-min E was well tolerated, with no significantadverse events as compared with placebo. This finding providessome reassurance for the conduct of large, longer-term trialsto address unanswered questions regarding vitamin E, such asits possible effects in preventing cancer.
Funded by the Medical Research Council of Canada, Natural SourceVitamin E Association, Negma, Hoechst–Marion Roussel,AstraZeneca, King Pharmaceuticals, and the Heart and StrokeFoundation of Ontario. Dr. Yusuf was supported by a Senior ScientistAward of the Medical Research Council of Canada and a Heartand Stroke Foundation of Ontario Research Chair.
We are indebted to W. Whitehill, F. Schutze, N. Bender, B. Rangoonwala,A. Ljunggren, G. Olsson, J.C. Dairon, J. Ghadiali, B. Carter,J.P. St. Pierre, W. Schulz, M. Jensen, L. Rios-Nogales, M. Bravo,J. Bourgouin, and C. Vint-Reed for support and to Karin Dearnessfor secretarial help.
* The investigators are listed in the Appendix of the Heart OutcomesPrevention Evaluation Study Investigators. Effects of an Angiotensin-Converting–EnzymeInhibitor, Ramipril, on Cardiovascular Events in High-Risk Patients.N Engl J Med 2000;342:145-53.
Source Information
The writing group (Salim Yusuf, D.Phil., Gilles Dagenais, M.D., Janice Pogue, M.Sc., Jackie Bosch, M.Sc., and Peter Sleight, D.M.) assumes responsibility for the overall content and integrity of the manuscript.
Address reprint requests to Dr. Salim Yusuf at the Canadian Cardiovascular Collaboration Project Office, Hamilton General Hospital, 237 Barton St. E., Hamilton, ON L8L 2X2, Canada, or at yusufs{at}fhs.mcmaster.ca.
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