Original Article

Final Report on the Aspirin Component of the Ongoing Physicians' Health Study

Steering Committee of the Physicians' Health Study Research Group*

N Engl J Med 1989; 321:129-135July 20, 1989DOI: 10.1056/NEJM198907203210301

Abstract

Abstract

The Physicians' Health Study is a randomized, double-blind, placebo-controlled trial designed to determine whether low-dose aspirin (325 mg every other day) decreases cardiovascular mortality and whether beta carotene reduces the incidence of cancer. The aspirin component was terminated earlier than scheduled, and the preliminary findings were published. We now present detailed analyses of the cardiovascular component for 22,071 participants, at an average follow-up time of 60.2 months.

There was a 44 percent reduction in the risk of myocardial infarction (relative risk, 0.56; 95 percent confidence interval, 0.45 to 0.70; P<0.00001) in the aspirin group (254.8 per 100,000 per year as compared with 439.7 in the placebo group). A slightly increased risk of stroke among those taking aspirin was not statistically significant; this trend was observed primarily in the subgroup with hemorrhagic stroke (relative risk, 2.14; 95 percent confidence interval, 0.96 to 4.77; P = 0.06). No reduction in mortality from all cardiovascular causes was associated with aspirin (relative risk, 0.96; 95 percent confidence interval, 0.60 to 1.54).

Further analyses showed that the reduction in the risk of myocardial infarction was apparent only among those who were 50 years of age and older. The benefit was present at all levels of cholesterol, but appeared greatest at low levels. The relative risk of ulcer in the aspirin group was 1.22 (169 in the aspirin group as compared with 138 in the placebo group; 95 percent confidence interval, 0.98 to 1.53; P = 0.08), and the relative risk of requiring a blood transfusion was 1.71.

This trial of aspirin for the primary prevention of cardiovascular disease demonstrates a conclusive reduction in the risk of myocardial infarction, but the evidence concerning stroke and total cardiovascular deaths remains inconclusive because of the inadequate numbers of physicians with these end points. (N Engl J Med 1989; 321: 129–35.)

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Table 1Confirmed Cardiovascular End Points in the Aspirin Component of the Physicians' Health Study, According to Treatment Group.*

Table 2Subcategories of Stroke, According to Treatment Group.*

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Article

ALTHOUGH chewing willow bark, which has L aspirin-like properties, was prescribed for pain relief by Hippocrates in the fifth century B.C., the possible role of aspirin in reducing the risk of cardiovascular disease has been recognized only very recently. Such a possibility derives from the capacity of aspirin in low doses to inhibit cyclooxygenase-dependent platelet enzymes virtually completely, resulting in the inhibition of aggregability for the life of the platelet.1 These effects are so profound that higher doses add little benefit but do increase the risk of side effects.2 Although an early case–control study3 raised the possibility of a large benefit, most observational studies4 ^, 5 have suggested a cardiovascular benefit of about 20 percent. In such circumstances, the amount of uncontrolled confounding in case–control or cohort studies may be as large as the small-to-moderate effects being sought6; consequently, conclusive data can result only from a randomized trial whose sample is sufficiently large.7 ^, 8

The Physicians' Health Study is a double-blind, placebo-controlled, randomized trial designed to test two primary-prevention hypotheses in a population of healthy male physicians: whether aspirin in low doses (Bufferin, Bristol-Myers Products, 325 mg every other day) reduces mortality from cardiovascular disease, and whether beta carotene (Lurotin, BASF, 50 mg on alternate days) decreases the incidence of cancer. Although the beta carotene component of the trial is continuing at least through 1990, the Data Monitoring Board recommended the early termination of the blinded aspirin component of the trial on December 18, 1987. This decision was based on all available evidence, including three major considerations: the presence of a significant (P<0.00001) reduction in the risk of total myocardial infarction among those in the aspirin group; the fact that no effect of aspirin on cardiovascular mortality could be detected in the trial until the year 2000 or later, because of the exceptionally low cardiovascular death rates among the participating physicians; and the fact that aspirin was subsequently prescribed for more than 85 percent of the participants who experienced nonfatal vascular events, which made any finding about cardiovascular mortality particularly difficult to interpret. The trial's preliminary findings were published on January 28, 1988.9 We report here the results of the final analyses of the cardiovascular component up to January 25, 1988, when the participants were told whether they had been assigned to the aspirin or the placebo group.

Methods

The subjects and methods of the Physicians' Health Study were described in detail in the preliminary report.9 Briefly, 22,071 physicians were randomly assigned, according to two-by-two factorial design,10 to one of four treatment groups: aspirin and beta carotene, aspirin and beta carotene placebo, aspirin placebo and beta carotene, or aspirin placebo and beta carotene placebo. Altogether, 11,037 physicians were assigned at random to receive aspirin and 11,034 to receive aspirin placebo. All 22,071 participants randomly assigned to a treatment group have been included in all analyses.

Every six months for the first year and annually thereafter, the participants were sent a supply of monthly calendar packs (provided by Bristol-Myers Products) containing white tablets (aspirin or placebo) for odd-numbered days and red capsules (beta carotene or placebo) for even-numbered days. They were also sent brief questionnaires asking about their compliance with the treatment regimen and the occurrence of any relevant events.

By January 25, 1988, the participants had been followed for an average of 60.2 months (range, 45.8 to 77.0); 99.7 percent were still providing information on morbidity, and the vital status of all 22,071 doctors was known. The reported consumption of aspirin or other platelet-active drugs was 85.71 percent in the aspirin group and 14.23 percent in the placebo group. A total of 1269 physicians (624 taking aspirin and 645 taking aspirin placebo) requested an enteric-coated preparation (supplied by Bristol-Myers Products), and an additional 29 (16 assigned to aspirin and 13 assigned to placebo) specifically requested Ecotrin or its placebo (supplied by Smith-Kline Beckman).

When a participant reported a relevant outcome event, written consent for the review of his medical records was obtained. The information was requested from hospitals and responsible physicians. Reported diagnoses of cardiovascular disease or deaths were considered confirmed only after the examination of all available information by an End Points Committee of physicians that included two internists, a cardiologist, and a neurologist, all blinded to the assigned treatment. When written consent or the relevant records could not be obtained, a reported event could not be confirmed. Records were available for review for 95.6 percent of the reported myocardial infarctions, 95.2 percent of the strokes, and 94.8 percent of all deaths. All our analyses were based on confirmed events.

The diagnoses of nonfatal myocardial infarction were confirmed with use of the criteria of the World Health Organization.11 Nonfatal stroke was defined as a typical neurologic deficit that was sudden or rapid in onset, lasted more than 24 hours, and was attributable to a cerebrovascular event. Strokes were further classified according to the severity of the residual impairment at the time of hospital discharge (mild, moderate, or severe) and according to the probable cause (ischemic or hemorrhagic) on the basis of medical records and the judgment of the neurologist. Death due to a cardiovascular cause was documented by convincing evidence of a cardiovascular mechanism from all available sources, including death certificates, hospital records, and — for death outside the hospital — observers' impressions.

For the end points of myocardial infarction and stroke (Tables 1Table 1Confirmed Cardiovascular End Points in the Aspirin Component of the Physicians' Health Study, According to Treatment Group.* and 2Table 2Subcategories of Stroke, According to Treatment Group.*), only the first event within each category was counted. For cardiovascular mortality (Table 3Table 3Confirmed Deaths, According to Treatment Group.), all deaths were included in the analyses. Thus, for the 15 subjects who had both a nonfatal myocardial infarction and a nonfatal stroke, both events were counted as end points. For the 23 who had a nonfatal myocardial infarction (or stroke) followed by death from a cardiovascular cause, the nonfatal event was included in our analysis of myocardial infarction (or stroke), and the fatal event was included in cardiovascular deaths. In addition, we performed analyses using as end points only the first cardiovascular event experienced by the participants — myocardial infarction, stroke, or cardiovascular death — and this method yielded virtually identical results. For the combined end point of nonfatal myocardial infarction, nonfatal stroke, and death from a cardiovascular cause, only a participant's first cardiovascular event was counted.

The relative risk was calculated as the number of events per person-year of observation in the aspirin group divided by the corresponding number in the placebo group after adjustment for age and for assignment to beta carotene treatment,12 even though no significant effect of beta carotene was observed on any of the major cardiovascular end points. Since the trial was so large, the adjusted ratios were, in practice, never materially different from the ratios of the crude numbers affected in each group.8 For each relative risk, the two-sided P value and the 95 percent confidence interval were calculated.12 Multiple logistic-regression analysis12 was used to control simultaneously for the joint effects of any small differences in base-line cardiovascular risk factors, although no individual factor differed significantly between the aspirin and placebo groups.

Results

There were 139 myocardial infarctions among those assigned to aspirin and 239 among those assigned to aspirin placebo (relative risk, 0.56; 95 percent confidence interval, 0.45 to 0.70; P<0.00001) (Table 1). This represents a 44 percent reduction in risk, and the benefits of aspirin were significant for both fatal and nonfatal myocardial infarction. In terms of absolute rates of events, the figures can be extrapolated to 254.8 per 100,000 per year in the aspirin group and 439.7 per 100,000 per year in the placebo group. As for total stroke, there were 119 events in the aspirin group and 98 in the placebo group — an increase in risk that was not statistically significant (relative risk, 1.22; 95 percent confidence interval, 0.93 to 1.60; P = 0.15). Strokes were then subdivided into ischemic and hemorrhagic events and, further, into those resulting in mild, moderate, or severe disability or death (Table 2). In the subgroup with hemorrhagic strokes, aspirin was associated with an increased risk that was of borderline statistical significance (relative risk, 2.14; 95 percent confidence interval, 0.96 to 4.77; P = 0.06). This subgroup included 10 mild hemorrhagic strokes in the aspirin group and 6 in the placebo group (relative risk, 1.67; 95 percent confidence interval, 0.61 to 4.57; P = 0.32), as well as 13 moderate-to-severe or fatal hemorrhagic strokes in the aspirin group and 6 in the placebo group (relative risk, 2.19; 95 percent confidence interval, 0.84 to 5.69; P = 0.11).

With respect to total cardiovascular mortality (Table 3), there were 81 deaths among those assigned to aspirin and 83 among those given placebo (relative risk, 0.96; 95 percent confidence interval, 0.60 to 1.54; P = 0.87). In the five categories of death from specific cardiovascular causes, there was only one statistically significant finding: a reduction in the rate of fatal myocardial infarction (10 in the aspirin group and 28 in the placebo group; P = 0.004). For sudden death, there was an apparent increase in risk that did not achieve statistical significance (22 in the aspirin group and 12 in the placebo group; P = 0.09). Combining the category of fatal acute myocardial infarction (ICD [International Classification of Diseases number] 410) with the categories of all other fatal ischemic heart disease (ICD 411 to 414) yielded 34 deaths in the aspirin group and 53 in the placebo group (relative risk, 0.60; 95 percent confidence interval, 0.37 to 0.98; P = 0.04). The addition of sudden death (ICD 798) resulted in 56 deaths in the aspirin group and 65 in the placebo group (relative risk, 0.86; 95 percent confidence interval, 0.60 to 1.22; P = 0.41). There was no reduction in the risk of all deaths from noncardiovascular causes (124 in the aspirin group vs. 133 in the placebo group; relative risk, 0.93; 95 percent confidence interval, 0.72 to 1.20; P = 0.59). Thus, there were 205 deaths with a confirmed cause in the aspirin group and 216 in the placebo group (relative risk, 0.95; 95 percent confidence interval, 0.79 to 1.15; P = 0.60).

To help clarify a risk-to-benefit ratio, we considered a combined end point consisting of nonfatal myocardial infarction, nonfatal stroke, and death from a cardiovascular cause. There were 307 important vascular events among those assigned to aspirin and 370 among those assigned to placebo (relative risk, 0.82; 95 percent confidence interval, 0.70 to 0.96; P = 0.01). This represents a statistically significant, 18 percent reduction in important vascular events among those assigned to aspirin.

As expected with a sample of 22,071 participants randomly assigned to treatment groups, there were no differences in the base-line characteristics — age, cigarette smoking, incidence of diabetes mellitus, parental history of myocardial infarction, cholesterol level, systolic blood pressure, diastolic blood pressure, alcohol use, amount of vigorous exercise, and body-mass index. When the possible effects of any differences in the joint distributions of these risk factors were taken into account through logistic regression, the relative risks for each cardiovascular end point were unchanged.

We also examined the possible effects of aspirin in subgroups of physicians with various cardiovascular risk factors. As shown in Table 4Table 4Risk of Total Myocardial Infarction Associated with Aspirin Use, According to Level of Coronary Risk Factors., the effects of aspirin on the risk of myocardial infarction were modified by two coronary risk factors — age and blood cholesterol level. The reduction in the risk of myocardial infarction associated with the use of aspirin was apparent only in those 50 years of age or older (P = 0.02). No consistent effect of age on the relation between aspirin and either stroke or cardiovascular mortality was observed. For cholesterol, the beneficial effects of aspirin on myocardial infarction were apparent at all levels but appeared greatest at low levels (P = 0.04). For cigarette smoking, the reduction in the risk of myocardial infarction associated with the use of aspirin was similar among those who had never smoked, past smokers, and current smokers. For stroke, cigarette smoking did not modify the effect of aspirin, but for cardiovascular mortality, it appeared to do so (P = 0.05). However, neither the observed reduction in risk among nonsmokers (P = 0.18) nor the apparently increased risk among current smokers (P = 0.20) was significant. Finally, blood-pressure levels had no consistent effect on the association between aspirin and myocardial infarction, stroke, or mortality from cardiovascular causes.

During the 60.2 months of follow-up, gastrointestinal discomfort was reported by 26.1 percent of the aspirin group and 25.6 percent of the placebo group; 0.5 percent was therefore attributable to the active drug, a nonsignificant excess (P = 0.45) (Table 5Table 5Side Effects According to Treatment Group.). For all gastrointestinal symptoms except ulcer, the corresponding figures were 34.8 percent and 34.2 percent, respectively (P = 0.48, also not significant). There were 169 participants with ulcer in the aspirin group and 138 in the placebo group (relative risk, 1.22; 95 percent confidence interval, 0.98 to 1.53; P = 0.08). Among those with ulcer, 38 of the participants taking aspirin experienced some hemorrhage, as compared with 22 taking placebo (relative risk, 1.77; 95 percent confidence interval, 1.07 to 2.94; P = 0.04).

With respect to bleeding, 2979 of the aspirin group and 2248 of those taking placebo reported problems such as easy bruising, hematemesis, melena, nonspecific gastrointestinal bleeding, epistaxis, or other bleeding (relative risk, 1.32; 95 percent confidence interval, 1.25 to 1.40; P<0.00001). Furthermore, 48 in the aspirin group and 28 in the placebo group required transfusion (relative risk, 1.71; 95 percent confidence interval, 1.09 to 2.69; P = 0.02). One death from gastrointestinal hemorrhage was reported. This occurred in the aspirin group, and the event was confirmed.

Discussion

The results just described were virtually identical to the findings presented in our preliminary report.9 Overall, there was a statistically significant, 44 percent reduction in the risk of myocardial infarction that included significant benefits of aspirin for both fatal and nonfatal events. There continued to be an apparent but not significantly increased risk of stroke — primarily in the subgroup of all hemorrhagic strokes — associated with the use of aspirin. In the subgroup of moderate-to-severe or fatal hemorrhagic stroke, the increased risk that we had observed previously was no longer statistically significant (13 events in the aspirin group and 6 in the placebo group; P = 0.11). No reduction in the risk of mortality from all cardiovascular causes was associated with aspirin. Our findings regarding stroke and cardiovascular mortality must be viewed in the context of the fact that the trial had too few events to evaluate either of these end points.

Even in a trial with our large sample, the ability to identify particular subgroups of participants more or less likely to benefit from aspirin is limited. We observed no significant modification of the effects of aspirin on any of the major manifestations of cardiovascular disease across the various risk-factor subgroups classified according to cigarette smoking, the history of diabetes mellitus, parental myocardial infarction, diastolic blood pressure, systolic blood pressure, alcohol use, amount of exercise, and body-mass index. The reduction in the risk of myocardial infarction associated with aspirin was apparent only among those 50 or older. More important, however, was the low absolute risk of myocardial infarction at younger ages, suggesting that any net benefit of aspirin would be greatest among physicians 50 years of age and older. For cholesterol, the beneficial effects of aspirin were apparent at all levels. The observation that the benefits of aspirin for myocardial infarction were greatest at low levels of cholesterol was unexpected. This observation may be correct or may reflect random fluctuations in the data from which it was derived. It is not possible on the basis of the present data to decide between these explanations. For stroke and cardiovascular mortality, there was no apparent modification of the effects of aspirin according to risk factors, with the possible exception of cigarette smoking (in relation only to cardiovascular mortality). The number of these end points was too small for us to detect whether overall results were meaningful; the analysis of these end points according to subgroup was therefore particularly difficult.

The only other randomized trial of the role of aspirin in the primary prevention of cardiovascular disease is a smaller study of British doctors.13 In contrast to the Physicians' Health Study, the British Doctors' Trial showed no significant differences for fatal or nonfatal myocardial infarction, but the 95 percent confidence intervals were very wide. As in the Physicians' Health Study, there were more strokes among those assigned to aspirin, although the difference was not significant, and there was no significant difference in mortality from all cardiovascular causes. There were differences in the design of the U.S. and British trials, including the doses (325 mg on alternate days vs. 500 mg daily), blinding (double-blind with placebo control vs. single-blind), compliance (85.71 percent in the aspirin group and 85.74 percent in the placebo group after 60.2 months vs. 70 percent in the aspirin group and 98 percent in the group without aspirin after 36 months of a 72-month follow-up), and definition of end points. Perhaps most relevant, however, was the difference in the sample size; 5139 subjects were randomly assigned to aspirin or control in the British trial, and 22,071 in the U.S. study. To minimize the effect of this difference in sample size, we undertook an overview of the two trials of primary prevention.14 Since the U.S. trial was so much larger, this overview showed a significant, 33 percent reduction in nonfatal myocardial infarction associated with aspirin (P<0.0002). A repeated analysis, in which data from this final report were used, gave virtually identical results.

The findings of this study of aspirin in the primary prevention of cardiovascular disease should be viewed in the context of all the evidence concerning the possible role of aspirin. In 1985 the Food and Drug Administration approved the labeling of aspirin as an agent to be prescribed for the treatment of patients with a previous myocardial infarction or unstable angina.15 A recent overview16 of 25 randomized trials of antiplatelet therapy (aspirin, dipyridamole, or sulfinpyrazone, alone or in combination) in patients with a history of cardiovascular disease demonstrated a 25 percent reduction in the incidence of subsequent important vascular events (nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascular disease), a 32 percent decrease in nonfatal myocardial infarction, a 27 percent reduction in nonfatal stroke, and a 15 percent reduction in cardiovascular mortality. All these reductions were statistically significant. Moreover, aspirin was at least as effective as dipyridamole or sulfinpyrazone. Most recently, the Second International Study of Infarct Survival17 evaluated the role of aspirin in evolving myocardial infarction in a randomized trial with 17,187 participants and demonstrated a 49 percent reduction in nonfatal myocardial infarction, a 46 percent decrease in nonfatal stroke, and a 23 percent reduction in cardiovascular death after five weeks. All these reductions were statistically significant.

Aspirin's benefits in reducing the incidence of subsequent myocardial infarction have been shown conclusively in the survivors of myocardial infarction and stroke and in patients with unstable angina, as well as in those with an evolving heart attack. Our trial demonstrates conclusively a benefit of aspirin in reducing the incidence of first myocardial infarction and thus extends the previous findings to healthy people. Benefits in reducing the incidence of subsequent stroke have been shown conclusively in survivors of myocardial infarction and stroke and in patients with unstable angina, as well as in those with an evolving heart attack. The findings of our trial of primary prevention, although not statistically significant, are compatible with an increase in the number of all strokes among aspirin users. It seems important to distinguish between ischemic stroke, in which one might expect aspirin to be of benefit, and hemorrhagic stroke, in which one might expect an adverse effect. The possibility of an increase in the incidence of hemorrhagic stroke among aspirin users is not unexpected, since any agent that decreases clotting may help prevent ischemic events but increase bleeding. To evaluate this matter further, future trials in which the sample size is adequate to distinguish between ischemic and hemorrhagic stroke are required.

Finally, aspirin's benefits in reducing the incidence of cardiovascular mortality have been shown conclusively in the survivors of myocardial infarction and stroke and in patients with unstable angina, as well as in those with an evolving heart attack. In our trial of primary prevention, however, no reduction in the risk of mortality from all cardiovascular causes was associated with aspirin. Although it may be tempting to speculate about possible explanations for this finding, the primary consideration must be that the cardiovascular mortality rate among the physicians in this trial was only 15 percent of that expected for a general population of white men with the same age distribution over a similar period. This reduction was even greater than our conservative estimates of the "healthy volunteer"6 effect had suggested. The chief consequence of this extremely low cardiovascular mortality rate was to render it impossible to detect reliably whether aspirin had any effect on total mortality from cardiovascular causes until at least the year 2000. In addition, over 85 percent of the participants who had a nonfatal myocardial infarction were being treated with aspirin, making any finding about cardiovascular mortality particularly difficult to interpret.

The side effects of aspirin are clearly related to the size of the dose. The Aspirin Myocardial Infarction Study18 tested a dose of 1000 mg a day, and gastrointestinal symptoms were reported by 23.7 percent of those assigned to active treatment and 14.9 percent of those assigned to placebo. In the recently completed United Kingdom Transient Ischemic Attack trial,2 those receiving 300 mg daily experienced 30 percent fewer side effects than those receiving 1200 mg — a significant reduction (P<0.0001). In the Physicians' Health Study, in which the dose was 325 mg on alternate days, the rate of gastrointestinal discomfort attributable to aspirin was relatively low (0.5 percent). As expected, increased risks of upper gastrointestinal ulcers and bleeding problems were attributable to aspirin in this trial. Of greater clinical relevance, however, were their relatively low rates of occurrence, due in part to the low dose and the frequency of administration, and also to our eligibility criteria and the prerandomization run-in phase of the study, which excluded participants unable to tolerate the drug.9 For all these reasons, the frequency and severity of gastrointestinal discomfort, ulcers, and bleeding complications attributable to aspirin were far lower than those reported in previous trials.

There is some suggestion that low doses of aspirin are at least as effective in reducing the risk of cardiovascular disease as high doses. An overview of the trials of secondary prevention indicated that patients receiving 300 mg a day gained the same beneficial effect as those receiving 1500 mg.16 The benefits of aspirin observed in both the Second International Study of Infarct Survival17 and the Physicians' Health Study resulted from low-dose therapy — 160 mg daily and 325 mg every other day, respectively. A dose of 325 mg of buffered or enteric-coated aspirin every other day completely inhibits platelet aggregation, with no recovery even 48 hours after the last dose.19 Pharmacologic studies have suggested that the dose of aspirin necessary to inhibit platelet aggregation may be lower than 80 mg.20 However, in the acute stage of a cardiovascular event (unstable angina, transient ischemic attack, or myocardial infarction), a dose of about 160 mg to give a more rapid antithrombotic effect might be prudent.17

Since both trials of aspirin in primary prevention were confined to men, there is no direct evidence on the role of aspirin in the primary prevention of cardiovascular disease in women. Both the overview15 and the Second International Study of Infarct Survival17 demonstrated aspirin's significant benefits for secondary prevention of the various manifestations of cardiovascular disease in women. One can consider generalizing the results of our primary-prevention trial to women, but any such clinical judgment must take into account their absolute risks of various cardiovascular events as well as the possibility that aspirin in low doses may have a different pharmacologic effect in women.21 The only way to evaluate this question directly is through a randomized trial of healthy women that has a sufficiently large sample to detect the most plausible small-to-moderate effects.

Since the publication of our preliminary report, 74 percent of the participating physicians who were assigned to placebo have requested that their calendar packs be changed to aspirin. For the general public, however, the decision whether to take aspirin to reduce the risks of cardiovascular disease should be an individual judgment made only with the advice of a physician or other health care provider. In the making of this decision, the cardiovascular risk profile of the patient and the risks and benefits of the drug should be weighed.

The dedicated and conscientious collaboration of our study's 22,071 physicians has provided important information and has made it possible to conduct the trial at a small fraction of the usual cost. With the continued commitment of the participating physicians, we shall collect more observational data on stroke and cardiovascular mortality. In addition, the ongoing randomized component of the trial should provide important information on the possible role of beta carotene in the prevention of cancer.

Supported by grants (HL-26490, HL-34595, CA-34944, and CA-40360) from the National Institutes of Health.

We are indebted to the staff of the Physicians' Health Study, particularly Mary Breen, Joanne Crowley, Medora Hearn, Michael Jonas, Jean MacFayden, Patrick McCormick, Geneva McNair, Ayn Stamper, Jemma Pierre, Leslie Power, Miriam Schvartz, M.D., and Phyllis Johnson Wojciechowski; and to Dominick Mellace of Bristol-Myers Products for his logistic support.

Source Information

From the Charming Laboratory, Departments of Medicine and Preventive Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston. Address reprint requests to Dr. Charles H. Hennekens at 55 Pond Ave., Brookline, MA 02146.

*The members of the Steering Committee and of the Physicians* Health Study Research Group are as follows: Steering Committee: Charlene Belanger, M.A., Julie E. Buring, Sc.D., Nancy Cook, Sc.D., Kimberley Eberlein, M.P.H., Samuel Z. Goldhaber, M.D., David Gordon, M.A., Charles H. Hennekens, M.D. (chairman), Sherry L. Mayrent, Ph.D., Richard Peto, F.R.S.. Bernard Rosner, Ph.D., Meir J. Stampfer, M.D., Fran Stubblefield, B.S., and Walter C. Willett, M.D. The Steering Committee also includes the members of the Data Monitoring Board, as well as Thomas Ryan, M.D., Thomas Blaszkowski, Ph.D., (ex officio), and Andrew Vargosko, Ph.D. (ex officio). Physicians' Health Study Research Group: Charlene Belanger, M.A., Eugene Braunwald, M.D., Julie E. Buring, Sc.D., Nancy Cook, Sc.D., Richard Doll, F.R.S., Kimberley Eberlein, M.P.H., Samuel Z. Goldhaber, M.D., David Gordon, M.A., Charles H. Hennekens, M.D. (principal investigator), Edward H. Kass, M.D., Janet Lang, Sc.D., JoAnn Manson, M.D., Micheline Mathews-Roth, M.D., Sherry L. Mayrent, Ph.D., Richard Peto, F.R.S., Bernard Rosner, Ph.D., Suzanne Satterfield, M.D., Frank E. Speizer, M.D., Meir J. Stampfer, M.D., Fran Stubblefield, B.S., James O.Taylor, M.D., and Walter C. Willett, M.D. End Points Committee: Harris Funkenstein, M.D., Samuel Z. Goldhaber, M.D., Meir J. Stampfer, M.D., and James O. Taylor, M.D. (chairman). Data Monitoring Board: Lawrence S. Cohen, M.D., Theodore Colton, Sc.D., David DeMets, Ph.D. (chairman), Daniel Deykin, M.D., Lawrence Friedman, M.D., and Bernard Rosner, Ph.D. Recently added members are John Cairns, M.D., Peter Greenwald, M.D., and Charles H. Hennekens, M.D. The retired chairman is George B. Hutchison, M.D.

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607. 607

     Stephen Scheidt. (1997) Changing Mortality from Coronary Heart Disease among Smokers and Nonsmokers over a 20-Year Interval. Preventive Medicine 26:4, 441-446
     

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     DaLi Feng, Carol McKenna, Jaime Murillo, Murray A. Mittleman, Otavio C. Gebara, Izabella Lipinska, James E. Muller, Geoffrey H. Tofler. (1997) Effect of Aspirin Dosage and Enteric Coating on Platelet Reactivity. The American Journal of Cardiology 80:2, 189-193
     

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     JURGEN REHM, MARY JANE ASHLEY, GERARD DUBOIS. (1997) Alcohol and health: individual and population perspectives. Addiction 92:s1, S109-S115
     

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     Ridker , Paul M. , Cushman , Mary , Stampfer , Meir J. , Tracy , Russell P. , Hennekens , Charles H. , . (1997) Inflammation, Aspirin, and the Risk of Cardiovascular Disease in Apparently Healthy Men. New England Journal of Medicine 336:14, 973-979
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     E. Giovannucci, M. J. Stampfer, K. Krithivas, M. Brown, A. Brufsky, J. Talcott, C. H. Hennekens, P. W. Kantoff. (1997) The CAG repeat within the androgen receptor gene and its relationship to prostate cancer. Proceedings of the National Academy of Sciences 94:7, 3320-3323
     

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     K. D. RAINSFORD, S. C. ROBERTS, S. BROWN. (1997) Ibuprofen and Paracetamol: Relative Safety in Non-prescription Dosages. Journal of Pharmacy and Pharmacology 49:4, 345-376
     

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     Susan E. Herz. (1997) Don't Test, Do Sell: Legal Implications of Inclusion and Exclusion of Women in Clinical Drug Trials. Epilepsia 38:s4, S42-S49
     

615. 615

     Petra Verhoef, Charles H Hennekens, Robert H Allen, Sally P Stabler, Walter C Willett, Meir J Stampfer. (1997) Plasma Total Homocysteine and Risk of Angina Pectoris With Subsequent Coronary Artery Bypass Surgery. The American Journal of Cardiology 79:6, 799-801
     

616. 616

     Paul M Ridker, Charles H Hennekens, Christian Schmitz, Meir J Stampfer, Klaus Lindpaintner. (1997) PIA1/A2 polymorphism of platelet glycoprotein IIIa and risks of myocardial infarction, stroke, and venous thrombosis. The Lancet 349:9049, 385-388
     

617. 617

     William W. Parmley. (1997) Nonlipoprotein risk factors for coronary heart disease: Evaluation and management. The American Journal of Medicine 102:2, 7-14
     

618. 618

     Pierre Throux. (1997) Antiplatelet therapy: Do the new platelet inhibitors add significantly to the clinicl benefits of aspirin?. American Heart Journal 134:5, s62
     

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     DaLi Feng, MD, Carol McKenna, RN, Jaime Murillo, MD, Murray A. Mittleman, MD, DrPH, Otavio C. Gebara, MD, Izabella Lipinska, PhD, James E. Muller, MD, Geoffrey H. Tofler, MD. (1997) Effect of Aspirin Dosage and Enteric Coating on Platelet Reactivity. The American Journal of Cardiology 80:2, 189
     

620. 620

     Ramon C. Hermida, Jose R. Fernández, Diana E. Ayala, Artemio Mojón, Manuel Iglesias. (1997) Influence of Aspirin Usage on Blood Pressure: Dose and Administration-Time Dependencies. Chronobiology International 14:6, 619-637
     

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     John H. Kurata, Aki N. Nogawa. (1997) Meta-analysis of Risk Factors for Peptic Ulcer. Journal of Clinical Gastroenterology 24:1, 2-17
     

622. 622

     Walter E. Smalley, Raymond N. DuBois. Colorectal Cancer and Nonsteroidal Anti-inflammatory Drugs. Elsevier, 1997:1-20.
     

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     Javier Muñiz, Darwin R. Labarthe, Rafael Juaneb, Alfonso Castro Beiras. (1997) Estudios experimentales en cardiología. Revista Española de Cardiología 50:4, 268-277
     

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     Raymond N. DuBois, Francis M. Giardiello, Walter E. Smalley. (1996) NONSTEROIDAL ANTI-INFLAMMATORY DRUGS, EICOSANOIDS, AND COLORECTAL CANCER PREVENTION. Gastroenterology Clinics of North America 25:4, 773-791
     

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     Mary D. Nettleman, Jonathan Alsip, Mary Schroder, Marilyn Schulte. (1996) Predictors of mortality after acute hip fracture. Journal of General Internal Medicine 11:12, 765-767
     

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     John V. L. Sheffield, Eric B. Larson. (1996) General internal medicine update. Journal of General Internal Medicine 11:10, 613-621
     

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     James H. O'Keefe, Robert D. Conn, Carl J. Lavie, Timothy M. Bateman. (1996) The New Paradigm for Coronary Artery Disease: Altering Risk Factors, Atherosclerotic Plaques, and Clinical Prognosis. Mayo Clinic Proceedings 71:10, 957-965
     

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     Karin B Michels, Bernard A Rosner. (1996) Data trawling: to fish or not to fish. The Lancet 348:9035, 1152-1153
     

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     J.Michael Gaziano. (1996) Antioxidants in cardiovascular disease: Randomized trials. Nutrition 12:9, 583-588
     

630. 630

     Geoffrey S. Ginsburg, Pamela S. Douglas. (1996) Why cardiologists should be interested in estrogen. The American Journal of Cardiology 78:5, 559-561
     

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     Robert D. Marks. (1996) Aspirin use and fecal occult blood testing. The American Journal of Medicine 100:6, 596-597
     

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     S. Vincent Rajkumar, Priya Sampathkumar, Anthony B. Gustafson. (1996) Number needed to treat is a simple measure of treatment efficacy for clinicians. Journal of General Internal Medicine 11:6, 357-359
     

633. 633

     Walter E. Smalley, Marie R. Griffin. (1996) THE RISKS AND COSTS OF UPPER GASTROINTESTINAL DISEASE ATTRIBUTABLE TO NSAIDS. Gastroenterology Clinics of North America 25:2, 373-396
     

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     Paul D. Greenberg, John P. Cello, Don C. Rockey. (1996) Asymptomatic chronic gastrointestinal blood loss in patients taking aspirin or warfarin for cardiovascular disease. The American Journal of Medicine 100:6, 598-604
     

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     Hennekens , Charles H. , Buring , Julie E. , Manson , JoAnn E. , Stampfer , Meir , Rosner , Bernard , Cook , Nancy R. , Belanger , Charlene , LaMotte , Frances , Gaziano , J. Michael , Ridker , Paul M. , Willett , Walter , Peto , Richard , . (1996) Lack of Effect of Long-Term Supplementation with Beta Carotene on the Incidence of Malignant Neoplasms and Cardiovascular Disease. New England Journal of Medicine 334:18, 1145-1149
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     David J. Maron. (1996) Nonlipid primary and secondary prevention strategies for coronary heart disease. Clinical Cardiology 19:5, 419-423
     

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     Guido B. Aranha Rosito, Geoffrey H. Tofler. (1996) HEMOSTATIC FACTORS AS TRIGGERS OF CARDIOVASCULAR EVENTS. Cardiology Clinics 14:2, 239-250
     

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     A. Rodgers, S. MacMahon. (1996) Antiplatelet therapy and the prevention of thrombosis. Australian and New Zealand Journal of Medicine 26:2, 210-215
     

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     Julie K. Fetters, Eric D. Peterson, Leslee J. Shaw, L.Kristin Newby, Robert M. Califf. (1996) Sex-specific differences in coronary artery disease risk factors, evaluation, and treatment: Have they been adequately evaluated?. American Heart Journal 131:4, 796-813
     

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     Joan B. Lehmann, Paulette S. Wehner, Christoph U. Lehmann, Linda M. Savory. (1996) Gender bias in the evaluation of chest pain in the emergency department. The American Journal of Cardiology 77:8, 641-644
     

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     Sidna M. Scheitel, Kevin C. Fleming, Darryl S. Chutka, Jonathan M. Evans. (1996) Geriatric Health Maintenance. Mayo Clinic Proceedings 71:3, 289-302
     

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     Anne S. Lindblad. (1996) The effects of treatment noncompliance on power in a 2 × 2 factorial design. Journal of Biopharmaceutical Statistics 6:3, 263-270
     

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     W Christen. (1996) Antioxidants and age-related eye disease current and future perspectives. Annals of Epidemiology 6:1, 60-66
     

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     Simonetta Salvini, Charles H. Hennekens, J.Steven Morris, Walter C. Willett, Meir J. Stampfer. (1995) Plasma levels of the antioxidant selenium and risk of myocardial infarction among U.S. physicians. The American Journal of Cardiology 76:17, 1218-1221
     

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     GERALD C. TIMMIS, EDWARD TERRIEN. (1995) The Treatment of Myocardial Infarction. Journal of Interventional Cardiology 8:s6, 730-751
     

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     Bronner , Leslie L. , Kanter , Daniel S. , Manson , JoAnn E. , . (1995) Primary Prevention of Stroke. New England Journal of Medicine 333:21, 1392-1400
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     M.J. Smith, K.G.D. Allen, J.F. Norman, M.A. Harris, C.W. Miller. (1995) Low-dose aspirin does not attenuate platelet aggregation or atherosclerosis in miniature swine but decreases production of aortic wall prostacyclin. Prostaglandins, Leukotrienes and Essential Fatty Acids 53:5, 331-340
     

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     Giovannucci , Edward , Egan , Kathleen M. , Hunter , David J. , Stampfer , Meir J. , Colditz , Graham A. , Willett , Walter C. , Speizer , Frank E. , . (1995) Aspirin and the Risk of Colorectal Cancer in Women. New England Journal of Medicine 333:10, 609-614
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     Laurent J. Feldman, Jeffrey M. Isner. (1995) Gene therapy for the vulnerable plaque. Journal of the American College of Cardiology 26:3, 826-835
     

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     C. Meinert. (1995) The inclusion of women in clinical trials. Science 269:5225, 795-796
     

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     Monica Kraft, Richard J. Martin. (1995) Chronobiology and chronotherapy in medicine. Disease-a-Month 41:8, 506-575
     

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     Boyd Spencer. (1995) Correlations, Sample Size, and Practical Significance: A Comparison of Selected Psychological and Medical Investigations. The Journal of Psychology 129:4, 469-475
     

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     Ridker , Paul M. , Hennekens , Charles H. , Lindpaintner , Klaus , Stampfer , Meir J. , Eisenberg , Paul R. , Miletich , Joseph P. , . (1995) Mutation in the Gene Coding for Coagulation Factor V and the Risk of Myocardial Infarction, Stroke, and Venous Thrombosis in Apparently Healthy Men. New England Journal of Medicine 332:14, 912-917
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     Lindpaintner , Klaus , Pfeffer , Marc A. , Kreutz , Reinhold , Stampfer , Meir J. , Grodstein , Francine , LaMotte , Fran , Buring , Julie , Hennekens , Charles H. , . (1995) A Prospective Evaluation of an Angiotensin-Converting–Enzyme Gene Polymorphism and the Risk of Ischemic Heart Disease. New England Journal of Medicine 332:11, 706-712
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656. 656

     Eliseo Guallar, Charles H. Hennekens, Frank M. Sacks, Walter C. Willett, Meir J. Stampfer. (1995) A prospective study of plasma fish oil levels and incidence of myocardial infarction in U.S. male physicians. Journal of the American College of Cardiology 25:2, 387-394
     

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     Barnett , Henry J.M. Eliasziw , Michael Meldrum , Heather E. . (1995) Drugs and Surgery in the Prevention of Ischemic Stroke. New England Journal of Medicine 332:4, 238-248
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     M Leutenegger, E Bertin. (1995) Diabète sucré et athérosclérose. Physiopathologie de la macroangiopathie diabétique. La Revue de Médecine Interne 16:1, 31-42
     

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     Peter H. Gann, Charles H. Hennekens, Francine Grodstein, Meir J. Stampfer, Christopher Longcope, Wendy Verhoek-Oftedahl. (1995) A prospective study of plasma hormone levels, nonhormonal factors, and development of benign prostatic hyperplasia. The Prostate 26:1, 40-49
     

660. 660

     Karin Müller-Decker, Kirsten Scholz, Friedrich Marks, Gerhard Fürstenberger. (1995) Differential expression of prostaglandin h synthase isozymes during multistage carcinogenesis in mouse epidermis. Molecular Carcinogenesis 12:1, 31-41
     

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     Alvan R. Feinstein. (1995) Meta-analysis: Statistical alchemy for the 21st century. Journal of Clinical Epidemiology 48:1, 71-79
     

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     Charles H Hennekens. (1994) Platelet inhibitors and antioxidant vitamins in cardiovascular disease. American Heart Journal 128:6, 1333-1336
     

663. 663

     Charles H. Hennekens, Julie E. Buring. (1994) Contributions of observational evidence and clinical trials in cancer prevention. Cancer 74:S9, 2625-2629
     

664. 664

     Julie E. Buring, I-Min Lee, Charles H. Hennekens. (1994) Nonsteroidal antiinflammatory drugs and colorectal cancer. A promising hypothesis but not yet proven. Cancer 74:7, 1837-1839
     

665. 665

     Krikor M. Berberian, Cornelia M. Duijn, Arno W. Hoes, Hans A. Valkenburg, Albert Hofman. (1994) Alcohol and mortality. European Journal of Epidemiology 10:5, 587-593
     

666. 666

     Robert S. Stern. (1994) Ocular Lens Findings in Patients Treated with PUVA.. Journal of Investigative Dermatology 103:4, 534-538
     

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     M. Angelo Trujillo, Harinder S. Garewal, Richard E. Sampliner. (1994) Nonsteroidal antiinflammatory agents in chemoprevention of colorectal cancer at what cost?. Digestive Diseases and Sciences 39:10, 2260-2266
     

668. 668

     T.W. Meade. (1994) 15 Haemostatic function, arterial disease and the prevention of arterial thrombosis. Baillière's Clinical Haematology 7:3, 733-755
     

669. 669

     J.Michael Gaziano. (1994) Antioxidant vitamins and coronary artery disease risk. The American Journal of Medicine 97:3, S18-S21
     

670. 670

     Charles H. Hennekens. (1994) Antioxidant vitamins and cancer. The American Journal of Medicine 97:3, S2-S4
     

671. 671

     William Gerard Christen. (1994) Antioxidants and eye disease. The American Journal of Medicine 97:3, S14-S17
     

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     John F. Dickson, Robert F. Willkens. (1994) Nonsteroidal Anti-Inflammatory Drugs in the Treatment of Rheumatoid Arthritis. Clinical Immunotherapeutics 2:3, 185-191
     

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     Dale M. Atrens. (1994) The questionable wisdom of a low-fat diet and cholesterol reduction. Social Science & Medicine 39:3, 433-447
     

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     A. BRÖIJERSÉN, M. ERIKSSON, P. T. LARSSON, O. BECK, L. BERGLUND, B. ANGELIN, P. HJEMDAHL. (1994) Effects of selective LDL-apheresis and pravastatin therapy on platelet function in familial hypercholesterolaemia. European Journal of Clinical Investigation 24:7, 488-496
     

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     Patrono , Carlo . (1994) Aspirin as an Antiplatelet Drug. New England Journal of Medicine 330:18, 1287-1294
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     Nicholas I. Kondo, Rosemarie Maddi, Bruce M. Ewenstein, Samuel Z. Goldhaber. (1994) Anticoagulation and Hemostasis in Cardiac Surgical Patients. Journal of Cardiac Surgery 9:4, 443-461
     

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     G. Domenighetti. (1994) From ethics of ignorance to consumers empowerment. Sozial- und Prventivmedizin SPM 39:3, 123-125
     

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     Edward J. Weiner, Arthur F. Stucchi, Thomas L. Foxall, Glenn T. Shwaery, Subbiah Yoganathan, Robert J. Nicolosi. (1994) The effects of doxazosin on platelet aggregation, platelet adhesion and blood coagulation in cynomolgus monkeys. Atherosclerosis 107:1, 35-44
     

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     Gerald Holtmann, Harald Goebell, Marianne Holtmann, Nicholas J. Talley. (1994) Dyspepsia in healthy blood donors. Digestive Diseases and Sciences 39:5, 1090-1098
     

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     The Alpha-Tocopherol Beta Carotene Cancer Prevention Study Group. (1994) The Effect of Vitamin E and Beta Carotene on the Incidence of Lung Cancer and Other Cancers in Male Smokers. New England Journal of Medicine 330:15, 1029-1035
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     P.M. Ridker, C.H. Hennekens, J.E. Manson, P.M. Ridker, D.E. Vaughan, M.J. Stampfer, D.E. Vaughan, C.H. Hennekens, M.J. Stampfer. (1994) Prospective study of endogenous tissue plasminogen activator and risk of stroke. The Lancet 343:8903, 940-943
     

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     Sherine E. Gabriel, Mary E. Campion, W. Michael O'Fallon. (1994) A Cost-Utility Analysis of Misoprostol Prophylaxis for Rheumatoid Arthritis Patients Receiving Nonsteroidal Antiinflammatory Drugs. Arthritis & Rheumatism 37:3, 333-341
     

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     Michael Lewis, Hannelore Lwel, Allmut Hrmann. (1994) Die Arzneimittelbehandlung von Herzinfarkt-patienten vor und nach dem Akutereignis: Ergebnisse des Herzinfarktregisters Augsburg. Sozial- und Prventivmedizin SPM 39:2, 75-85
     

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     Martin H. Huber, Waun Ki Hong. (1994) Biology and chemoprevention of head and neck cancer. Current Problems in Cancer 18:2, 86-140
     

685. 685

     Julie E. Buring, Charles H. Hennekens. (1994) Randomized trials of primary prevention of cardiovascular disease in women. Annals of Epidemiology 4:2, 111-114
     

686. 686

     Jules Y.T. Lam, Jean-Gilles Latour, Jacques Lespérance, David Waters. (1994) Platelet aggregation, coronary artery disease progression and future coronary events. The American Journal of Cardiology 73:5, 333-338
     

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     Cristina Escudero, Lourdes Alvarez, Javier de Haro, José González, María Victoria Alvarez, Isabel Millán, Eduardo Jorge-Herrero, JoséLuis Castillo-Olivares. (1994) Prevention of arterial thrombosis by a monoclonal antibody against the 100 to 109 amino acid sequence stretch of the beta-subunit of the human platelet fibrinogen receptor: A comparative study with low dose aspirin. Journal of the American College of Cardiology 23:2, 483-486
     

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     Paul R. Eisenberg. (1994) Thrombosis and Fibrinolysis in Acute Myocardial Infarction. Alcoholism: Clinical and Experimental Research 18:1, 97-104
     

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     Margus Viigimaa, Tiiu Jôudu, Enn Hendrikson, Yelena Shandrik, Rein Teesalu. (1994) Antiaggregative Therapy with Acetylsalicylic Acid and Diclofenac in Patients with Acute Myocardial Infarction. Upsala Journal of Medical Sciences 99:2, 131-138
     

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     Paul M. Ridker. (1994) Plasma concentration of endogenous tissue plasminogen activator and the occurrence of future cardiovascular events. Journal of Thrombosis and Thrombolysis 1:1, 35-40
     

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     Kenneth B. Schechtman, Mae O. Gordon. (1994) The effect of poor compliance and treatment side effects on sample size requirements in randomized clinical trials. Journal of Biopharmaceutical Statistics 4:2, 223-232
     

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     T.C. Fisher, H.J. Meiselmann. (1994) Polymorphonuclear leukocytes in ischemic vascular disease. Thrombosis Research 74, S21-S34
     

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     Jussi K. Huttunen, O. P. Heinonen, V. Manninen, P. Koskinen, T. Hakulinen, L. Teppo, M. Mänttäri, M. H. Frick. (1994) The Helsinki Heart Study: an 8.5-year safety and mortality follow-up. Journal of Internal Medicine 235:1, 31-39
     

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     H. Tohgi, H. Takahashi, K. Tamura. (1994) Antiplatelet Medication in Cerebrovascular Disease: Potential Sources of Controversies and Future Strategies. Platelets 5:1, 13-19
     

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     Karen A. Johnson, Leslie G. Ford, Barnett Kramer, Peter Greenwald. (1994) Overview of U.S. National Cancer Institute (USNCI) Chemoprevention Research. Acta Oncologica 33:1, 5-11
     

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     (1994) Clinical development plan: Aspirin. Journal of Cellular Biochemistry 56:S20, 74-85
     

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     Kazuo Hakoi, Kenji Irimura, Takashi Makita. (1993) Ultrastructural study of magnesium dependent adenosine triphosphatase (Mg-ATPase) activity in rat liver peroxisomes after administration of aspirin and clofibrate. Medical Electron Microscopy 26:3-4, 161-168
     

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     Millicent Higgins, Claude Lenfant. (1993) Dissent “Consider what a long way you've come” —The white queen to Alice. Journal of Clinical Epidemiology 46:12, 1347-1350
     

700. 700

     Loretta M. Itri. (1993) Cancer chemoprevention. Cancer 72:S11, 3374-3380
     

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     James R. Couch. (1993) Antiplatelet therapy in the treatment of cerebrovascular disease. Clinical Cardiology 16:10, 703-710
     

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     Carlo Patrono, Giovanni Davì. (1993) Antiplatelet agents in the prevention of diabetic vascular complications. Diabetes / Metabolism Reviews 9:3, 177-188
     

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     Charles H. Hennekens, Michael A. Jonas, Julie E. Buring. (1993) Antiplatelet therapy and risk of stroke. Annals of Epidemiology 3:5, 568-570
     

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     Carl J. Lavie, Richard V. Milani, Andrew B. Littman. (1993) Benefits of cardiac rehabilitation and exercise training in secondary coronary prevention in the elderly. Journal of the American College of Cardiology 22:3, 678-683
     

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     Mark L. Dyken. (1993) Overview of trends in management and prognosis of stroke. Annals of Epidemiology 3:5, 535-540
     

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     Michael J. Klag, Jiang He, Lucy A. Mead, Daniel E. Ford, Thomas A. Pearson, David M. Levine. (1993) Validity of physicians' self-reports of cardiovascular disease risk factors. Annals of Epidemiology 3:4, 442-447
     

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     P.M. Ridker, D.E. Vaughan, Je Manson, Ch Hennekens, Mj Stampfer. (1993) Endogenous tissue-type plasminogen activator and risk of myocardial infarction. The Lancet 341:8854, 1165-1168
     

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     A. NORDØY. (1993) Haemostatic factors in coronary heart disease. Journal of Internal Medicine 233:5, 377-383
     

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     David M. Najman, Jeanine M. Walenga, Jawed Fareed, Roque Pifarré. (1993) Effects of aprotinin on anticoagulant monitoring: Implications in cardiovascular surgery. The Annals of Thoracic Surgery 55:3, 662-666
     

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     PJ Roderick, HC Wilkes, TW Meade. (1993) The gastrointestinal toxicity of aspirin: an overview of randomised controlled trials.. British Journal of Clinical Pharmacology 35:3, 219-226
     

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     Robert W. Hobson, William C. Krupski, David G. Weiss. (1993) Influence of aspirin in the management of asymptomatic carotid artery stenosis. Journal of Vascular Surgery 17:2, 257-265
     

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     Paulette Mehta, Jawahar L. Mehta. (1993) Effects of aspirin in arterial thrombosis: Why don't animals behave the way humans do?. Journal of the American College of Cardiology 21:2, 511-513
     

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     Kenneth B. Schechtman, Mae E. Gordon. (1993) A comprehensive algorithm for determining whether a run-in strategy will be a cost-effective design modification in a randomized clinical trial. Statistics in Medicine 12:2, 111-128
     

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     (1993) The Hypertension Optimal Treatment Study (The HOT Study): The Hot Study Group. Blood Pressure 2:1, 62-68
     

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     TRACY L. JOHNSON. (1993) Position Paper: A Women's Health Research Agenda. Journal of Women's Health 2:2, 95-98
     

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     Gordon W. Pledger. (1993) Confidence intervals versus ρ-values for interpretation of clinical trial results: introduction. Journal of Biopharmaceutical Statistics 3:2, 237-242
     

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     Paul A. Schulte, Nathaniel Rothman, Melissa A. Austin. Cardiovascular Disease. In: Molecular Epidemiology. Elsevier, 1993:341-363.
     

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     Henk C.S. Wallenburg, Henk A. Bremer. (1992) 9 Principles and applications of manipulation of prostaglandin synthesis in pregnancy. Baillière's Clinical Obstetrics and Gynaecology 6:4, 859-891
     

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     B. H. CHONG. (1992) Aspirin and dipyridamole in the prevention of coronary disease and coronary artery bypass graft occlusion. Internal Medicine Journal 22:6, 645-646
     

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     B. H. CHONG. (1992) Aspirin and dipyridamole in the prevention of coronary disease and coronary artery bypass graft occlusion. Australian and New Zealand Journal of Medicine 22:6, 645-646
     

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     W. Virgil Brown. (1992) When do we treat hypercholesterolemia?. Clinical Cardiology 15:S3, 10-14
     

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     SJ Gray, H. Giles, J. Posner. (1992) The effect of a prostaglandin DP-receptor partial agonist (192C86) on platelet aggregation and the cardiovascular system in healthy volunteers.. British Journal of Clinical Pharmacology 34:4, 344-351
     

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     Patricia A. Buffler, Julie E. Buring. (1992) Women and health. Annals of Epidemiology 2:5, 759-760
     

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     Lamas , Gervasio A. , Pfeffer , Marc A. , Hamm , Peggy , Wertheimer , John , Rouleau , Jean-Lucien , Braunwald , Eugene , . (1992) Do the Results of Randomized Clinical Trials of Cardiovascular Drugs Influence Medical Practice?. New England Journal of Medicine 327:4, 241-247
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     Willard , John E. Lange , Richard A. Hillis , L. David . (1992) The Use of Aspirin in Ischemic Heart Disease. New England Journal of Medicine 327:3, 175-181
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     Paul M. Ridker, JoAnn E. Manson, Samuel Z. Goldhaber, Charles H. Hennekens, Julie E. Buring. (1992) Comparison of delay times to hospital presentation for physicians and nonphysicians with acute myocardial infarction. The American Journal of Cardiology 70:1, 10-13
     

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     S.Z. Goldhaber, J.E. Manson, M.J. Stampfer, F. LaMotte, B. Rosner, J.E. Buring, C.H. Hennekens. (1992) Low-dose aspirin and subsequent peripheral arterial surgery in the Physicians' Health Study. The Lancet 340:8812, 143-145
     

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     James E. Muller, Geoffrey H. Tofler. (1992) Triggering and hourly variation of onset of arterial thrombosis. Annals of Epidemiology 2:4, 393-405
     

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     Larry A. Weinrauch, John A. D'Elia, Anthony P. Monaco, Ray E. Gleason, Francine Welty, Peter C. Nishan, Richard W. Nesto. (1992) Preoperative evaluation for diabetic renal transplantation: Impact of clinical, laboratory, and echocardiographic parameters on patient and allograft survival. The American Journal of Medicine 93:1, 19-28
     

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     Barry J. Materson, Richard A. Preston. (1992) Antihypertensive Drug Therapy Does Not Perturb the Circadian Blood Pressure Pattern. The Journal of Clinical Pharmacology 32:7, 627-629
     

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