Commentaries:
Increased dose increased bleeding. What´s the mre convenient dose of Aspirin?
Initial Aspirin Dose and Outcome Among ST-Elevation Myocardial Infarction Patients Treated With Fibrinolytic Therapy
Circulation
Volume 117, Issue 2; January 15, 2008
Jeffrey S. Berger, MD, MS; Amanda Stebbins, MS; Christopher B. Granger, MD; Eric M. Ohman, MD; Paul W. Armstrong, MD; Frans Van de Werf, MD, PhD; Harvey D. White, DSc; R. John Simes, MD; Robert A. Harrington, MD; Robert M. Califf, MD; Eric D. Peterson, MD, MPH
Background— Although treatment with immediate aspirin reduces morbidity and mortality in ST-elevation myocardial infarction, the optimal dose is unclear. We therefore compared the acute mortality and bleeding risks associated with the initial use of 162 versus 325 mg aspirin in fibrinolytic-treated ST-elevation myocardial infarction patients.
Methods and Results— Using combined data from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO I) and Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO III) trials (n=48 422 ST-elevation myocardial infarction patients), we compared the association between initial aspirin dose of 162 versus 325 mg and 24-hour and 7-day mortality, as well as rates of in-hospital moderate/severe bleeding. Results were adjusted for previously identified mortality and bleeding risk factors. Overall, 24.4% of patients (n=11 828) received an initial aspirin dose of 325 mg, and 75.6% (n=36 594) received 162 mg. The 24-hour mortality rates were 2.9% versus 2.8% (P=0.894) for those receiving an initial aspirin dose of 325 versus 162 mg. Mortality rates at 7 and 30 days were 5.2% versus 4.9% (P=0.118) and 7.1% versus 6.5% (P=0.017) among patients receiving the 325 versus 162 mg aspirin. After adjustment, aspirin dose was not associated with 24-hour (odds ratio [OR], 1.01; 95% CI, 0.82 to 1.25), 7-day (OR, 1.00; 95% CI, 0.87 to 1.17), or 30-day (OR, 0.99; 95% CI, 0.87 to 1.12) mortality rates. No significant difference was noted for myocardial infarction or the composite of death or myocardial infarction between groups. In-hospital moderate/severe bleeding occurred in 9.3% of those treated with 325 mg versus 12.2% among those receiving 162 mg (P<0.001). After adjustment, 325 mg was associated with a significant increase in moderate/severe bleeding (OR, 1.14; 95% CI, 1.05 to 1.24; P=0.003).
Conclusion— These data suggest that an initial dose of 162 mg aspirin may be as effective as and perhaps safer than 325 mg for the acute treatment of ST-elevation myocardial infarction.
Showing posts with label Aspirin. Show all posts
Showing posts with label Aspirin. Show all posts
Tuesday, January 22, 2008
Saturday, January 19, 2008
Aspirin 'resistance' linked to increased CV morbidity
Aspirin 'resistance' linked to increased CV morbidity
By Caroline Price
18 January 2008
Br Med J 2008; Advance online publication
MedWire News: Patients who do not respond to aspirin therapy are at increased long-term risk for cardiovascular (CV) morbidity, the results of a systematic review and meta-analysis show.
Such patients, labeled "aspirin resistant," had an approximately four-fold increased risk for nonfatal and fatal cardiovascular, cerebrovascular, or vascular events when taking aspirin compared with those classified as sensitive to aspirin.
"Not only did aspirin resistance have an effect on clinical outcome but this risk was not ameliorated by currently used adjunct antiplatelet therapies," the study authors note.
It is not clear why a significant number of CV disease patients derive no benefit from aspirin therapy, nor how these patients may be identified, explain Michael Buchanan (McMaster University, Hamilton, Ontario, Canada) and colleagues.
Such patients have been termed aspirin resistant because their platelets are not affected in the same way as platelets from individuals who seem to benefit from aspirin therapy. Yet it remains unknown whether these patients simply receive too low an aspirin dose, are not compliant, have differing abilities to absorb aspirin, or have an underlying genetic disposition that makes aspirin ineffective. Furthermore, few studies have addressed the impact of aspirin resistance on clinical outcomes.
To look for any relationship between aspirin resistance and clinical outcomes, Buchanan and team reviewed the literature and conducted a meta-analysis on 20 studies involving 2930 patients with CV disease who were receiving aspirin as an antithrombotic. Patients were classified as aspirin resistant if their platelet response was not inhibited in vitro by aspirin.
Overall, 810 (28%) patients were classified as aspirin resistant. These patients, regardless of underlying clinical symptoms, had a greater risk for death, acute coronary syndrome, failure in vascular intervention, or a new cerebrovascular event.
Indeed, 39% of aspirin-resistant compared with 16% of aspirin-sensitive patients had any cardiovascular event, giving an odds ratio of 3.85 (p<0.001).
The odds ratios for acute coronary syndrome, graft failure, and new cerebrovascular event in aspirin resistant compared with aspirin sensitive patients were 4.06, 4.35, and 3.78, respectively.
Moreover, the odds ratio for mortality for aspirin resistant patients was 5.99 (p<0.003).
A planned sensitivity analysis revealed no evidence of a dose-response relationship between aspirin resistance and any cardiovascular outcome among patients who received aspirin alone or who received a second antiplatelet. Furthermore, patients who were aspirin resistant had no benefit from concomitant therapy with clopidogrel or tirofiban, or both.
Italian cardiologists Giuseppe Biondi-Zoccai (University of Turin) and Marzia Lotrionte (Catholic University, Rome) commented in an accompanying editorial that further trials are needed to clarify whether aspirin resistance is just a nonmodifiable risk factor, or whether more aggressive antithrombotic regimens will benefit patients with aspirin resistance.
However, they cautioned that although clinical trials will help "fill in the gaps," there may be another factor generating interest in aspirin resistance.
"Drug companies may be keen to downgrade aspirin from its leading role as an effective drug in CV disease so that they can substitute it with much more expensive but marginally more effective alternatives," they stated.
Journal
By Caroline Price
18 January 2008
Br Med J 2008; Advance online publication
MedWire News: Patients who do not respond to aspirin therapy are at increased long-term risk for cardiovascular (CV) morbidity, the results of a systematic review and meta-analysis show.
Such patients, labeled "aspirin resistant," had an approximately four-fold increased risk for nonfatal and fatal cardiovascular, cerebrovascular, or vascular events when taking aspirin compared with those classified as sensitive to aspirin.
"Not only did aspirin resistance have an effect on clinical outcome but this risk was not ameliorated by currently used adjunct antiplatelet therapies," the study authors note.
It is not clear why a significant number of CV disease patients derive no benefit from aspirin therapy, nor how these patients may be identified, explain Michael Buchanan (McMaster University, Hamilton, Ontario, Canada) and colleagues.
Such patients have been termed aspirin resistant because their platelets are not affected in the same way as platelets from individuals who seem to benefit from aspirin therapy. Yet it remains unknown whether these patients simply receive too low an aspirin dose, are not compliant, have differing abilities to absorb aspirin, or have an underlying genetic disposition that makes aspirin ineffective. Furthermore, few studies have addressed the impact of aspirin resistance on clinical outcomes.
To look for any relationship between aspirin resistance and clinical outcomes, Buchanan and team reviewed the literature and conducted a meta-analysis on 20 studies involving 2930 patients with CV disease who were receiving aspirin as an antithrombotic. Patients were classified as aspirin resistant if their platelet response was not inhibited in vitro by aspirin.
Overall, 810 (28%) patients were classified as aspirin resistant. These patients, regardless of underlying clinical symptoms, had a greater risk for death, acute coronary syndrome, failure in vascular intervention, or a new cerebrovascular event.
Indeed, 39% of aspirin-resistant compared with 16% of aspirin-sensitive patients had any cardiovascular event, giving an odds ratio of 3.85 (p<0.001).
The odds ratios for acute coronary syndrome, graft failure, and new cerebrovascular event in aspirin resistant compared with aspirin sensitive patients were 4.06, 4.35, and 3.78, respectively.
Moreover, the odds ratio for mortality for aspirin resistant patients was 5.99 (p<0.003).
A planned sensitivity analysis revealed no evidence of a dose-response relationship between aspirin resistance and any cardiovascular outcome among patients who received aspirin alone or who received a second antiplatelet. Furthermore, patients who were aspirin resistant had no benefit from concomitant therapy with clopidogrel or tirofiban, or both.
Italian cardiologists Giuseppe Biondi-Zoccai (University of Turin) and Marzia Lotrionte (Catholic University, Rome) commented in an accompanying editorial that further trials are needed to clarify whether aspirin resistance is just a nonmodifiable risk factor, or whether more aggressive antithrombotic regimens will benefit patients with aspirin resistance.
However, they cautioned that although clinical trials will help "fill in the gaps," there may be another factor generating interest in aspirin resistance.
"Drug companies may be keen to downgrade aspirin from its leading role as an effective drug in CV disease so that they can substitute it with much more expensive but marginally more effective alternatives," they stated.
Journal
Thursday, January 10, 2008
Low-dose aspirin benefit shown in stable CVD patients
Low-dose aspirin benefit shown in stable CVD patients
By Caroline Price
09 January 2008
Am J Med 2008; 121: 43-49
MedWire News: Low-dose aspirin is associated with a significant reduction in the risk for major cardiovascular events and all-cause mortality, and a significant increase in the risk for major bleeding in patients with stable cardiovascular disease (CVD), meta-analysis findings show.
Despite the increased bleeding risk, "the totality of evidence demonstrated the benefit of aspirin in this high-risk group of subjects," comment the authors.
Recommendations for aspirin in secondary prevention are based on analyses of all anti-platelet therapies at all doses and in both stable and unstable patients, such that the role of low-dose aspirin in stable patients remains poorly defined, explain Jeffrey Berger (Duke University, Durham, North Carolina) and colleagues.
To address this issue, the team searched the MEDLINE database for secondary prevention trials of low-dose aspirin in stable CVD patients published between 1966 and 2006.
They identified six randomized placebo-controlled trials, one (Cardiff-I) that enrolled patients with a prior myocardial infarction (MI), one (Swedish Angina Pectoris Asprin Trial) that included patients with chronic stable angina, and four (Danish Low Dose, UK Transient Ischemic Attack, Swedish Aspirin Low-Dose Trial, and European Stroke Prevention Study-2) that included patients with a prior stroke or transient ischemic attack.
The aspirin dose ranged from 50 to 300 mg daily. Overall, there were 1718 cardiovascular events (nonfatal MIs, nonfatal strokes, and cardiovascular deaths) in these studies during a mean follow-up of 33.3 months.
There were significantly fewer cardiovascular deaths among patients taking aspirin (15.8%) than those taking placebo (19.1%), representing a 21% reduction in the odds for cardiovascular events with aspirin use (p<0.01).
Aspirin therapy was also associated with a 13% reduction in the odds for all-cause mortality (p=0.03), a 26% reduction in the odds for nonfatal MI (p<0.01), and a 25% reduction in the odds for stroke (p<0.01).
Against these findings, patients who received aspirin had a more than two-fold increased risk for major bleeding. However, the authors note that the low absolute risk for major bleeding meant that the number needed to treat to cause a major bleed was 111.
Furthermore, the data indicated that treating 1000 patients with low-dose aspirin would prevent around 33 major cardiovascular events, 12 nonfatal MIs, 25 nonfatal strokes, and 14 deaths, while causing just nine major bleeds, the researchers report in the American Journal of Medicine.
Of note, the decreased risk for major cardiovascular events was driven primarily by a reduction in the risk for MI in the two trials including patients with ischemic heart disease, and primarily by a reduction in the risk for stroke in the four trials that enrolled patients who had suffered cerebrovascular events.
Sub-group analyses showed that the effects of aspirin were similar at doses of 50-100 mg/day and 300 mg/day.
Berger and team conclude: "Future studies should focus on proper patient selection and management options to reduce the bleeding risk and the most optimal aspirin dose in each clinical setting for the long-term reduction in CVD and mortality."
Free abstract
By Caroline Price
09 January 2008
Am J Med 2008; 121: 43-49
MedWire News: Low-dose aspirin is associated with a significant reduction in the risk for major cardiovascular events and all-cause mortality, and a significant increase in the risk for major bleeding in patients with stable cardiovascular disease (CVD), meta-analysis findings show.
Despite the increased bleeding risk, "the totality of evidence demonstrated the benefit of aspirin in this high-risk group of subjects," comment the authors.
Recommendations for aspirin in secondary prevention are based on analyses of all anti-platelet therapies at all doses and in both stable and unstable patients, such that the role of low-dose aspirin in stable patients remains poorly defined, explain Jeffrey Berger (Duke University, Durham, North Carolina) and colleagues.
To address this issue, the team searched the MEDLINE database for secondary prevention trials of low-dose aspirin in stable CVD patients published between 1966 and 2006.
They identified six randomized placebo-controlled trials, one (Cardiff-I) that enrolled patients with a prior myocardial infarction (MI), one (Swedish Angina Pectoris Asprin Trial) that included patients with chronic stable angina, and four (Danish Low Dose, UK Transient Ischemic Attack, Swedish Aspirin Low-Dose Trial, and European Stroke Prevention Study-2) that included patients with a prior stroke or transient ischemic attack.
The aspirin dose ranged from 50 to 300 mg daily. Overall, there were 1718 cardiovascular events (nonfatal MIs, nonfatal strokes, and cardiovascular deaths) in these studies during a mean follow-up of 33.3 months.
There were significantly fewer cardiovascular deaths among patients taking aspirin (15.8%) than those taking placebo (19.1%), representing a 21% reduction in the odds for cardiovascular events with aspirin use (p<0.01).
Aspirin therapy was also associated with a 13% reduction in the odds for all-cause mortality (p=0.03), a 26% reduction in the odds for nonfatal MI (p<0.01), and a 25% reduction in the odds for stroke (p<0.01).
Against these findings, patients who received aspirin had a more than two-fold increased risk for major bleeding. However, the authors note that the low absolute risk for major bleeding meant that the number needed to treat to cause a major bleed was 111.
Furthermore, the data indicated that treating 1000 patients with low-dose aspirin would prevent around 33 major cardiovascular events, 12 nonfatal MIs, 25 nonfatal strokes, and 14 deaths, while causing just nine major bleeds, the researchers report in the American Journal of Medicine.
Of note, the decreased risk for major cardiovascular events was driven primarily by a reduction in the risk for MI in the two trials including patients with ischemic heart disease, and primarily by a reduction in the risk for stroke in the four trials that enrolled patients who had suffered cerebrovascular events.
Sub-group analyses showed that the effects of aspirin were similar at doses of 50-100 mg/day and 300 mg/day.
Berger and team conclude: "Future studies should focus on proper patient selection and management options to reduce the bleeding risk and the most optimal aspirin dose in each clinical setting for the long-term reduction in CVD and mortality."
Free abstract
Friday, December 28, 2007
Aspirin Therapy Can Impair Prostate Cancer Treatment
Aspirin Therapy Can Impair Prostate Cancer Treatment
MedPage Today
BOSTON, Dec. 27 -- Regular use of even low-dose aspirin may interfere with androgen suppression therapy for men with prostate cancer.
Men who used baby aspirin were significantly more likely to have abnormal liver function test results (P=0.02) among men in a study of the antiandrogen flutamide (Eulexin), reported Anthony V. D'Amico, M.D., Ph.D., of the Dana-Farber Cancer Institute here, and colleagues.
Abnormal liver function test results led to premature discontinuation of flutamide in 37% of aspirin users but only 16% of non-users, they said in a letter to the editors published in the Dec. 27 issue of the New England Journal of Medicine.
Oncologists, in collaboration with the patient's cardiologist, need to decide whether he should come off aspirin during hormonal therapy or whether the cardiovascular risk is great enough to forego hormonal therapy if liver function drops, Dr. D'Amico said, especially in view of evidence that antiandrogen therapy may increase heart attack risk.
"It's a trade off," he said. "It's going to have to be decided on an individual basis."
The finding may also have implications for oncologists beyond cautioning about drug-drug interactions, said Philip W. Kantoff, M.D., of Dana-Farber, a co-author of the letter.
"From a prostate cancer standpoint," he said, "this finding raises the potential value of more complete androgen blockade being of great importance in treating early prostate cancer."
In previous studies of high-dose aspirin use for rheumatoid arthritis or osteoarthritis, abnormal liver function tests have been reported in 5% of patients. And an animal study suggested that low testosterone levels contribute to slow metabolism of aspirin.
"In men with prostate cancer," they said, this effect "could have clinical importance because the antiandrogen component of hormone therapy is discontinued when liver function tests become abnormal."
So they retrospectively analyzed the impact of low-dose aspirin in a prospective, randomized controlled trial of radiation therapy with or without at least six months of a luteinizing hormone-releasing hormone agonist and flutamide.
The study included 206 patients with clinically localized prostate cancer and a PSA of at least 10 ng/mL, a Gleason score of at least seven, or radiographic evidence of extraprostatic disease.
The primary outcomes, published in the Journal of the American Medical Association in 2004, showed increased five-year survival (88% versus 78%, P=0.04) and decreased prostate cancer-specific mortality (P=0.02) with the addition of androgen suppression therapy.
Among the other findings of the current report at 7.6 years of follow-up, men who completed six months on a luteinizing hormone-releasing hormone agonist but stopped flutamide early were at 3.50 times higher relative risk of death (95% confidence interval: 1.03 to 11.80, P=0.04) than those who completed six months of both.
Radiation therapy alone was associated with 6.10-fold risk (95% CI: 2.30 to 16.20, P<0.001) compared with radiation therapy plus six months of hormone therapy.
Whereas men who used baby aspirin were more likely to have abnormal liver function test results (P=0.02), those on another common drug, atorvastatin (Lipitor) were not (P=0.13).
"Care givers should be aware of drug-drug interactions when treating cancer patients," Dr. Kantoff concluded, "including the interactions of cancer drugs with [other] prescription and non-prescription drugs, that could decrease the ability to deliver the cancer drug or diminish its effectiveness."
For men who would normally take the occasional aspirin for pain, Dr. D'Amico suggested using non-aspirin painkillers instead during hormonal therapy.
"These medicines don't have the same implications that aspirin appears to have in the setting of hormonal therapy," he said.
MedPage Today
BOSTON, Dec. 27 -- Regular use of even low-dose aspirin may interfere with androgen suppression therapy for men with prostate cancer.
Men who used baby aspirin were significantly more likely to have abnormal liver function test results (P=0.02) among men in a study of the antiandrogen flutamide (Eulexin), reported Anthony V. D'Amico, M.D., Ph.D., of the Dana-Farber Cancer Institute here, and colleagues.
Abnormal liver function test results led to premature discontinuation of flutamide in 37% of aspirin users but only 16% of non-users, they said in a letter to the editors published in the Dec. 27 issue of the New England Journal of Medicine.
Oncologists, in collaboration with the patient's cardiologist, need to decide whether he should come off aspirin during hormonal therapy or whether the cardiovascular risk is great enough to forego hormonal therapy if liver function drops, Dr. D'Amico said, especially in view of evidence that antiandrogen therapy may increase heart attack risk.
"It's a trade off," he said. "It's going to have to be decided on an individual basis."
The finding may also have implications for oncologists beyond cautioning about drug-drug interactions, said Philip W. Kantoff, M.D., of Dana-Farber, a co-author of the letter.
"From a prostate cancer standpoint," he said, "this finding raises the potential value of more complete androgen blockade being of great importance in treating early prostate cancer."
In previous studies of high-dose aspirin use for rheumatoid arthritis or osteoarthritis, abnormal liver function tests have been reported in 5% of patients. And an animal study suggested that low testosterone levels contribute to slow metabolism of aspirin.
"In men with prostate cancer," they said, this effect "could have clinical importance because the antiandrogen component of hormone therapy is discontinued when liver function tests become abnormal."
So they retrospectively analyzed the impact of low-dose aspirin in a prospective, randomized controlled trial of radiation therapy with or without at least six months of a luteinizing hormone-releasing hormone agonist and flutamide.
The study included 206 patients with clinically localized prostate cancer and a PSA of at least 10 ng/mL, a Gleason score of at least seven, or radiographic evidence of extraprostatic disease.
The primary outcomes, published in the Journal of the American Medical Association in 2004, showed increased five-year survival (88% versus 78%, P=0.04) and decreased prostate cancer-specific mortality (P=0.02) with the addition of androgen suppression therapy.
Among the other findings of the current report at 7.6 years of follow-up, men who completed six months on a luteinizing hormone-releasing hormone agonist but stopped flutamide early were at 3.50 times higher relative risk of death (95% confidence interval: 1.03 to 11.80, P=0.04) than those who completed six months of both.
Radiation therapy alone was associated with 6.10-fold risk (95% CI: 2.30 to 16.20, P<0.001) compared with radiation therapy plus six months of hormone therapy.
Whereas men who used baby aspirin were more likely to have abnormal liver function test results (P=0.02), those on another common drug, atorvastatin (Lipitor) were not (P=0.13).
"Care givers should be aware of drug-drug interactions when treating cancer patients," Dr. Kantoff concluded, "including the interactions of cancer drugs with [other] prescription and non-prescription drugs, that could decrease the ability to deliver the cancer drug or diminish its effectiveness."
For men who would normally take the occasional aspirin for pain, Dr. D'Amico suggested using non-aspirin painkillers instead during hormonal therapy.
"These medicines don't have the same implications that aspirin appears to have in the setting of hormonal therapy," he said.
Thursday, October 18, 2007
The influence of gender on the effects of aspirin in preventing myocardial infarction
The influence of gender on the effects of aspirin in preventing myocardial infarction
Todd Yerman, Wen Q Gan and Don D Sin
BMC Medicine 2007, 5:29doi:10.1186/1741-7015-5-29
Background
There is considerable variation in the effect of aspirin therapy reducing the risk of myocardial infarction (MI). Gender could be a potential explanatory factor for the variability. We conducted a systematic review and meta-analysis to determine whether gender mix might play a role in explaining the large variation of aspirin efficacy across primary and secondary MI prevention trials.
Methods
Randomized placebo-controlled clinical trials that examined the efficacy of aspirin therapy on MI were identified by using the PUBMED database (1966 to October 2006). Weighted linear regression technique was used to determine the relationship between log-transformed relative risk (RR) of MI and the percentage of male participants in each trial. The reciprocal of the standard error of the RR in each trial (1/SE) was used as the weight.
Results
A total of 23 trials (n = 113 494 participants) were identified. Overall, compared with placebo, aspirin reduced the risk of non-fatal MI (RR = 0.72, 95% confidence interval (CI) 0.64-0.81, p < 0.001) but not of fatal MI (RR = 0.88, 95% CI 0.75-1.03, p = 0.120). A total of 27% of the variation in the non-fatal MI results could be accounted for by considering the gender mix of the trials (p = 0.017). Trials that recruited predominantly men demonstrated the largest risk reduction in non-fatal MI (RR = 0.62, 95% CI 0.54-0.71), while trials that contained predominately women failed to demonstrate a significant risk reduction in non-fatal MI (RR = 0.87, 95% CI 0.71-1.06).
Conclusions
Gender accounts for a substantial proportion of the variability in the efficacy of aspirin in reducing MI rates across these trials, and supports the notion that women might be less responsive to aspirin than men.
Todd Yerman, Wen Q Gan and Don D Sin
BMC Medicine 2007, 5:29doi:10.1186/1741-7015-5-29
Background
There is considerable variation in the effect of aspirin therapy reducing the risk of myocardial infarction (MI). Gender could be a potential explanatory factor for the variability. We conducted a systematic review and meta-analysis to determine whether gender mix might play a role in explaining the large variation of aspirin efficacy across primary and secondary MI prevention trials.
Methods
Randomized placebo-controlled clinical trials that examined the efficacy of aspirin therapy on MI were identified by using the PUBMED database (1966 to October 2006). Weighted linear regression technique was used to determine the relationship between log-transformed relative risk (RR) of MI and the percentage of male participants in each trial. The reciprocal of the standard error of the RR in each trial (1/SE) was used as the weight.
Results
A total of 23 trials (n = 113 494 participants) were identified. Overall, compared with placebo, aspirin reduced the risk of non-fatal MI (RR = 0.72, 95% confidence interval (CI) 0.64-0.81, p < 0.001) but not of fatal MI (RR = 0.88, 95% CI 0.75-1.03, p = 0.120). A total of 27% of the variation in the non-fatal MI results could be accounted for by considering the gender mix of the trials (p = 0.017). Trials that recruited predominantly men demonstrated the largest risk reduction in non-fatal MI (RR = 0.62, 95% CI 0.54-0.71), while trials that contained predominately women failed to demonstrate a significant risk reduction in non-fatal MI (RR = 0.87, 95% CI 0.71-1.06).
Conclusions
Gender accounts for a substantial proportion of the variability in the efficacy of aspirin in reducing MI rates across these trials, and supports the notion that women might be less responsive to aspirin than men.
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