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Aspirin Lowers Risk of Blood Clot Risk in Women and
Men
Findings challenge earlier claims of little benefit
for women
March 22, 2006 - A once-daily pill of low-dose
aspirin helps lower the potential for clot-forming blood cells - in both
men and women - to stick together in narrow blood vessels, says a new
study that included senior citizens up to age 80. In what is
believed to be the first direct comparison of blood cell testing in both
sexes of 81 milligrams of acetyl salicylic acid a day, Johns Hopkins
researchers found aspirin therapy prevents the clumping together of
these clot-forming cells, called platelets. Clots in blood vessels of
the heart and brain can cause heart attacks and strokes.
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Health & Medicine |
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However, while the drug's overall effects on blood
cell function were the same for men and women, the investigators found
that women's platelets reacted somewhat more strongly to aspirin before
the start of therapy, and remained so even after treatment.
The study findings appear in the Journal of the
American Medical Association online March 21, and challenge the
conclusions from several other recent studies, including the federal
Women's Health Study, which showed low-dose aspirin had no effect in
preventing heart attacks in women, even though it worked in men.
Previous results, the researchers say, were not likely caused by the
failure of aspirin to prevent platelets from clumping together and
forming blood clots in women.
"Women are clearly benefiting from taking aspirin
and should continue to take it to improve their cardiovascular health,"
says study senior investigator Diane Becker, M.P.H., Sc.D., a professor
at The Johns Hopkins University School of Medicine and Bloomberg School
of Public Health.
"Aspirin has been proven by all previous studies to
lower the risk of stroke and, as our latest findings show, it also
reduces platelet aggregation that can lead to potentially fatal clots in
blood vessels."
"Our results show that aspirin does what it is
supposed to do in both men and women," says platelet biologist and study
co-author Nauder Faraday, M.D., an associate professor at Hopkins.
"But
women started at a higher baseline level of platelet aggregation and
remained slightly higher even after taking aspirin. So, it remains
unclear if the residual differences in platelet function impact the
drug's overall beneficial effects, and if the doses used in earlier
studies were sufficient to decisively prevent heart attacks in women."
"Further research is required to get a definitive
answer as to whom aspirin really benefits, under what circumstances it
does work and does not work, and just how much is required in different
people," he adds.
Results in both men and women showed that aspirin,
taken daily for a two-week period, works by inhibiting key biological
pathways that lead to platelet clumping.
Using an electrical measure of how well platelets
stick together, researches found that in aspirin-treated men, clumping
decreased by 15.1 ohms. The decrease was statistically the same in
aspirin-treated women, at 17.3 ohms. In this test, an ohm is the measure
of electrical resistance caused by platelets as they impede the flow of
electricity in a wire probe inside a test tube filled with blood.
Moreover, platelet aggregation was largely
suppressed in at least three other key pathways related to their
function when platelets were stimulated with substances that normally
trigger clot formation. Each of these tests involved mixing whole blood,
or platelet-rich plasma, from aspirin-treated men and women with various
concentrations of each of the main chemical compounds involved in the
pathways -- collagen, adenosine diphosphate, and epinephrine - to see
how platelets responded.
For example, in aspirin-treated men, platelet
clumping went down by 14.6 ohms when 1 microgram of collagen per
milliliter was added to whole blood, and decreased by 2.4 ohms when
exposed to a higher dose of 5 micrograms per milliliter. In treated
women, reductions were the same, at 14.9 ohms and 2.42 ohms,
respectively.
When 10 micromoles per liter of adenosine
diphosphate were added to whole blood, platelet aggregation decreased
the same amount, 0.19 ohms in men and 0.21 ohms in women. Addition of 2
micromoles per liter of epinephrine to platelet-rich plasma produced
significantly greater reductions in platelet clumping in treated women,
a drop of 36.9 percent, while it was less of a reduction for men, at
31.5 percent. Again, the researchers say, these changes would have been
zero if aspirin had had no effect.
Further analysis of results highlighted mainly two
factors, platelet reactivity levels before therapy starts and gender, as
having played a significant role in predicting the effects of aspirin
therapy on platelet clumping. Other factors, such as age, race or known
risk factors for heart disease, including smoking, obesity and high
blood pressure, were not found to be good predictors of aspirin's
beneficial effects.
More than 500 men and 700 women participated in the
study, called the Genetic Study of Aspirin Responsiveness (GeneSTAR).
Conducted solely at Hopkins from June 2004 to November 2005, the study
enrolled participants from across the country who ranged in age from 21
to 80; 31 percent were black and the rest were white. None had previous
histories of heart problems, such as a heart attack, but all were
considered to be at slightly increased risk of heart disease because of
a family history. Fifty percent of women participants were
postmenopausal.
Blood testing was conducted both before and after
treatment. In total, more than 200 different tests of platelet
reactivity were performed and analyzed in the study. Because whole blood
contains other cells that affect platelet aggregation, testing was
repeated using a purified version of test samples made up of strictly
platelet-rich plasma.
At the start of the experiment, laboratory tests of
blood platelets in women were found four times more likely than in men
to aggregate when exposed to arachidonic acid, a clot-inducing chemical
in the pathway that is most suppressed by aspirin.
While taking aspirin, participants maintained a
strict and consistent dietary and exercise regimen, with no smoking or
consumption of foods that by themselves affect platelet activity, such
as caffeine, chocolate, wine or grapefruit juice. Physical examinations
and pill counts were conducted to ensure that all participants adhered
to the study protocol. Because aspirin reaches its maximal effect in the
body at five days, the researchers say a longer study testing period was
not required to determine the drug's effects on platelet function.
Funding was provided by the National Heart, Lung
and Blood Institute, a member of the National Institutes of Health, and
the Johns Hopkins Clinical Research Center.
Besides Becker and Faraday, other investigators in
this research were Jodi Segal, M.D.; Dhananjay Vaidya, M.D., Ph.D.; Lisa
Yanek, M.P.H.; J. Enrique Herrera-Galeano, M.S.; Paul Bray, M.D.; Taryn
Moy, M.S.; and Lewis Becker, M.D.
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