NEW YORK (Reuters Health) Mar 24 - Clinical trials have suggested that aspirin prophylaxis is less effective in preventing MI in women than in men, although women do benefit from a similar reduction in risk of ischemic stroke. However, new study results show that the lower efficacy in women is not due to a failure of aspirin to suppress platelet aggregation, as has been proposed.

"Women are clearly benefiting from taking aspirin and should continue to take it to improve their cardiovascular health," Dr. Diane M. Becker states in a Johns Hopkins press release. "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."

To explore why aspirin seems to exert different effects in men and women, Dr. Becker, from Johns Hopkins Medical Institutions in Baltimore, and her team studied the effects of 14 days of aspirin therapy on platelet reactivity in unaffected individuals from families with premature coronary disease. They report their findings in the Journal of the American Medical Association for March 22/29.

Included in the study were unaffected healthy siblings of 403 patients with coronary heart disease events before 60 years of age, along with their adult offspring (571 men, 711 women). Platelet function was assessed at baseline and after 14 days of aspirin 81 mg daily, upon exposure to several agonists.

At baseline, platelet aggregation in reaction to all agonists was higher in women than in men, though the differences were "modest," the authors note.

For example, whole blood exposed to arachidonic acid 0.5 mM (which directly measures the cyclooxygenase-1 pathway, considered to be the most protective against MI), aggregation was 94.9% in men and 98.0% in women. Corresponding values after exposure to collagen 1 g/mL were 20.9% and 22.0%.

After aspirin treatment, most men and women demonstrated zero aggregation after exposure to arachidonic acid.

In platelet aggregation assays indirectly related to COX-1 (exposure to collagen, adenosine diphosphate and epinephrine), women demonstrated more inhibition but still had modestly but significantly more residual aggregation.

Closure time was measured in whole blood loaded into cartridges containing collagen and epinephrine. It was similar between men and women at baseline, but after aspirin, 32.4% of men and 50.8% of women had platelet function analyzer closure times of less than 300 seconds.

Multivariable analyses showed that the greatest contribution to the total variance in aggregation outcomes after exposure to agonists was the baseline level of aggregation. In most analyses, sex was not a significant predictor after adjustment for baseline aggregation.

"Although women in our study still retained a modest residual platelet reactivity that exceeds that of men, regardless of age," Dr. Becker's team concludes, "there is virtually total suppression of the COX-1 direct platelet function pathways in most women."