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Low-Dose Aspirin in Pregnancy

From the Departments of Obstetrics and Gynecology, Pediatrics, Medicine-Hematology, and Physiology and Biophysics, University of Tennessee, Memphis, Tennessee.

In a prospective study, we evaluated the effects of low-dose aspirin on maternal and neonatal plasma 6-keto-prostaglandin (PG) F₁ concentration, platelet aggregation, platelet thromboxane production, and neonatal transitional circulation. Forty women, at a mean (± SD) of 37 ± 2 weeks' gestation, were randomized to receive (N = 10 each) placebo or 20, 60, or 80 mg of aspirin per day until delivery. Maternal serum 6-keto-PGF₁ levels were not affected by these doses of aspirin, whereas thromboxane B₂ generated during clotting of maternal blood was decreased significantly by 60 and 80 mg of aspirin by 1 week of therapy. Maternal platelet thromboxane B₂ production in response to adenosine diphosphate or collagen was reduced 98% by the 80-mg dose after 1 week of aspirin therapy. The 60-mg dose reduced maternal platelet thromboxane B₂ production in response to adenosine diphosphate (50% decrease) or collagen (60% decrease) after 1 week of treatment, a nonsignificant difference. After 2 weeks of treatment with 60 mg of aspirin, platelet thromboxane B₂ production induced by both collagen and adenosine diphosphate was inhibited significantly (P < .01). Neonatal serum levels of 6-keto-PGF₁ and thromboxane B₂ were not affected by any doses of aspirin. Further, neonatal platelet aggregation in response to platelet stimulation by collagen and adenosine diphosphate was not inhibited. All neonates had echocardiographic evidence of a patent ductus arteriosus, and noninvasive estimates of pulmonary arterial pressure were similar among the groups of infants. We conclude that 60–80 mg of aspirin per day in the third trimester of pregnancy selectively inhibits maternal platelet cyclooxygenase without affecting neonatal platelet aggregation or pulmonary circulation.

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