Evaluation of platelet function in pregnancy. Comparative studies in non-smokers and smokers

We have evaluated the possible role of platelet functional abnormalities as a contributory cause of thrombosis during pregnancy and to the increased fetal mortality and morbidity among women who smoke. Fifty-three pregnant women were enrolled and evaluated on two separate prenatal visits held between the 20th and 36th week of pregnancy and, when possible, post partum. Smoking status was evaluated by personal statement and alveolar carbon monoxide levels. Women in the smoking group deliberately avoided cigarettes for at least 20 minutes before sampling. Plasma levels of beta-thromboglobulin, thromboxane B2, and 6-Keto PGF1 alpha were evaluated. A significant increase in 6-Keto PGF1 alpha was noted among smoking women as pregnancy advanced. 6-Keto PGF1 alpha levels decreased among non-smoking women while beta-thromboglobulin increased significantly between the 20th and 33rd week of pregnancy in non-smokers. Platelet aggregation, both in platelet rich plasma and in whole blood (by impedance aggregometry), was evaluated by five different parameters and four different aggregating agents. Significant differences between the non-smoking and smoking pregnant women were noted for selected age cohorts and aggregating agents. An increase in platelet reactivity among smokers was observed in whole blood by impedance aggregometry with adenosine diphosphate and in two age cohorts using platelet rich plasma. In two groups in which aggregation was significantly accelerated among non-smokers, epinephrine was used as the aggregating agent.