The effect of low-dose aspirin on platelet function during pregnancy compared to placebo: An explorative study. A letter to the Editor

Abstract

We read with interest Bij de Weg et al.’s, recent mechanistic report on the inhibitory effect of Aspirin on platelet function in patients with pre-eclampsia [1]. Compared to placebo, this study found that 80 mg of generic Aspirin demonstrated significant inhibitory effect on platelet function as evidenced by surrogate markers of platelet function (Verify Now® Aspirin Reaction Units [450.5 vs 648.0, p = 0.017]; Chronolog LTA [9.5% vs 94.5%, p = 0.009]; serum thromboxane B2 (TXB2) levels [11.9 ng/mL versus 175.9 ng/mL, p = 0.030] [1]. Despite the relatively small sample size of this exploratory study, its point estimates appear consistent with what has been reported from other studies examining Aspirin pharmacodynamics in different morbidities other than pregnancy [2].It is noteworthy that Bij de Weg et al.’s study did not provide information on the Aspirin formulation used in the study; although it still remains uncertain if enteric coating of aspirin would have significantly impacted the point estimate of platelet inhibition reported in that study. Enteric coating of Aspirin has recently generated intense mechanistic debate regarding its role in aspirin non responsiveness (as evidence by surrogate markers such as the proportion of TXB2 inhibition) [3]. Indeed, in a comprehensive proof-of-concept examination of prospectively recruited ethnically diverse patients with ischemic stroke (N = 42), we recently reported for the first-time absence of differential aspirin non responsiveness between stroke patients randomized to enteric coated (EC-ASA) vs. those allocated to the plain preparation (P-ASA).