Effects of different aspirin formulations on platelet aggregation times and on plasma salicylate concentrations.
BACKGROUND
Early aspirin treatment is widely used to inhibit platelet activity and to reduce morbidity and mortality in patients presenting with an acute myocardial infarction or a stroke. A number of different aspirin formulations have been used for this purpose; however, a comparison of their effectiveness in inhibiting early platelet aggregation has not been determined.


METHODS
In this study, we determined plasma salicylate concentrations and platelet inhibitory activities at various times after ingestion of three commonly used aspirin formulations: soluble aspirin (Alka-Seltzer), 325 mg, chewed baby aspirin, 324 mg, and whole compressed non-enteric coated aspirin, 324 mg. Twenty-four healthy volunteers, 18-39 years of age, participated in the prospective single-blinded triple-crossover study. Plasma salicylate concentrations and inhibition of arachidonic acid-induced platelet aggregation were determined on post-dose blood samples collected at 2.5, 5.0, 7.5, 10, 15, 20, 25, 30, and 40 min. All subjects crossed over to the other two formulations with at least 2 weeks between ingestions.


RESULTS
The median platelet inhibition times for the chewed, soluble, and whole aspirin formulations were 7.5, 7.5, and 10.0 min, respectively. Soluble and chewed aspirin were found to inhibit platelet aggregation faster than whole aspirin (p<0.001); however, there were no significant differences in platelet aggregation times between the soluble and chewed formulations (p<0.163). Inhibition of platelet aggregation was found to occur at an average plasma salicylate concentration of 2.46 microg/mL, regardless of method of ingestion.


CONCLUSIONS
The results indicate that soluble and chewed aspirin inhibit platelet aggregation in a shorter period of time than does whole aspirin. The results suggest that chewing baby aspirin or taking soluble buffered aspirin may be the preferred route of administration for early platelet inhibition.
Schwertner
H A
HA
Clinical Research, Wilford Hall Medical Center, Lackland, AFB, TX 78236-5300, USA. harvey.schwertner@lackland.af.mil
McGlasson
D
D
Christopher
M
M
Bush
A C
AC
D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D016718:Arachidonic Acid / Q000037:antagonists & inhibitors / Q000494:pharmacology; D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology*; D018592:Cross-Over Studies; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage* / Q000494:pharmacology; D011446:Prospective Studies; D012016:Reference Values; D012459:Salicylates / Q000097:blood*; D016037:Single-Blind Method; D012995:Solubility; D013608:Tablets, Enteric-Coated; D013997:Time Factors
D010975:Platelet Aggregation Inhibitors; D012459:Salicylates; D013608:Tablets, Enteric-Coated; D016718:Arachidonic Acid; D001241:Aspirin