Background:
Aspirin is the most commonly used
antiplatelet agent for the prevention of
cardiovascular diseases. However, a certain proportion of patients do not respond to
aspirin therapy. The mechanisms of
aspirin non-response remain unknown. The unique metabolomes in platelets of patients with
coronary artery disease (CAD) with
aspirin non-response may be one of the causes of
aspirin resistance. Materials and Methods: We enrolled 29 patients with CAD who were
aspirin non-responders, defined as a study subject who were taking
aspirin with a platelet aggregation time less than 193 s by PFA-100, and 31 age- and sex-matched patients with CAD who were responders. All subjects had been taking 100 mg of
aspirin per day for more than 1 month. Hydrophilic metabolites from the platelet samples were extracted and analyzed by nuclear magnetic resonance (NMR). Both 1D 1H and 2D J-resolved NMR spectra were obtained followed by spectral processing and multivariate statistical analysis, such as partial least squares discriminant analysis (PLS-DA). Results: Eleven metabolites were identified. The PLS-DA model could not distinguish
aspirin non-responders from responders. Those with low serum
glycine level had significantly shorter platelet aggregation time (mean, 175.0 s) compared with those with high serum
glycine level (259.5 s). However, this association became non-significant after correction for multiple tests. Conclusions: The hydrophilic metabolic profile of platelets was not different between
aspirin non-responders and responders. An association between lower
glycine levels and higher platelet activity in patients younger than 65 years suggests an important role of
glycine in the pathophysiology of
aspirin non-response.