Plasma triglycerides as predictors of platelet responsiveness to aspirin in patients after first ischemic stroke

Background: Although aspirin (ASA) remains the most popular and accepted agent for secondary stroke prevention, its efficacy does not exceed 25%. Platelet function monitoring in ASA users suggests that some individuals exhibit a reduced or even absent antiplatelet response after ASA. This phenomenon, also known as 'resistance', is prevalent in stroke survivors. We sought to evaluate the blood lipid profile in poststroke ASA users dependent on their antiplatelet response to ASA. Methods: Ninety-six consecutive ASA users after first-ever ischemic stroke confirmed by imaging were prospectively enrolled. The platelet function analyzer (PFA-100, Dade Behring, USA) was utilized to assess the response after ASA. The lipid profile (total cholesterol, high-density lipoprotein, low-density lipoprotein and triglycerides) was measured using the Cardiochek instrument (Polymer Technology, USA) from the autologuos blood samples. Results: The poststroke duration was 3-26 months, and all patients were treated with ASA for at least 3 months. The allowed daily ASA doses were from 75 up to 325 mg, with a mean of 158 mg. The mean age of the patients was 71 years, almost 60% were women, and over 85% of the patients were treated with statins. Thirty-seven patients were identified as low ASA responders, while 59 patients exhibited an adequate response. There were no differences between ASA responders and nonresponders with regard to demographics, clinical characteristics, risk factors and concomitant medications. The lipid profile biomarkers were similar between groups with the exception of triglycerides, which were significantly increased in the patients with ASA resistance, compared with ASA responders. Conclusion: The fact that hypertriglyceridemia affects platelet response to ASA has potential practical implications in light of growing evidence that ASA may exert antiplatelet properties beyond the cyclooxygenase pathway. The mechanism of such an association is unclear but may be related to the diminished platelet membrane fluidity and inability of ASA to downregulate such 'strong' protected platelets.