Plasma Triglycerides as Predictors of Platelet Responsiveness to Aspirin in Patients after First Ischemic Stroke

Abstract

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.

Aspirin resistance in patients with acute ischemic stroke

“…Similarly, Bennett et al [17] did not find any significant differences between aspirin-resistant and aspirin-sensitive patients, although they reported a trend towards lower rates of diabetes, carotid stenosis and hypercholesterolemia among resistant patients. While Boncoraglio et al [26] also did not find any significant difference between aspirin responders and nonresponders, Karepov et al [27] pointed out that the only significant difference between patients with and without aspirin resistance was the triglyceride levels. Jeon et al [28] reported that patients with aspirin resistance had higher NIHSS scores.…”

“…Other mechanisms such as activation of pathways other than the cyclooxygenase-thromboxane pathway, increased platelet turnover during thrombotic events and increased expression of platelet surface P-selectin might also be important in the development of aspirin resistance after acute stroke [39]. Even plasma triglycerides were suggested to be a predictor of platelet responsiveness to aspirin in patients with ischemic stroke [27].…”

Antiplatelet Treatment in Ischemic Stroke Treatment

“…In an early small retrospective clinical study, hyperlipidemia has been found to enhance the risk of ASA failure in patients after first-ever ischemic stroke [53]. Later it has been reported that hyperlipidemia may serve as an independent predictor of ASA resistance in poststroke cohorts [54]-However, how the blood lipid profile affects ASA resistance has not been extensively studied.…”

“…Later it has been reported that hyperlipidemia may serve as an independent predictor of ASA resistance in poststroke cohorts [54]-However, how the blood lipid profile affects ASA resistance has not been extensively studied. Therefore, Karepov et al [53] sought to define the potential association of conventional components of blood lipids with platelet responsiveness in poststroke ASA users. These authors studied ninety-six consecutive ASA users after first-ever ischemic stroke confirmed by imaging were prospectively enrolled.…”

Glycated albumin predicts the effect of dual and single antiplatelet therapy on recurrent stroke

“…24,25 We have adjusted these factors and found that GA remained to have an independent effect on antiplatelet therapy and the outcomes. This association was independent of history of diabetes mellitus.…”