Objective: The aim of this study was to evaluate the prevalence of aspirin non-responsiveness using whole blood multiple electrode aggregometry and to investigate the role of different clinical and laboratory variables associated with the lack of response.
Methods: The present study included 116 aspirin treated patients presented with acute coronary syndromes or stroke. Response to aspirin was assessed by impedance aggregometry using arachidonic acid as agonist, in a final concentration of 0.5 mM (ASPI test).
Results: In our data set 81% (n=94) were responders and 19% (n=22) non-responders showing high-on-aspirin platelet reactivity. Correlation analysis showed that the ward of admittance, low-density lipoproteins (LDL), concomitant antibiotic treatment, beta-adrenergic receptor blockers, history of myocardial infarction as well as PCI performed on Cardiology patients have different degrees of association with aspirin response.
Conclusion: Concomitant treatment with beta-adrenergic receptor inhibitors, history of myocardial infarction and Cardiology ward admittance significantly increased the chance of responding to aspirin treatment whereas antibiotic therapy and low-density lipoproteins cholesterol seemed to increase the risk of high-on-aspirin residual platelet reactivity.
Tag Archives: ischemic stroke
Genetic Polymorphism TNFα -308G>A and Ischemic Stroke in Northern Romania
Introduction: Stroke is one of the leading causes of death in Romania. Evidence in supporting the role of the pro-inflammatory cytokine TNF-alpha in ischemic pathogenesis is now well established. The aim of the present study is to evaluate the relationship between TNFα -308G>A polymorphism and ischemic stroke in a Northern Romanian population group and to determine whether it has an influence on the risk of cerebral events. This is a cross-sectional, randomized, case-control study for the evaluation of TNFα -308G>A polymorphism alleles frequency among patients with ischemic stroke.
Material and method: The study included 108 patients diagnosed with ischemic stroke (neurological and CT scan examination), and 118 healthy unrelated controls. TNFα -308G>A genotyping was carried out using PCR-RFLP technique. The amplification of the relevant gene fragment was subjected to restriction enzyme digestion, followed by gel electrophoresis.
Results: Molecular analysis did not reveal an increased frequency of GA mutant genotype in the study group compared to the control group (p = 0.879, OR = 0.928, CI = 0.512–1.682).
Conclusions: We found no significant differences in distribution of the TNFα -308G>A polymorphism between ischemic stroke patients and controls.