Urinary 11-dehydrothromboxane B2 levels were significantly higher in aspirin-treated stable coronary artery disease patients with a history of major adverse cardiovascular events compared to those without.
Cross-Sectional (n=82)
Does urinary 11-dehydrothromboxane B2 level correlate with a history of MACE in patients with stable coronary artery disease taking aspirin?
High urinary 11-dehydrothromboxane B2 levels are associated with a history of MACE in patients with stable coronary artery disease on aspirin, suggesting its utility as a marker of aspirin resistance.
Absolute Event Rate: 587.8% vs 438.3%
p-value: p=0.001
Introduction. Acetylsalicylic acid (ASA, aspirin) resistance is the inability to reduce thromboxane A2 synthesis in platelets and inhibit platelets activation and aggregation while taking ASA. Assessment of urinary 11-dehydrothromboxane B2 (11-dhTxB2) levels is one of the methods to identify aspirin resistance. Our research aimed to investigate whether urinary 11-dhTxB2 levels and other clinical and laboratory parameters are associated with a history of major adverse cardiovascular events (MACE) including myocardial infarction and ischaemic stroke in aspirin-treated patients with stable coronary artery disease. Patients and methods. In a cross-sectional study we investigated 82 patients with stable coronary artery disease who took ASA at doses of 75–150 mg/day. We used the evaluation of the urinary 11-dhTxB2 levels standardized by creatinine as a method to identify aspirin resistance. Statistical analysis was performed using Mann-Whitney U-test, ROC-analysis and multivariable logistic regression. Results. The medians of urinary 11-dehydrothromboxane B2 level in patients with and without MACE were 587.8 (Q1-Q3 512.8–800.3) pg/mg creatinine and 438.3 (Q1–Q3 337.6–577.9) pg/mg creatinine, respectively (p=0.001). The threshold level of urinary 11-dhTxB2, which predicted a high risk of aspirin resistance, was 521.1 pg/mg creatinine, and in 36 (43.9 %) patients the concentration of the 11-dhTxB2 exceeded this level. The regression model characterising the dependence of the presence of a history of MACE was constructed. It included platelet count, urinary levels of 11-dhTxB2 and the presence of type 2 diabetes. Sensitivity and specificity of the model were 55 % and 88.9 %, respectively. Conclusions. The results of the study demonstrate that the antiplatelet effect of aspirin is weaker in stable coronary artery disease patients with a history of MACE than in those without a history of MACE.
Lukianets et al. (Wed,) conducted a cross-sectional in Stable coronary artery disease (n=82). Acetylsalicylic acid vs. Patients without a history of major adverse cardiovascular events (MACE) was evaluated on Median urinary 11-dehydrothromboxane B2 level (pg/mg creatinine) (p=0.001). Urinary 11-dehydrothromboxane B2 levels were significantly higher in aspirin-treated stable coronary artery disease patients with a history of major adverse cardiovascular events compared to those without.