Systemic thromboxane generation appears to increase the risk of all-cause and cardiovascular mortality regardless of aspirin use, reveals a study. Hence, its measurement may help inform therapy modification, especially in individuals without cardiovascular disease (CVD).
A total of 3,044 participants (mean age 66 years, 53.8 percent women) in the Framingham Heart Study were included in the analysis. The authors measured stable thromboxane B2 metabolites (TXB2-M) using enzyme-linked immunosorbent assay in banked urine of these individuals. Finally, they assessed the link of TXB2-M to survival over a median observation period of 11.9 years by multivariable modeling.
At the index examination, median TXB2-M were lower in 1,363 (44.8 percent) participants on aspirin than in nonusers (1.147 vs 4,179 pg/mg creatinine; p<0.0001).
TXB2-M significantly correlated with all-cause and cardiovascular mortality regardless of aspirin use (hazard ratio [HR], 1.96 and 2.41, respectively; p<0.0001 for both). The significant association persisted even after adjusting for mortality risk factors for similarly aged individuals (HR, 1.49 and 1.82, respectively; p≤0.005 for both).
Among 2,353 participants without CVD, TXB2-M also correlated with cardiovascular mortality in aspirin nonusers (adjusted HR, 3.04, 95 percent confidence interval [CI], 1.29‒7.6), but not in aspirin users. On the other hand, aspirin use correlated with all-cause mortality in those with low (adjusted HR, 1.46, 95 percent CI, 1.14‒1.87) but not elevated TXB2-M.
“Persistent systemic thromboxane generation, predominantly from nonplatelet sources, in aspirin users with CVD is a mortality risk factor,” the authors said.