High Risk of Cardiovascular Events in Patients, Biosynthesis of Aspirin-Resistant Thromboxane And The Risk Of Stroke, Myocardial Infarction Or Death

In a higher-risk group, we investigated if aspirin resistance, which is defined as inability to reduce production of thromboxane, enhanced the risk for cardiovascular disease. Methods: The Cardiac Outcome Preventive Assessment Study collected baseline urine samples from 5000 patients. A level of urinary 11-dehydro-thromboxane B2 was measured, which is a marker of within vitro cell generation of thromboxane, in 400 cured patients with aspirin having a cardiovascular death, stroke and infarction, stroke during a 5-year follow-up and in 400 age - and matching sex control subjects, which did not have an event, using a nested case-control design. Result: After accounting for baseline differences, the risks of infarction, strokes, or cardiac mortality rose with every fourth of 11-dihydro-thromboxane B2, with individuals in the top fourth section having a 1.9-fold greater threat than those from the lower portion (“OR, 1.9; 95% CI, 1.3 to 2.8; p=0.009). The upper quartile showed a 2-fold increased myocardial infarction risk ("OR, 2.1; 95% CI, 1.3 to 3.5; p=0.07) and a 3.6-fold elevated risk of cardiac death ("OR, 3.6; 95% CI, 1.78to 7.5; p=0.01) than the lower quartile. Conclusions: the 11-dehydro thromboxane B2 level in urine, better determine the risk of cardiovascular events or cardiovascular death in aspirin-treated patients. These findings also depicts that patients with elevated urine 11-dehydro thromboxane B2 concentrations are more impervious to aspirin, and could profit from greater antiplatelet medications or therapies that even more efficiently stop thromboxane generation in vivo or activities.