"We investigated markers of platelet reactivity and low-grade inflammation, and their association with early markers of vascular disease in subjects with prediabetes and new onset type 2 diabetes (NDOM)."

"Platelet reactivity was evaluated as 11-dehydrothromboxane B₂ urinary levels (TXB2)"

"TXB2 urinary levels were independently associated with hs-CRP, fibrinogen and HbA1c in multiple regression analysis."

"Digoxin use was shown to be associated with an increased risk of cardiovascular events in atrial fibrillation (AF). We hypothesized that digoxin may affect cardiovascular risk by increasing platelet activation. Urinary excretion of 11-dehydro-thromboxane B₂ (TxB₂), a marker of platelet activation, and serum digoxin concentration (SDC) were measured. Patients in the upper tertile of SDC showed higher 11-dehydro-TxB₂ compared with non-digoxin users. In vitro study showed an increased basal platelet activation in patients with AF compared with healthy subjects."

"Thromboxane (TX)-dependent platelet activation and lipid peroxidation, as reflected in vivo by the urinary excretion of 11-dehydro-TXB₂ and 8-iso-prostaglandin (PG)F_2a, play a key role in atherothrombosis in obesity and type 2 diabetes mellitus (T2DM) since the earlier stages."

"After achievement of the weight loss target, a comparable reduction in U-11-dehydro-TXB₂ (between-group p = 0.679) and 8-iso-PGF-_2a (p = 0.985) was observed in both arms in parallel with a comparable improvement in glycemic control, insulin sensitivity, SAT, high-sensativity C-reactive protein (hs-CRP)." 

"The antiplatelet effect of aspirin is attributed to platelet cyclooxygenase-1 inhibition.  Controversy exists on the prevalence of platelet resistance to aspirin in patients with coronary artery disease and effects of aspirin dose on inhibition.  Our primary aim was to determine the degree of platelet aspirin responsiveness in patients, as measured by commonly used methods, and to study the relation of aspirin dose to platelet inhibition."

"Meta-analyses of clinical trials have indicated that aspirin treatment of patients with vascular disease is associated with a 25% to 44% reduction in adverse cardiovascular events.  The antithrombotic effect of aspirin has been primarily attributed to the irreversible blockade of the cyclooxygenase-1 (COX-1) enzyme in platelets that leads to attenuation in the production of an important platelet agonist, thromboxane A_2.  In recent years, an increasing number of reports about aspirin resistance has led to a growing concern among clinicians and patients about the efficacy of aspirin treatment.  Various studies have evaluated the antiplatelet effect of aspirin therapy and have reported the prevalence of aspirin resistance to be between 9.4% to 35%."