Our aim was to determine the prevalence of platelet dysfunction using an end point of assembly into a stable thrombus after severe injury.
OBJECTIVES: This study sought to determine the prevalence of platelet aspirin resistance using methods that directly indicate the degree of platelet cyclooxygenase inhibition.
Controversy exists on the prevalence of platelet resistance to aspirin in patients with coronary artery disease and effects of aspirin dose on inhibition.
Compared to matched controls, prevalence of platelet-mediated clumping was higher in cases (P = .019), in children presenting with prostration (P = .049) and in children with severe anaemia (P = .025).025
The most likely reason is the higher prevalence of platelet aggregates in feline samples, which have been reported in 64% of feline samples [ 20].
We observed a higher prevalence of thrombocytopenia (platelets ≤125.0×10/μl) in HIV-infected compared to HIV-uninfected women, but no association between thrombocytopenia and CD4 count within HIV-infected women.
To evaluate the prevalence of dual platelet inhibition in cases of severe retrobulbar hemorrhage following retrobulbar and peribulbar anesthesia.
The prevalence of high platelet reactivity (HPR) in patients who have switched from clopidogrel to prasugrel during maintenance phase after an acute coronary syndrome (ACS) event is unknown.
A meta-regression, based on the individual trials, of the prevalence of anti-platelet therapy on relative risk of ischaemic heart disease gave a similar result (p = 0.056).
Finally, ticagrelor was extremely effective in reducing the prevalence of high residual platelet reactivity using previously defined cutoffs; nearly all patients during ticagrelor therapy, irrespective of clopidogrel response status, had platelet reactivity below the cutoffs associated with increased ischaemic risk.
Prevalence and level of platelet-mediated clumping was significantly higher in isolates from severe cases compared to matched controls, both when the assays were conducted with unadjusted parasitemias (Table 2 and 3) and when parasitemias were adjusted to 1% (Table S1).
