Key result
Thienopyridine nonresponders show higher platelet activation, but ~20% of responders retain high thrombin responsiveness.
Why the study?
Do thienopyridine nonresponders exhibit higher susceptibility to thrombin- and ADP-inducible platelet activation compared to responders in patients undergoing angioplasty and stenting?
Population
317 patients undergoing angioplasty and stenting for cardiovascular disease receiving thienopyridines
Comparison
High on-treatment residual ADP-inducible… vs Adequate thienopyridine-mediated platelet…
Design
Cohort
Authors
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Suggests potential benefit of thrombin inhibition even among responders; leaves open whether this improves outcomes after stenting.
Observational (n=317)
Do thienopyridine nonresponders exhibit higher susceptibility to thrombin- and ADP-inducible platelet activation compared to responders in patients undergoing angioplasty and stenting?
p-value: p=≤0.02
Thienopyridine nonresponders have higher susceptibility to thrombin- and ADP-inducible platelet activation, and even adequate responders often retain preserved responsiveness to thrombin, suggesting a potential benefit for additional thrombin inhibition.
Gremmel et al. (2013) conducted an observational in Cardiovascular disease (n=317). High on-treatment residual ADP-inducible platelet reactivity (HRPR) vs. Adequate thienopyridine-mediated platelet inhibition was evaluated on TRAP-6- and ADP-inducible P-selectin expression, activated GPIIb/IIIa and monocyte-platelet aggregate (MPA) formation (p=≤0.02). Thienopyridine nonresponders exhibited significantly higher TRAP-6- and ADP-inducible platelet activation than responders (P≤0.02), though ~20% of responders retained high thrombin responsiveness.
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