Abstract
Introduction: Despite routine thromboprophylaxis with aspirin, thromboembolism (TE) continues to be a significant complication after the Fontan procedure. Data suggest that suboptimal ex-vivo aspirin-induced platelet inhibition-known as High on-Aspirin Platelet Reactivity (HAPR) is an independent risk factor for breakthrough TE. The occurrence of HAPR may potentially increase the risk of aspirin prophylaxis failure in children who underwent Fontan procedure. However, HAPR has not been adequately studied in this patient population. Hypothesis: There is a high incidence of HAPR in children after the Fontan procedure. Methods: We conducted a single-center, prospective, observational pilot study of children requiring Fontan procedure. Thromboelastography with platelet mapping (TEG-PM), platelet CD62P expression by flow-cytometry and urinary 11-dehydro-thromboxane B2 (11-dhTxB2) were measured at baseline prior to starting aspirin at 5 mg/kg/day and after at least 5 days of continuous therapy. HAPR was defined as less than 30% Arachidonic Acid (AA)-induced platelet aggregation inhibition as measured by TEG-PM. Results: 17 patients (11 males and 6 females, median age 3 years) were enrolled. HAPR was identified in 9/17 (53%) with 3/9 (33%) patients exhibiting no detectable AA-induced platelet aggregation inhibition. There was no significant effect of aspirin on percentage of activated platelets (i.e.: platelets expressing CD62P marker) in children with or without HAPR. In contrast to children with HAPR, aspirin therapy in children without HAPR led to significant reduction in urinary 11-dhTxB2 levels (Table 1). Conclusions: A significant proportion of children with single ventricle physiology exhibited HAPR in the immediate post-operative period after Fontan procedure. Further studies are needed to examine association of HAPR with increased risk of TE in this patient population.
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