Thromboembolic Complications in Fontan Patients: Population-Based Prevalence and Exploration of the Etiology
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Thromboembolic Complications in Fontan Patients : Population-Based Prevalence and Exploration of the Etiology. / Idorn, L; Jensen, A S; Juul, K; Reimers, J.I.; Johansson, P I; Sørensen, K E; Ostrowski, S R; Søndergaard, L.
In: Annals of Pediatric Cardiology, Vol. 34, No. 2, 2013, p. 262-72.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Thromboembolic Complications in Fontan Patients
T2 - Population-Based Prevalence and Exploration of the Etiology
AU - Idorn, L
AU - Jensen, A S
AU - Juul, K
AU - Reimers, J.I.
AU - Johansson, P I
AU - Sørensen, K E
AU - Ostrowski, S R
AU - Søndergaard, L
PY - 2013
Y1 - 2013
N2 - After the Fontan procedure, patients face an increased risk for thromboembolic events (TE). The etiology for this increased thrombogenecity is incompletely understood. This study aimed to determine the prevalence of TE in Danish Fontan patients and to bring new insights into the etiology of TE. Using a population-based design, we retrospectively identified all TEs in 210 Fontan patients. Whole blood assays (thromboelastography, thromboelastography functional fibrinogen and Multiplate) reflecting global hemostasis, clot strength and platelet aggregation were analyzed prospectively in 112 patients and plasma was analyzed in 76 patients for biomarkers reflecting endothelial-, glycocalyx-, platelet-, and fibrinolysis function (histone-complexed DNA fragments, Protein C, soluble CD40 ligand, soluble thrombomodulin, syndecan-1, tissue-type plasminogen activator). The results were compared in groups stratified according to age, antithrombotic therapy, TE, and glycocalyx degradation (syndecan-1
AB - After the Fontan procedure, patients face an increased risk for thromboembolic events (TE). The etiology for this increased thrombogenecity is incompletely understood. This study aimed to determine the prevalence of TE in Danish Fontan patients and to bring new insights into the etiology of TE. Using a population-based design, we retrospectively identified all TEs in 210 Fontan patients. Whole blood assays (thromboelastography, thromboelastography functional fibrinogen and Multiplate) reflecting global hemostasis, clot strength and platelet aggregation were analyzed prospectively in 112 patients and plasma was analyzed in 76 patients for biomarkers reflecting endothelial-, glycocalyx-, platelet-, and fibrinolysis function (histone-complexed DNA fragments, Protein C, soluble CD40 ligand, soluble thrombomodulin, syndecan-1, tissue-type plasminogen activator). The results were compared in groups stratified according to age, antithrombotic therapy, TE, and glycocalyx degradation (syndecan-1
U2 - 10.1007/s00246-012-0431-4
DO - 10.1007/s00246-012-0431-4
M3 - Journal article
C2 - 22843202
VL - 34
SP - 262
EP - 272
JO - Annals of Pediatric Cardiology
JF - Annals of Pediatric Cardiology
SN - 0974-2069
IS - 2
ER -
ID: 48549164