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- W2992128432 abstract "We previously reported the presence of an acquired von Willebrand factor (vWF) abnormality characterized by absence of the highest molecular weight (raw) multimers in 12 children with non-cyanotic congenital cardiac lesions. In order to determine the prevalence and define the mechanism of the vWF defect, a prospective series of 17 children were studied at the time of cardiac catheterization. In addition to standard coagulation and vWF assays, vWF multimeric patterns were determined by SDS agarose electrophoresis using two agarose concentrations, low concentration (0.65%) and high concentration (3.0%). Nine of the 17 children had absence of high mw vWF multimers on 0.65% agarose gels as follows: Of 5 children with absence of high mw vWF multimers on 0.65% agarose gels, 4 had 3% agarose gel patterns similar to that seen in patients with Type IIA von Willebrand disease (vWd). Two of 3 studied had the presence of vWF:frag on crossed immunoelectrophoresis. The patterns were not different when samples were drawn into a cocktail of proteolytic inhibitors. There was no correlation of abnormal vWF multimers with elevated B thromboglobulin, low dose ristocetin induced platelet aggregation or abnormal platelet vWF subunits. Thus, abnormal vWF multimers are commonly associated with non-cyanotic congenital cardiac lesions, particularly VSD. The lack of abnormality in platelet vWF multimers, absent low dose ristocetin aggregation, and presence of vWF:frag suggests that these alterations may be secondary to fragmentation or are of endothelial cell origin." @default.
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- W2992128432 date "1987-01-01" @default.
- W2992128432 modified "2023-09-26" @default.
- W2992128432 title "ABNORMAL vWF IN CONGENITAL CARDIAC DISEASE: EVIDENCE FOR FRAGMENTATION" @default.
- W2992128432 doi "https://doi.org/10.1055/s-0038-1644086" @default.
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