Hydrogels are a versatile tool for a multitude of applications in biomedical research and clinical practice. Especially collagen and fibrin hydrogels are distinguished by their excellent biocompatibility, natural capacity for cell adhesion and low immunogenicity. In many ways, collagen and fibrin represent an ideal biomaterial, as they can serve as a scaffold for tissue regeneration and promote the migration of cells, as well as the ingrowth of tissues. On the other hand, pure collagen and fibrin materials are marked by poor mechanical properties and rapid degradation, which limits their use in practice. This paper will review methods of modification of natural collagen and fibrin materials to next-generation materials with enhanced stability. A special focus is placed on biomedical products from fibrin and collagen already on the market. In addition, recent research on the in vivo applications of collagen and fibrin-based materials will be showcased.

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.

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