Abstract 1389: Epicardial Wave Break and Arrhythmogenicity after Fibrin Sealant Injections: a Novel Cell Delivery Scaffold
Background: Advances in cell culture as well as delivery and implantation methods have created enthusiasm for cell-based therapies as a feasible means to treat ischemic heart disease, cardiomyopathy, and arrhythmias. The injection of cells in a “scaffold”, such a fibrin sealant (Crosseal), has been proposed as a means to improve cell survival during implantation. It is unknown if injections with fibrin sealant are arrhythmogenic.
Methods: We used optical mapping techniques to study the effects of linear injections on wavefront activation and arrhythmogenicity in Langendorff-perfused rabbit and dog hearts. Using a 25 gauge needed, fibrin sealant (6 dogs, 2 rabbits), ethanol (3 dogs), or saline (3 dogs) were injected in a line from the base to the apex to the base of the epicardial surface of the right ventricle. Each injection was 0.25 ml for a total of 1 (rabbits) or 4 (dogs) ml.
Results: In both rabbits (100%) and 5 (83%) of the dogs that received fibrin sealant injections, conduction block, verified with apical and medial-lateral pacing maneuvers, was manifested as wave break along the injection line. In contrast, 0 saline dogs and 1 (33%) of the ethanol dogs developed similar conduction block. Shortly after the creation of the injection line with fibrin sealant, both rabbits developed VT originated at the apical portion of the line that degenerated to VF. In 3 (50%) of the fibrin sealant dogs, monomorphic VT was observed shortly after the linear line was created that degenerated to VF also at the apical portion of the line. In the other 3 (50%) fibrin sealant dogs, spontaneous VF was observed. In contrast, no spontaneous arrhythmias were observed in the saline or ETOH treated dogs over a 30 minute observation period.
Conclusions: Optical mapping consistently recorded conduction block, VT, and VF after linear fibrin sealant injections. The fibrin sealant line altered the underlying electrophysiologic substrate facilitating the occurrence of spontaneous ventricular arrhythmias. These data suggest cellular scaffolds developed to enhance cell survival may result in untoward arrhythmias and require further investigation for prevention of this complication.