RESUMEN
The atrioventricular (AV) node is permanently damaged in approximately 3 percent of congenital heart surgery operations, requiring implantation of a permanent pacemaker. Improvements in pacemaker design and in alternative treatment modalities require an effective in vivo model of complete heart block (CHB) before testing can be performed in humans. Such a model should enable accurate, reliable, and detectable induction of the surgical pathology. Through our laboratorys efforts in developing a tissue engineering therapy for CHB, we describe here an improved in vivo model for inducing chronic AV block. The method employs a right thoracotomy in the adult rabbit, from which the right atrial appendage may be retracted to expose an access channel for the AV node. A novel injection device was designed, which both physically restricts needle depth and provides electrical information via electrocardiogram interface. This combination of features provides real-time guidance to the researcher for confirming contact with the AV node, and documents its ablation upon formalin injection. While all animals tested could be induced to acute AV block, those with ECG guidance were more likely to maintain chronic heart block >12 h. Our model enables the researcher to reproduce both CHB and the associated peripheral fibrosis that would be present in an open congenital heart surgery, and which would inevitably impact the design and utility of a tissue engineered AV node replacement.
Asunto(s)
Animales , Femenino , Conejos , Nodo Atrioventricular/cirugía , Ablación por Catéter/métodos , Bloqueo Cardíaco/cirugía , Toracotomía/métodos , Modelos Animales de Enfermedad , Electrocardiografía , Fluoroscopía , Bloqueo Cardíaco/etiologíaRESUMEN
The atrioventricular (AV) node is permanently damaged in approximately 3% of congenital heart surgery operations, requiring implantation of a permanent pacemaker. Improvements in pacemaker design and in alternative treatment modalities require an effective in vivo model of complete heart block (CHB) before testing can be performed in humans. Such a model should enable accurate, reliable, and detectable induction of the surgical pathology. Through our laboratory's efforts in developing a tissue engineering therapy for CHB, we describe here an improved in vivo model for inducing chronic AV block. The method employs a right thoracotomy in the adult rabbit, from which the right atrial appendage may be retracted to expose an access channel for the AV node. A novel injection device was designed, which both physically restricts needle depth and provides electrical information via electrocardiogram interface. This combination of features provides real-time guidance to the researcher for confirming contact with the AV node, and documents its ablation upon formalin injection. While all animals tested could be induced to acute AV block, those with ECG guidance were more likely to maintain chronic heart block >12 h. Our model enables the researcher to reproduce both CHB and the associated peripheral fibrosis that would be present in an open congenital heart surgery, and which would inevitably impact the design and utility of a tissue engineered AV node replacement.
Asunto(s)
Nodo Atrioventricular/cirugía , Ablación por Catéter/métodos , Bloqueo Cardíaco/cirugía , Toracotomía/métodos , Animales , Modelos Animales de Enfermedad , Electrocardiografía , Femenino , Fluoroscopía , Bloqueo Cardíaco/etiología , ConejosRESUMEN
OBJECTIVES: The objective was to study the impact of nonadherence on late rejection after pediatric heart transplantation. STUDY DESIGN: This was a retrospective cohort study of cardiac transplant recipients surviving >6 months (n = 50). Patients were stratified by episodes of late rejection. End points were defined by cyclosporin A (CSA) level, CSA level variability, and patient admission of nonadherence. RESULTS: In 15 patients there were 49 episodes of late rejection, and 37 (76%) were associated with nonadherence. Of these patients, 7 of 15 died, and 3 of 15 had transplant coronary artery disease. Risk factors for the rejection were single-parent home, non-white, older age, and higher CSA level variability. In 35 nonrejectors there were 4 deaths from sepsis, post-transplant lymphoproliferative disease, renal failure, and encephalomyelitis. CONCLUSION: Late rejection after pediatric heart transplantation is associated with nonadherence, is common during adolescence, and is associated with poor outcome.