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Malignant arrhythmias are a major cause of sudden cardiac death in adults with congenital heart disease. We developed a model to serially investigate electrophysiological properties in an animal model of right ventricular hypertrophy and failure.
We created models of compensated (cHF; n=11) and decompensated (dHF; n=11) right ventricular failure in Wistar rats by pulmonary trunk banding. Healthy controls underwent sham operation (Control; n=13). Surface electrocardiography was recorded from extremities, and inducibility of ventricular tachycardia was evaluated in vivo by programmed stimulation. Isolated right ventricular myocardium was analysed for mRNA expression of selected genes.
Banding caused an increased mRNA expression of both connexin 43 and the voltage-gated sodium channel 1.5, as well as a prolongation of PQ, QRS and QTc intervals. Ventricular tachycardia was induced in the majority of banded animals compared with none in the healthy control group. No differences were found between the two degrees of failure in neither the electrophysiological parameters nor inducibility.
The electrophysiological properties of rat hearts subjected to pulmonary trunk banding were significantly changed with increased susceptibility to ventricular tachycardia, but no differences were found between compensated and decompensated right ventricular failure. Furthermore, we demonstrate that in vivo electrophysiological evaluation is a sensitive method to characterise the cardiac electric phenotype in an experimental rat model.
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