Key result
Chronic rapid ventricular pacing for at least 4 weeks significantly prolonged the P-R interval in a porcine model of tachycardiomyopathy compared to unpaced controls.
Why the study?
Does chronic ventricular pacing prolong the P-R interval in a porcine model of tachycardia-induced cardiomyopathy?
Does chronic ventricular pacing prolong the P-R interval in a porcine model of tachycardia-induced cardiomyopathy?
p-value: p=<0.001
In a porcine model of tachycardia-induced cardiomyopathy, chronic ventricular pacing leads to prolonged P-R intervals, indicating electrical or structural remodeling of the cardiac conductive tissue.
May indicate conduction remodeling in tachycardiomyopathy; hypothesis-generating in this animal model and leaves human translation open.
The aim of the study was to assess the atrioventricular conduction in the model of porcine pacing induced tachycardiomyopathy. Fifty-one swine were examined: 27 were paced and 24 served as a control group. Every 4 weeks, the animals were anaesthetised for 1 h and an ECG Holter was performed. Thirty minutes after the onset of anaesthesia, P-R and R-R intervals were measured. Each result was assigned to the subgroup according to the animal’s weight and the presence or absence of previous pacing. P-R interval was longer in animals after at least 4 weeks of rapid ventricular stimulation than in adjusted group of the animals according to the body mass. Multivariate analysis has showed that longer P-R interval was related to male gender, higher body mass, slower heart rate, and history of previous pacing. Chronic ventricular pacing led to the slowing of atrioventricular conduction. The presence of differences in the duration of R-R intervals between groups was only found in swine weighing 120-139 kg. The R-R interval was shorter in paced animals, whereas PR interval was longer in that group, indicating that PR prolongation is related to electrical or structural remodelling of the cardiac conductive tissue but not increased sympathetic nervous system activity, which is expected to produce corresponding changes in PR and R-R intervals.
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Skrzypczak et al. (2013) studied Tachycardia-induced cardiomyopathy (n=51). Chronic rapid ventricular pacing vs. No chronic pacing was evaluated on P-R interval duration (p=<0.001). Chronic rapid ventricular pacing for at least 4 weeks significantly prolonged the P-R interval in a porcine model of tachycardiomyopathy compared to unpaced controls.
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