Abstract
During the last two decades an increasing body of evidence has built up that ventricular pacing causes abnormal, asynchronous electrical activation of the ventricles, and thereby also causes abnormal contraction patterns and reduced pump function [1]. During asynchronous contraction workload, myocardial blood flow and oxygen consumption are reduced in early-activated and increased in late-activated regions [1]. Long-term ventricular pacing induces ventricular dilatation and asymmetric hypertrophy, the latter due to local variation in myocyte size and proportional increase in collagen [2]. The latter study cited is an elegant demonstration that local myocardial load regulates local myocardial growth. However, the degree of hypertrophy appears to depend on the degree of initial hypertrophy. Left ventricular (LV) pacing in normal dog hearts induced circa 40% hypertrophy in the late-activated septum. In contrast, right ventricular (RV) pacing in hearts that were hypertro- phying due to aortic banding showed no excessive hypertrophy in the late-activated LV free wall, but rather a reduction in hypertrophy of the early-activated septum [3]. Moreover, the asymmetry of hypertrophy appears to depend on the site of pacing: around 40% in case of LV pacing versus around 10% in the caseof RV pacing.
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References
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© 2004 Springer-Verlag Italia
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Peschar, M., Vos, M.A., Prinzen, F.W. (2004). Reverse Structural and Contractile Remodeling without Reverse Electrical Remodeling by Biventricular and Right Ventricular Apex Pacing in Dogs with Chronic AV Block. In: Raviele, A. (eds) Cardiac Arrhythmias 2003. Springer, Milano. https://doi.org/10.1007/978-88-470-2137-2_102
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DOI: https://doi.org/10.1007/978-88-470-2137-2_102
Publisher Name: Springer, Milano
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