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Cardiovascular Research 2001 49(4):771-778; doi:10.1016/S0008-6363(00)00313-8
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Remodeling by ventricular pacing in hypertrophying dog hearts

Matthijs F.M van Oosterhouta, Theo Artsb, Arno M.M Muijtjensc, Robert S Renemana and Frits W Prinzena,*

aDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University and University Hospital, P.O. Box 616, 6200 MD Maastricht, The Netherlands
bDepartment of Biophysics, Cardiovascular Research Institute Maastricht, Maastricht University and University Hospital, Maastricht, The Netherlands
cDepartment of Medical Informatics, Cardiovascular Research Institute Maastricht, Maastricht University and University Hospital, Maastricht, The Netherlands

* Corresponding author. Tel.: +31-43-388-1200/1080; fax: +31-43-388-4166 frits.prinzen{at}fys.unimaas.nl

Objective: Asynchronous electrical activation of the left ventricle (LV), induced by ventricular pacing (VP), reduces mechanical load in early- and enhances it in late-activated regions. Consequently, chronic VP leads to asymmetric hypertrophy. We investigated whether such locally induced myocardial hypertrophy also occurs in the presence of pressure overload hypertrophy (POH). Methods: POH was induced by aortic banding in puppies. At age 9 months, seven dogs were paced at the right ventricular (RV) apex at physiological heart rate for 6 months (POH-pace group), while four POH dogs served as POH-control group. Changes in volume of the LV cavity and the total LV wall and of five LV wall sectors were measured by means of 2D-echocardiography and X-ray marker detection. Results: During the last 6 months of the protocol the volume of the five LV wall sectors increased in the POH-control group, ranging from 27±9 to 30±5% (mean±S.D.). In POH-pace animals sector wall volume in the four sectors at intermediate to long distance from the pacing site increased to a similar extent (ranging from 31±16 to 35±17%), but wall volume in the early-activated apical septum increased significantly less (17±21%). In these hearts myocyte diameter was significantly smaller in the apical septum than in the lateral LV wall. The regional difference in wall volume changes (19±21%) was significantly smaller in the POH-pace group than in chronically paced, non-hypertrophic, canine hearts in a previous study from our laboratory (43±14%). Conclusions: In hypertrophying hearts chronic pacing at the RV apex suppresses the development of hypertrophy in the early-activated apical septum but does not cause additional hypertrophy in late-activated regions, as is the case in non-hypertrophic hearts. The latter suggests that the local growth response is reduced in hypertrophying hearts.

KEYWORDS Hypertrophy; Remodeling; Ventricular function


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