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(Circulation. 1998;98:588-595.)
© 1998 American Heart Association, Inc.

Basic Science Reports

Asynchronous Electrical Activation Induces Asymmetrical Hypertrophy of the Left Ventricular Wall

Matthijs F. M. van Oosterhout, MD; Frits W. Prinzen, PhD; Theo Arts, PhD; Jan J. Schreuder, MD, PhD; Ward Y. R. Vanagt, MSc; Jack P. M. Cleutjens, PhD; ; Robert S. Reneman, MD, PhD

From the Departments of Physiology (M.F.M.v.O., F.W.P., W.Y.R.V., R.S.R.), Biophysics (T.A.), Anesthesiology (J.J.S.), and Pathology (J.P.M.C.), Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, the Netherlands.

Correspondence to Frits W. Prinzen, PhD, Department of Physiology, Cardiovascular Research Institute Maastricht, University of Maastricht, PO Box 616, 6200 MD Maastricht, Netherlands. E-mail frits.prinzen{at}fys.unimaas.nl

Background—Asynchronous electrical activation, induced by ventricular pacing, causes regional differences in workload, which is lower in early- than in late-activated regions. Because the myocardium usually adapts its mass and structure to altered workload, we investigated whether ventricular pacing leads to inhomogeneous hypertrophy and whether such adaptation, if any, affects global left ventricular (LV) pump function.

Methods and Results—Eight dogs were paced at physiological heart rate for 6 months (AV sequential, AV interval 25 ms, ventricular electrode at the base of the LV free wall). Five dogs were sham operated and served as controls. Ventricular pacing increased QRS duration from 47.2±10.6 to 113±16.5 ms acutely and to 133.8±25.2 ms after 6 months. Two-dimensional echocardiographic measurements showed that LV cavity and wall volume increased significantly by 27±15% and 15±17%, respectively. The early-activated LV free wall became significantly (17±17%) thinner, whereas the late-activated septum thickened significantly (23±12%). Calculated sector volume did not change in the LV free wall but increased significantly in the septum by 39±13%. In paced animals, cardiomyocyte diameter was significantly (18±7%) larger in septum than in LV free wall, whereas myocardial collagen fraction was unchanged in both areas. LV pressure-volume analysis showed that ventricular pacing reduced LV function to a similar extent after 15 minutes and 6 months of pacing.

Conclusions—Asynchronous activation induces asymmetrical hypertrophy and LV dilatation. Cardiac pump function is not affected by the adaptational processes. These data indicate that local cardiac load regulates local cardiac mass of both myocytes and collagen.

Key Words: hypertrophy • pacing • hemodynamics • remodeling • echocardiography

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