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Cardiovascular Research 2000 48(1):120-128; doi:10.1016/S0008-6363(00)00149-8
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Regional electrophysiological effects of left ventricular hypertrophy in isolated rabbit hearts under normal and ischaemic conditions

Robert Wolka, Kenneth P. Sneddonb, John Dempsterc, Kathleen A. Kanec, Stuart M. Cobbeb and Martin N. Hicksb,*

aDepartment of Cardiology, Medical Center for Postgraduate Education, Grochowski Hospital, Grenadierow 51/59, 04-073 Warsaw, Poland
bDepartment of Medical Cardiology, Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, UK
cDepartment of Physiology and Pharmacology, University of Strathclyde, Strathclyde Institute for Biomedical Sciences, 27 Taylor Street, Glasgow, G4 0NR, UK

* Corresponding author. Tel.: +44-141-211-0461; fax: +44-141-552-4683 m.n.hicks{at}clinmed.gla.ac.uk

Objectives: Left ventricular hypertrophy (LVH) has been reported to produce differential electrophysiological effects in isolated epicardial and endocardial cells. This study aimed to examine regional electrophysiological effects of LVH in normal and ischaemic conditions in the whole heart. Methods: LVH was secondary to perinephritis-induced hypertension. Monophasic action potential duration (MAPD90), effective refractory period (ERP) and conduction delay were measured in paced, isolated working rabbit hearts either at one right ventricular and two left ventricular sites (apical and basal epicardium) or at three left ventricular sites (apical and basal epicardium, apical endocardium). The hearts were subjected to 30 min of regional ischaemia and 15 min of reperfusion. Results: In non-ischaemic conditions, LVH produced uniform prolongation of MAPD90 and ERP in the left ventricular epicardium, but not in the endocardium. After coronary artery occlusion, LVH significantly increased ischaemia-induced transepicardial dispersion of repolarisation, but not refractoriness. LVH did not affect arrhythmogenesis in either non-ischaemic or ischaemic conditions. Conclusions: Differential effects of LVH on epicardial and endocardial electrophysiological parameters are also observed in the whole heart. In addition, the sensitivity of hypertrophied myocardium to ischaemia is increased and leads to an increase in ischaemia-induced dispersion of repolarisation. However, neither dispersion of refractoriness nor arrhythmogenesis are affected by LVH in non-ischaemic or ischaemic conditions in this experimental model.

KEYWORDS Hypertrophy; Ischaemia; Repolarisation; Ventricular arrhythmias


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