Abnormal Action Potential Conduction in Isolated Human Hypertrophied Left Ventricular Myocardium

Authors

  • HUGH McINTYRE M.D., MRCP,

    1. Institute of Urology and Nephrology, University College, London, United Kingdom
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      Dr. Hugh McIntyre, Consultant Physician. The Conquest Hospital, The Ridge, St. Leonards-on-Sea. E. Sussex TN37 7RD. United Kingdom.

  • CHRISTOPHER H. FRY Ph.D., D.Sc.

    Corresponding author
    1. Institute of Urology and Nephrology, University College, London, United Kingdom
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  • We are grateful to the British Heart Foundation for financial assistance.

Address for correspondence: Christopher H. Fry, Ph.D., D.Sc Institute of Urology, 67 Riding House St., London WIP 7PN, United Kingdom. Fax: 171-636-5053; E-mail:chris.fry@uc.ac.uk

Abstract

AP Conduction in Hypertrophied Myocardium. Introduction: Cardiac hypertrophy is associated with an increased incidence of arrhythmias that result from altered action potential configuration or propagation velocity. These variables were measured in isolated preparations of human left ventricular myocardium and correlated with the degree of hypertrophy.

Methods and Results: Cardiac mass was estimated by echocardiography and cell diameter was measured from fixed isolated specimens; the two variables correlated significantly. Action potential duration was measured under field stimulation but was independent of the degree of hypertrophy; however, the duration was longer in septal preparations (405 ± 12 msec, 37°C, 1-Hz stimulation) than in papillary muscles (342 ± 11 msec). Conduction velocity decreased progressively as cell diameter increased both in septal and papillary muscle preparations. Cable analysis showed that the variation of conduction velocity could be accounted for adequately by an increase of the intracellular resistivity of the preparations.

Conclusion: The data suggest that conduction defects occur in a progressive manner in human hypertrophy, which would provide an important substrate for dysrhythmias in human left ventricular hypertrophy and could result from a decrease of electrical coupling between adjacent myocardial cells.

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