Supported by grants from the National Institutes of Health (HL-47678), the American Heart Association, New York State Affiliate, and the Masons of New York State and Florida.
The M Cell:
Its Contribution to the ECG and to Normal and Abnormal Electrical Function of the Heart
Article first published online: 20 APR 2007
Journal of Cardiovascular Electrophysiology
Volume 10, Issue 8, pages 1124–1152, August 1999
How to Cite
ANTZELEVITCH, C., SHIMIZU, W., YAN, G.-X., SICOURI, S., WEISSENBURGER, J., NESTERENKO, V. V., BURASHNIKOV, A., DI DIEGO, J., SAFFITZ, J. and THOMAS, G. P. (1999), The M Cell:. Journal of Cardiovascular Electrophysiology, 10: 1124–1152. doi: 10.1111/j.1540-8167.1999.tb00287.x
- Issue published online: 20 APR 2007
- Article first published online: 20 APR 2007
- Manuscript received 28 January 1999; Accepted for publication 27 April 1999.
- long QT syndrome;
- early afterdepolarization;
- T wave
Characteristics of the M Cell. The discovery and characterization of the M cell, a unique cell type residing in the deep layers of the ventricular myocardium, has opened a new door in our understanding of the electrophysiology and pharmacology of the heart in both health and disease. The hallmark of the M cell is the ability of its action potential to prolong much more than that of other ventricular myocardial cells in response to a slowing of rate and/or in response to agents that act to prolong action potential duration. Our goal in this review is to provide a comprehensive characterization of the M cell, its contribution to transmural heterogeneity, and its role in the normal electrical function of the heart, in the inscription of the ECG (particularly the T wave), and in the development of QT dispersion, T wave alternans, long QT intervals, and cardiac arrhythmias, such as torsades de pointes. Our secondary goal is to address the controversy that has arisen relative to the functional importance of the M cell in the normal heart. The controversy derives largely from the failure of some investigators to demonstrate transmural heterogeneity of repolarization in the dog in vivo under control conditions and after administration of quinidine. The inability to demonstrate transmural heterogeneity under these conditions may he due to the use of bipolar recording techniques that, in our experience, seriously underestimate transmural dispersion of repolarization (TDK). The use of sodium pentobarhital and α-chloralose as anesthesia also is problematic, because these agents reduce or eliminate TDR by affecting a variety of ion channel currents. Finally, attempts to amplify transmural dispersion of repolarization with an agent such as quinidine must take into account that relatively high concentrations can result in effects opposite to those desired due to drug inhibition of multiple ion channels. These observations may explain the inability of earlier studies to detect the M cell.