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M cells in the human heart.

See related articles, pages 981–991 

Dispersion of repolarization across the ventricular wall has been suggested to underlie the inscription of the normal electrocardiographic T wave and when amplified to contribute prominently to the development of cardiac arrhythmias.1–3

The magnitude of transmural dispersion of repolarization (TDR) is attributable to intrinsic differences in the action potential duration (APD) of the 3 principal cell types that comprise the ventricular myocardium and the extent to which these repolarization differences are damped by electrotonic forces. An increase in tissue resistivity in the deep subepicardium,4 attributable to a sharp transition in cell orientation,3 reduced expression of connexin 435,6 and increased density of collagen7 in this region, contributes to the expression of repolarization heterogeneities across the ventricular wall by limiting the degree of electrotonic interaction between the myocardial layers. Thus, the degree of electrotonic coupling, together with the intrinsic differences in APD, determines the extent to which TDR is expressed and its impact on arrhythmogenesis, as well as on the morphology of the T wave. It is noteworthy that even in the absence of any difference in final repolarization time, electrotonic forces generated by transmural differences in the shape of the action potential can inscribe an upright T wave in the ECG. Theoretical studies have also been helpful in our understanding of the role of electrical coupling in the expression of TDR.8

TDR is in large part attributable to the presence of M cells between the endocardial and epicardial layers of the heart. The M cell, discovered in the early 1990s and named in memory of Gordon K. Moe,9,10 has as its hallmark the ability to prolong its action potential more than that of normal epicardium or endocardium in response to a slowing of rate or exposure to agents …