It is well established that repolarization heterogeneities are important to the initiation of reentrant arrhythmias. For example, transmural repolarization heterogeneities in canine wedge preparations have been implicated as an underlying substrate for reentry in animal models of long QT syndrome type 2 (LQT2), Brugada syndrome, and heart failure. However, the transmural distribution of electro-physiologically similar cell types remains a topic of considerable debate. The reason for the debate is that a subpopu-lation of cells has been identified within the transmural depth that are neither epicardial nor endocardial cell types and are often referred to as M-cells. However, M-cells should not be confused with the generic midmyocardial cell labeling because M-cells may reside in islands
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