Ventricular Microanatomy, Arrhythmias, and the Electrochemical Driving Force for Na+
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A well-known feature of the electrophysiological activity of the mammalian heart is that it can be regulated by tissue microanatomy. This occurs both on a cell-to-cell basis and regionally, that is, within defined structures in the cardiac syncytium.1,2 The initiation and conduction of the action potential and its ability to trigger and regulate contraction are modulated by connexin-mediated intercellular communication at well defined gap junctions.3 Recent results strongly suggest that the expression of some of the ion channels responsible for the cardiac action potential is not uniform on the surface membrane or sarcolemma of each myocyte. For example, Na+ channels seem to be preferentially expressed and in fact concentrated at the intercalated disc regions between ventricular myocytes, where connexins are also located.4,5 These features (Figure), when combined with the fact that in the adult myocardium, myocytes are often arranged in trabeculae (tightly packed cylindrical structures) can also result in activity- or rate-dependent changes in the electrolyte composition of the immediately adjacent restricted extracellular space or “clefts”.3 A well-known example is the extracellular potassium accumulation that has been studied in detail in the ventricle6 and the Purkinje conduction system.7