Following the seminal paper by Madison Spach and Mark Josephson, clinicians have been aware of anisotropic re-entry as an established mechanism of arrhythmogenesis, although the exact mechanisms responsible remain uncertain.[1] Nevertheless, changes in microanatomical structures, such as cellular coupling, gap junction distribution and function and fibre disarray, lead to anisotropic conduction, i.e. dependence of myocardial velocity on myocyte orientation.[2] Anisotropic conduction was initially attributed to conduction tissue, such as the atrioventricular (AV) node, but we know now that in cardiac tissue, in general, conduction velocity is anisotropic. Particularly in disease states, such as postinfarction myocardium, anisotropic conduction and spatial inhomogeneity of refractoriness may be implicated in the genesis of re-entrant, or even focal, arrhythmias. The length of the re-entrant pathway is determined by subtle electrophysiological–anatomical changes, and there may be an excitable gap.
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