Anisotropic structural complexities in the genesis of reentrant arrhythmias.

T he paper by Brugada et a1l in this issue of Circulation adds importantly to mounting evidence that the anisotropic passive electri- cal properties of cardiac muscle play an important role in atrial2-4 and ventricular5-6 reentrant arrhyth- mias.The anisotropic properties involved are deter- mined at a microscopic size scale (<200 jam) by the alignment of cardiac myocytes, their complex shapes, the distribution of their interconnections (gap junc- tions), and the geometry of interstitial (extracellular) space.These electrical properties are different in the atria and ventricles of normal adult hearts.For descriptive purposes, the different types of anisotro- pic properties have been characterized simply as "uniform" and "nonuniform" anisotropy.7 Normal ventricular muscle generally has uniform anisotropic properties due to the presence of frequent side-to- side electrical connections between cells and groups of cells8,9; such bundles produce low amplitude smooth unipolar extracellular waveforms when prop- agation occurs across cells (transverse propaga- tion).7'8In many normal adult atrial bundles, how- ever, the side-to-side connections are sparse, pro- See p 1296 and 1307 ducing nonuniform anisotropic properties.During transverse conduction this results in small multiphasic (fragmented) extracellular waveforms due to asynchronous firing of adjacent cells or groups of cells.8Additionally, the anisotropic properties of the same structure change from uniform to nonuniform during development following birth,3 with aging,8 and in the border zone of healed myocardial infarcts.10-14 Functionally, the different anisotropic properties behave differently in response to the same interven- tion.For example, in human and canine atrial and ventricular bundles early premature stimuli and so- dium channel-blocking drugs produce unidirectional longitudinal conduction disturbances in nonuniform anisotropic bundles but not in uniform anisotropicThe opinions expressed in this editorial comment are not neces- sarily those of the editors or of the American Heart Association.