Abstract

A critical requirement for arrhythmogenesis in myopathic hearts is the establishment of functional conduction block, which leads to both the initiation and the maintenance of reentrant excitation. We studied diseased left ventricular trabecular muscle (n 2) using a combined floating microelectrode and optical mapping technique to characterize the mechanism of conduction block in human hearts. Figure 1 shows trabecular muscle that is being paced (120 beats per minute [BPM]) via a Purkinje fibre. The spread of activation is in the longitudinal plane parallel to myocyte fibre orientation seen in the top image of Figure 1 (A), with 2:1 conduction block seen distally on the dominant frequency (DF) map. The amplitude ratio demonstrates that amplitude alternans occurs proximal to the region of block, with the magnitude of alternans increasing closer to the region of block. At the region of block, fibre anisotropy was observed where the fibre orientation changes from longitudinal to transverse (B) with minimal fibrosis (C, picrosirius red stain). Figure 2 reports microelectrode recordings from 3 sites: A, B (3 mm away from A), and C (6 mm away from A). With increasing activation rates from 60, 150, and 200, to 300 beats per minute, progressive conduction

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