OBJECTIVES: We investigated whether transmural mechanics could yield insight into the transmural electrical sequence. BACKGROUND: Although the concept of transmural dispersion of repolarization has helped explain a variety of arrhythmias, its presence in vivo is still disputable. METHODS: We studied the time course of transmural myofiber mechanics in the anterior left ventricle of normal canines in vivo (n = 14) using transmural bead markers under biplane cineradiography. In 4 of these animals, plunge electrodes were placed in the myocardial tissue within the bead set to measure transmural electrical sequence. RESULTS: The onset of myofiber shortening was earliest at endocardial layers and progressively delayed toward epicardial layers (p < 0.001), resulting in transmural dispersion of myofiber shortening of 39 ms. The onset of myofiber relaxation was earliest at epicardial layers and most delayed at subendocardial layers (p = 0.004), resulting in transmural dispersion of myofiber relaxation of 83 ms. There was no significant transmural gradient in electrical repolarization (p = NS). CONCLUSIONS: Despite lack of evidence of significant transmural gradient in electrical repolarization in vivo, there is transmural dispersion of myofiber relaxation as well as shortening.
OBJECTIVES: We investigated whether transmural mechanics could yield insight into the transmural electrical sequence. BACKGROUND: Although the concept of transmural dispersion of repolarization has helped explain a variety of arrhythmias, its presence in vivo is still disputable. METHODS: We studied the time course of transmural myofiber mechanics in the anterior left ventricle of normal canines in vivo (n = 14) using transmural bead markers under biplane cineradiography. In 4 of these animals, plunge electrodes were placed in the myocardial tissue within the bead set to measure transmural electrical sequence. RESULTS: The onset of myofiber shortening was earliest at endocardial layers and progressively delayed toward epicardial layers (p < 0.001), resulting in transmural dispersion of myofiber shortening of 39 ms. The onset of myofiber relaxation was earliest at epicardial layers and most delayed at subendocardial layers (p = 0.004), resulting in transmural dispersion of myofiber relaxation of 83 ms. There was no significant transmural gradient in electrical repolarization (p = NS). CONCLUSIONS: Despite lack of evidence of significant transmural gradient in electrical repolarization in vivo, there is transmural dispersion of myofiber relaxation as well as shortening.
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