Yue, Arthur M., Betts, Tim R., Roberts, Paul R. and Morgan, John M.
Global dynamic coupling of activation and repolarization in the human ventricle
Circulation, 112, (17), . (doi:10.1161/CIRCULATIONAHA.104.510412).
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Background: The ability to determine spatial and dynamic changes in ventricular repolarization may help to understand arrhythmogenic mechanisms in humans. We hypothesized that noncontact mapping could be used to investigate global activation-repolarization coupling in the human ventricle during steady state and premature extrastimulation.
Methods and Results: Activation-recovery intervals (ARIs) determined from reconstructed unipolar electrograms by the Ensite system were analyzed during sinus rhythm, constant pacing, spontaneous ventricular ectopic beats, and premature stimulation at intermediate and short coupling intervals in the left or right ventricle of 13 patients (6 female; mean age, 48 years) without structural myocardial disease. ARIs were measured from 32 sites in each ventricle with the use of a method validated with monophasic action potential recordings and unipolar contact electrograms. Global T-wave distribution was displayed on a 3-dimensional geometry of the ventricle, with polarities opposite to the direction of activation during steady state and premature stimulation. There was a significant inverse correlation between activation times and ARIs during sinus rhythm, ventricular ectopy, and premature stimulation (r=0.72, slope=–0.76, P<0.001). Premature stimuli at short coupling intervals flattened the regression slope compared with sinus rhythm (–0.61 versus –0.81; P=0.05), but the global pattern of repolarization was preserved. In comparison to our method, the Wyatt method of ARI measurement failed to demonstrate significant coupling between activation and repolarization (r=0.34, slope=0.19).
Conclusions: Global, dynamic repolarization mapping of the human ventricle is feasible. An inverse coupling of activation and repolarization during steady state and premature stimulation may preserve electric stability in the normal ventricle.
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