Japanese Journal of Electrocardiology
Online ISSN : 1884-2437
Print ISSN : 0285-1660
ISSN-L : 0285-1660
Volume 9, Issue 5
Displaying 1-3 of 3 articles from this issue
  • J.A. Abildskov
    1989 Volume 9 Issue 5 Pages 555-556
    Published: September 10, 1989
    Released on J-STAGE: December 10, 2010
    JOURNAL FREE ACCESS
    The T wave is a sensitive but nonspecific marker of heart disease and certain extracardiac states. Its physiologic basis has been partially defined in terms of the distribution of ventricular recovery properties and changes of these properties in some disease states. The mechanism of the normal gradients of recovery properties is uncertain and various possibilities including temperature, tension, neural effects, electrotonic interactions of Purkinje and myocardial fibers and electrical loading conditions have been considered. Further understanding and improved medical utility of the T wave is likely to involve more detailed definition of ionic mechanisms, effects of anisotropy on repolarization and improved description of the electrocardiographic expressions of medically important conditions.
    One of the areas in which greater utility of the T wave is likely is the prediction of ventricular arrhythmias by detection of arrhythmogenic conditions of repolarization. Disparate recovery of excitability has been clearly related to reentrant arrhythmias and the QRST deflection area is a marker of that disparity. A growing body of evidence suggests that body surface mapping of the QRST area reflects locally disparate ventricular recovery related to reentrant arrhythmias. To further understand and define this relation a computer model of propagated excitation is being used to investigate vulnerability and electrocardiographic waveform features including distributions of QRST area.
    The model includes nonuniform cycle length dependent recovery of excitability and slow propagation of excitation during incomplete recovery.Vulnerability is assessed as the duration of train stimulation required to initiate selfsustained reentrant propagation and ECG waveforms are calculated from simulated voltage gradients in the model. Findings show the expected direct relation of vulnerability to disparate recovery and confirm QRST area distributions in which the magnitude of nonuniformity relates to vulnerability. In the model the mechanism of the relation between vulnerability and disparate recovery is the degree of nonuniformity of propagation per premature response to train stimulation. Findings also show an inverse relation of vulnerability to the mean repolarization duration due to the number of premature responses to train stimulation per unit time. This suggests that electrocardiographic prediction of ventricular arrhythmias might be improved by considering both range and duration of recovery. An index based on the distributions of both QRST area and QT interval seems appropriate although the optimum combination is not yet certain.
    Other findings pertinent to the electrocardiographic estimation of vulnerability include evidence that nonuniform conduction defects permit simulated fibrillation even in the presence of uniform recovery properties. The conduction defects are reflected in QRS area distributions as are nonuniform recovery properties in the QRST area, suggesting that estimation of vulnerability might be further improved by consideration of both distributions.
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  • 1989 Volume 9 Issue 5 Pages 557-575
    Published: September 10, 1989
    Released on J-STAGE: September 09, 2010
    JOURNAL FREE ACCESS
    Download PDF (1943K)
  • 1989 Volume 9 Issue 5 Pages 577-713
    Published: September 10, 1989
    Released on J-STAGE: September 09, 2010
    JOURNAL FREE ACCESS
    Download PDF (17214K)
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