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Publication Detail
A cellular basis for the primary long Q-T syndromes.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Attwell D, Lee JA
  • Publication date:
  • Pagination:
    1136, 1139
  • Journal:
  • Volume:
  • Issue:
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  • Keywords:
    Action Potentials, Adrenergic beta-Antagonists, Arrhythmias, Cardiac, Electrocardiography, Heart, Heart Rate, Humans, Long QT Syndrome, Sympathetic Nervous System
In several syndromes sudden death is associated with a long Q-T interval on the electrocardiogram. Current treatment is aimed at correcting a notional imbalance of cardiac sympathetic drive. Although this approach can be effective, the primary disorder may be a defect in the cellular mechanism that alters the length of the ventricular action potential, and hence the Q-T interval, in response to a change of heart rate. Such defects may be underdiagnosed because the long Q-T syndromes are defined simply in terms of a prolonged Q-T interval, without consideration of the fact that susceptibility to arrhythmias is likely to be due, not to a lengthened Q-T per se, but to an absence or alteration of the normal Q-T shortening in response to an increase of heart rate. People susceptible to R-on-T related arrhythmias could be identified by measurement of the dependence of the Q-T interval on heart rate and how quickly the Q-T interval adapts to a change in rate.
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