["Critical interval of the dispersion of refractoriness" in the pathogenesis of ventricular extrasystole in the long QT syndrome].
B Domenichelli
Abstract
B Domenichelli
Abstract
The reentry mechanism (R.M.) has been demonstrated to be relevant in the genesis of experimental extrasystoles. The extrapolation of these observations to the ventricular extrasystoles (V.E.) observed in clinical situations is still debated. However, the V.E. related to the long QT syndromes have been commonly considered to be caused by R.M. In fact an abnormal prolongation of the repolarization time favors the dispersion of the myocardial recovery time. A critical lengthening of the QT interval has been observed by several Authors to underlie the appearance of V.E. That after a further critical prolongation of the QT the V.E. disappear, has not been so far described. We report a patient with long QT syndrome in whom the ECG demonstrated an extreme variability of the QT interval. The V.E. appeared only when the QT interval was greater than 580 msec, whereas they disappeared when the QT interval was greater than 660 msec. Thus, a critical interval of refractoriness dispersion (C.I.R.D.) between 580 and 660 msec was established. We suggest that in our case the V.E. were probably due to R.M., caused by regional lengthening of the repolarization; a further prolongation of repolarization time probably induced either an antegrade block in both limbs of the circuit or a retrograde block in the reentry pathway and consequently the abolition of R.M. The identification of a C.I.R.D. suggest a possible R.M. in the pathogenesis of clinical ventricular extrasystoles.
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The reentry mechanism (R.M.) has been demonstrated to be relevant in the genesis of experimental extrasystoles. The extrapolation of these observations to the ventricular extrasystoles (V.E.) observed in clinical situations is still debated. However, the V.E. related to the long QT syndromes have been commonly considered to be caused by R.M. In fact an abnormal prolongation of the repolarization time favors the dispersion of the myocardial recovery time. A critical lengthening of the QT interval has been observed by several Authors to underlie the appearance of V.E. That after a further critical prolongation of the QT the V.E. disappear, has not been so far described. We report a patient with long QT syndrome in whom the ECG demonstrated an extreme variability of the QT interval. The V.E. appeared only when the QT interval was greater than 580 msec, whereas they disappeared when the QT interval was greater than 660 msec. Thus, a critical interval of refractoriness dispersion (C.I.R.D.) between 580 and 660 msec was established. We suggest that in our case the V.E. were probably due to R.M., caused by regional lengthening of the repolarization; a further prolongation of repolarization time probably induced either an antegrade block in both limbs of the circuit or a retrograde block in the reentry pathway and consequently the abolition of R.M. The identification of a C.I.R.D. suggest a possible R.M. in the pathogenesis of clinical ventricular extrasystoles.
Key concepts: Medicine, QT interval, Repolarization, Prolongation, Reentry, Refractory period, Cardiology, Internal medicine