Key result
A 100-ms QT dispersion cutoff identifies beta-blocker nonresponders in LQTS with ~80% accuracy.
Why the study?
QT interval dispersion is a marker of ventricular repolarization dispersion and cardiac electrical instability. The study tested the hypothesis that dispersion of ventricular repolarization is differently affected by interventions providing complete or incomplete protection against malignant arrhythmias in patients with long QT syndrome.
Does QT dispersion predict the efficacy of antiadrenergic therapy in patients with long QT syndrome?
Observational (n=43)
Does QT dispersion predict the efficacy of antiadrenergic therapy in patients with long QT syndrome?
QT dispersion is a useful clinical marker to predict the efficacy of antiadrenergic therapy in patients with long QT syndrome.
BACKGROUND: QT interval dispersion, measured as interlead variability of QT, is a marker of dispersion of ventricular repolarization and, hence, of cardiac electrical instability. We tested the hypothesis that dispersion of ventricular repolarization may be differently affected by interventions destined to provide complete or incomplete protection against malignant arrhythmias in patients with long QT syndrome (LQTS). Twenty-eight patients affected by the Romano Ward form of LQTS entered the study and were divided into three groups: LQTS patients before institution of therapy, patients who did respond to beta-blocker therapy, and patients who continued to have syncope and cardiac arrest despite beta-blockade and who underwent left cardiac sympathetic denervation. A group of 15 healthy volunteers served as control subjects. METHODS AND RESULTS: Dispersion of QT and QTc were calculated using two indexes: the difference between the longest and the shortest value measured in each of the 12 ECG leads (QTmax-QTmin, QTcmax-QTcmin) and the relative dispersion of QT and QTc (standard deviation of QT/QT average x100, standard deviation of QTc/QTc average x100). Both indexes of dispersion of repolarization were higher in the LQTS patients than in control subjects; also, patients not responding to beta-blockers had a significantly higher dispersion of repolarization than responders. A cutoff value of 100 milliseconds for QTmax-QTmin had an 80% sensitivity and 82% specificity in discriminating between responders and nonresponders. A cutoff value of 6 for QT relative dispersion yielded similar results. The LQTS patients who did not respond to beta-blockade underwent left cardiac sympathetic denervation and thereafter remained asymptomatic (mean follow-up, 5 +/- 4 years). In this group, dispersion of repolarization was significantly reduced by the surgical denervation to values similar to that of the responders to beta-blockade. CONCLUSIONS: These data indicate that QT dispersion is a useful clinical tool to predict efficacy of antiadrenergic therapy in LQTS patients.
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Priori et al. (1994) conducted an observational in Idiopathic long QT syndrome (Romano Ward form) (n=43). Beta-blocker therapy and left cardiac sympathetic denervation vs. Healthy volunteers and untreated/beta-blocker nonresponder LQTS patients was evaluated on QT and QTc dispersion (QTmax-QTmin, QTcmax-QTcmin, and relative dispersion) and discrimination between beta-blocker responders and nonresponders. A QTmax-QTmin cutoff of 100 ms discriminated beta-blocker responders from nonresponders in long QT syndrome with 80% sensitivity and 82% specificity.
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