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Background: The efficacy of beta-blocker treatment in type 3 long QT syndrome (LQT3) remains debated., Objectives: The purpose of this study was to test the hypothesis that beta-blocker use is associated with cardiac events (CEs) in a French cohort of LQT3 patients., Methods: All patients with a likely pathogenic/pathogenic variant in the SCN5A gene (linked to LQT3) were included and followed-up. Documented ventricular tachycardia/ventricular fibrillation, torsades de pointes, aborted cardiac arrest, sudden death, and appropriate shocks were considered as severe cardiac events (SCEs). CEs also included syncope., Results: We included 147 patients from 54 families carrying 23 variants. Six of the patients developed symptoms before the age of 1 year and were analyzed separately. The 141 remaining patients (52.5% male; median age at diagnosis 24.0 years) were followed-up for a median of 11 years. The probabilities of a CE and an SCE from birth to the age of 40 were 20.5% and 9.9%, respectively. QTc prolongation (hazard ratio [HR] 1.12 [1.0-1.2]; P = .005]) and proband status (HR 4.07 [1.9-8.9]; P <.001) were independently associated with the occurrence of CEs. Proband status (HR 8.13 [1.7-38.8]; P = .009) was found to be independently associated with SCEs, whereas QTc prolongation (HR 1.11 [1.0-1.3]; P = .108) did not reach statistical significance. The cumulative probability of the age at first CE/SCE was not lower in patients treated with a beta-blocker., Conclusion: In agreement with the literature, proband status and lengthened QTc were associated with a higher risk of CEs. Our data do not show a protective effect of beta-blocker treatment., Competing Interests: Disclosures The authors have no conflicts to disclose., (Copyright © 2023 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: In the long QT syndrome (LQTS) the effects of beta-blocker treatment on prevention of cardiac events differs according to the genotype. We aimed to assess the effect of beta-blocker treatment on QT/QTc duration in Type 1 LQTS (LQT1) and Type 2 LQTS (LQT2) patients., Methods: 24-hour digital Holter ECG were recorded before and after beta-blocking therapy initiation in LQT1 (n = 30) and LQT2 patients (n = 16). QT duration was measured on consecutive 1-minute averaged QRS-T complexes leading to up to 1440 edited QT-RR pairs for each recording. We computed subject- and treatment-specific log/log QT/RR relationships which were used to correct the QT intervals. The QT duration was also evaluated at predefined heart rates and after correction using Bazett and Fridericia coefficients., Results: At baseline, individual QT/RR coefficients were higher in LQT2 than in LQT1 patients (0.53 ± 0.10 vs. 0.40 ± 0.11, P < 0.001) and QT1000 was longer in LQT2 than in LQT1 patients (521 ± 38 vs. 481 ± 39 ms, P < 0.01). Beta-blockers significantly prolonged the mean RR interval (from 827 ± 161 to 939 ± 197 ms, P < 0.0001). The individual QT/RR coefficients were not significantly modified by beta-blockers. Beta-blocker treatment was associated with a prolongation of the QT1000 interval (from 481 ± 39 to 498 ± 43 ms, P < 0.01) in LQT1 patients but with a shortening in LQT2 patients (from 521 ± 38 to 503 ± 32 ms, P < 0.01)., Conclusions: The effect of beta-adrenergic blockade on QTc duration is different in LQT1 and LQT2 patients. Our data suggest that, in LQT1 patients, the well-known positive effect of beta-blockade might be associated with a prolongation of QTc duration. The mechanisms of beta-blockade protection may be different in LQT1 and in LQT2 patients., (©2013, Wiley Periodicals, Inc.)

This study compares the ability of 2 semiautomated methods with a fully automated method for QT measurement to minimize the sample size required to detect a moxifloxacin effect and exclude a placebo effect in a thorough QT/QTc study. The fully automated and 1 of 2 semiautomated methods used a global QT measurement in 12 leads, whereas the other semiautomated method used a tangent method on single lead raw complexes. Mean QTcF intervals were greater when measured on a global QT electrocardiogram than on raw complexes, but the mean magnitudes of DeltaQTcF were similar for all methods. The 3 methods detected a statistically significant increase in QTcF for moxifloxacin compared to placebo and were able to exclude a placebo effect on QTcF in all 62 participants. However, due to a smaller variability, the semiautomated methods allowed these detections with fewer than 20 participants, whereas the fully automated required at least 27 participants.

Exercise testing may be used to assess symptoms occurring on effort, to search for and evaluate arrhythmias or conduction defects, antiarrhythmic drugs, pacemakers or implantable cardioverter defibrillators. Interpretation of exercise testing is difficult because of the complexity of the factors in play. Exercise itself induces changes in myocardial metabolism and the autonomic nervous system, the nature and importance of which are influenced by the underlying cardiac disease and the presence of cardiac failure or myocardial ischaemia. This is particularly true when studying the behaviour of arrhythmias on effort, which depends on many parameters, in that they may appear or disappear during exercise, irrespective of their relationship to autonomic nervous system activation. The main problem lies in the interpretation of changes in the heart rate before the onset of an arrhythmia. The sinus rhythm is both a passive indicator of the vago-sympathetic equilibrium and one of the determining factor of the arrhythmia (relationship to the rate), but it is, itself, dependent on the presence of myocardial dysfunction, a source of arrhythmias, and its changes then become difficult to interpret. These reasons explain why exercise testing is certainly a valuable tool in assessing arrhythmias but the poor reproducibility, especially in the evaluation of ventricular arrhythmias, advises prudence in the interpretation of results.

The efficacy of beta-blockers in preventing sudden death after myocardial infarction would seem to be greater in patients with cardiac failure and proportional to the reduction in heart rate induced by these drugs. In addition, a reduction in heart rate variability measured by the standard deviation from the average cardiac cycle over 24 hours has been reported to be an independent bad prognostic factor after myocardial infarction. This study compares the heart rates and the standard deviations from the mean cardiac cycle over 24 hours in 41 patients divided into 3 groups of comparable age (group I: normal subjects, n = 15; group II: hypertrophic cardiomyopathy without cardiac failure, n = 13; group III: cardiac failure, n = 13) before and after administration of acebutolol (10 mg/kg). The average 24 hour heart rates, the maximum 8-hour diurnal and minimum average 4-hour nocturnal heart rates, day-night ratio and standard deviations from the average 24 hour heart rate and at the hours of maximum and minimum average heart rates were measured by Holter monitoring with an ATREC II system. The 24 hour heart rates were slower in groups II (-18.1 p. 100) and III (-19.1 p. 100) than in group I (-9.5 p. 100), p less than 0.01, the basal heart rates being comparable and the heart rates after acebutolol being significantly lower in groups II and III. The degree of change was comparable during the diurnal and nocturnal periods.(ABSTRACT TRUNCATED AT 250 WORDS)