The Efficacy of Beta-Blockers in Patients With Long QT Syndrome 1–3 According to Individuals’ Gender, Age, and QTc Intervals: A Network Meta-analysis

Abstract

Long QT syndrome (LQTS) is an arrhythmic heart disease caused by congenital genetic mutations, and results in increased occurrence rates of polymorphic ventricular tachyarrhythmias and sudden cardiac death (SCD). Clinical evidence from numerous previous studies suggested that beta blockers (BBs), including atenolol, propranolol, metoprolol, and nadolol, exhibit different efficacies for reducing the risk of cardiac events (CEs), such as syncope, arrest cardiac arrest (ACA), and SCD, in patients with LQTS. In this study, we identified relevant studies in MEDLINE, PubMed, embase, and Cochrane databases and performed a meta-analysis to assess the relationship between the rate of CEs and LQTS individuals with confounding variables, including different gender, age, and QTc intervals. Moreover, a network meta-analysis was not only established to evaluate the effectiveness of different BBs, but also to provide the ranked efficacies of BBs treatment for preventing the recurrence of CEs in LQT1 and LQT2 patients. In conclusion, nadolol was recommended as a relatively effective strategy for LQT2 in order to improve the prognosis of patients during a long follow-up period.

A Systematic Review on the Role of Βeta-Blockers in Reducing Cardiac Arrhythmias in Long QT Syndrome Subtypes 1-3

“…The main limitation was that their recommendation was geared primarily toward female patients, given limited male patient data. These findings nonetheless were also supported by Saadeh , nadolol appears to be the ideal potential β-blocker of choice in all LQT subtypes, and atenolol followed by propranolol offers viable alternatives in types 1 [1,2,5,24].…”

“…Ahn et al supported the use and role of nadolol in risk reduction in LQT1 and LQT2 [ 1 ]. Han et al supported this; they focused heavily on the significant reduction in ACE in LQT1 and LQT2 by β-blockers, and the role of nadolol was seen as being ideal in both types, with atenolol a possible substitute in LQT1 [ 2 ]. Saadeh et al 2020 confirmed the role of β-blockers in LQTS as a whole and emphasized the efficacy and role of nadolol in LQTS 3, where previously β-blockers were thought to be contraindicated [ 5 ].…”

“…Diagnosis of LQTS is done by clinical symptoms in conjunction with EKG assessment and is best done using the Schwartz Diagnostic Criteria for LQTS, which is highlighted in In treating this arrhythmia syndrome, the mainstay of medical management is supported by β-blocker therapy [1,2,6]. Additional treatment modalities include medical via mexiletine, ranolazine, and/or flecainide, as well as procedural, via left cardiac sympathetic denervation and implantable cardiac defibrillator (ICD) [11][12][13].…”

“…Long QT syndrome (LQTS) is both an inherited and acquired condition that is characterized by an abnormal prolongation of the QT-interval on electrocardiogram (EKG) monitoring and action potential duration (APD), which increases the risk of fatal ventricular, arrhythmias, sudden cardiac death (SCD), and milder adverse cardiac eventsACE such as syncope [ 1 - 2 ]. This condition was first officially coined and supported by EKG evidence in 1957 and has since been recognized as one of the most commonly inherited channelopathies/arrhythmia syndromes with a prevalence of 1:2000 [ 2 ]. Congenital LQTS has more than 15 genotypes of which the most common genes are LQT1, LQT2, and LQT3 [ 3 ].…”

“…In treating this arrhythmia syndrome, the mainstay of medical management is supported by β-blocker therapy [ 1 , 2 , 6 ]. Additional treatment modalities include medical via mexiletine, ranolazine, and/or flecainide, as well as procedural, via left cardiac sympathetic denervation and implantable cardiac defibrillator (ICD) [ 11 - 13 ].…”