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Background: The use of intravenous (IV) sotalol loading following recent U.S. Food and Drug Administration (FDA) approval of a 1-day loading protocol has reduced the obligatory 3-day hospital stay for sotalol initiation when given orally. Several studies have recently demonstrated the safety and feasibility of IV loading for patients with atrial arrhythmias. However, there is a paucity of data on the feasibility and safety of IV sotalol loading for patients with ventricular arrhythmias. This study aims to assess the safety, feasibility, and length of stay (LOS) outcomes of IV sotalol loading for the prevention of ventricular arrhythmias.
Methods: A retrospective analysis was performed of all patients undergoing IV sotalol loading and oral sotalol initiation for ventricular arrhythmias, or IV sotalol loading for atrial arrhythmias between August 2021 and December 2023 at Northwestern University. Baseline characteristics, success of sotalol initiation/loading, changes in heart rate (HR) and QT/QTc, safety, and LOS were compared between patients undergoing sotalol loading/initiation for ventricular arrhythmias (IV vs. PO) and between patients undergoing IV sotalol loading for ventricular arrhythmias vs. for atrial arrhythmias.
Results: A total of 28 patients underwent sotalol loading/initiation for ventricular arrhythmias (N = 15 IV and N = 13 PO) and 41 patients underwent IV sotalol loading for atrial arrhythmias. Baseline characteristics of congestive heart failure history and left ventricular ejection fraction were worse in the ventricular arrhythmias group. There was no significant difference in the successful completion of IV sotalol loading for ventricular arrhythmias compared to oral sotalol initiation for ventricular arrhythmias or IV sotalol loading for atrial arrhythmias (86.7% vs. 92.3% vs. 90.2%, p = 0.88). There was a significant increase in ΔQTc following IV sotalol infusion for ventricular arrhythmias compared to following PO sotalol initiation for ventricular arrhythmias (46.4 ± 29.2 ms vs. 8.9 ± 32.6 ms, p = 0.004) and following IV sotalol infusion for atrial arrhythmias (46.4 ± 29.2 ms vs. 24.0 ± 25.1 ms, p = 0.018). ΔHR following IV sotalol infusion for ventricular arrhythmias was similar to ΔHR following PO sotalol initiation for ventricular arrhythmias and ΔHR following IV sotalol infusion for atrial arrhythmias (- 7.5 ± 8.7 bpm vs. - 8.5 ± 13.9 bpm vs. - 8.3 ± 13.2 bpm, p = 0.87). There were no significant differences in discontinuation for QTc prolongation (6.7% vs. 1.7% vs. 2.4%, p = 0.64) and bradycardia (13.3% vs. 7.7% vs. 9.8%, p = 0.88) between IV sotalol loading for ventricular arrhythmias, PO sotalol initiation for ventricular arrhythmias, and IV sotalol loading for atrial arrhythmias. There were no instances of hypotension, life-threatening ventricular arrhythmias, heart failure, or death. Length of stay was significantly shorter for IV sotalol loading compared to PO sotalol initiation for ventricular arrhythmias (1.1 ± 0.36 days vs. 4.2 ± 1.0 days, p < 0.0001).
Conclusion: IV sotalol loading appears feasible and safe for use in ventricular arrhythmias and results in a decreased length of stay. Despite increased comorbidities and greater increase in QTc interval following IV sotalol infusion in the ventricular arrhythmias group, there were no significant differences in successful completion of loading or adverse outcomes when compared to PO sotalol initiation for ventricular arrhythmias and IV loading for atrial arrhythmias.
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http://dx.doi.org/10.1007/s10840-024-01829-4 | DOI Listing |
Circ Arrhythm Electrophysiol
September 2025
Department of Congenital Heart Disease, Evelina London Children's Hospital, United Kingdom (S. Chivers, T.V., V.Z., S.M., G.M., W.R., E.R., D.F.A.L., T.G.D., O.I.M., G.K.S., J.M.S.).
Background: Fetal tachycardias can cause adverse fetal outcomes including ventricular dysfunction, hydrops, and fetal demise. Postnatally, ECG is the gold standard, but, in fetal practice, echocardiography is used most frequently to diagnose and monitor fetal arrhythmias. Noninvasive extraction of the fetal ECG (fECG) may provide additional information about the electrophysiological mechanism and monitoring of intermittent arrhythmias.
View Article and Find Full Text PDFHeart Rhythm
September 2025
Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, United States. Electronic address:
Background: Electronic nicotine delivery systems (ENDS) utilize "E-liquids" in order to generate "E-vapor", an inhalable aerosolized mixture containing nicotine and flavors. Flavored ENDS are very popular among teens who vape, however, the possible cardiac electrophysiological harm of inhalation exposure to flavored ENDS are not fully understood.
Objective: To test if inhalation exposure to flavoring carbonyls in e-liquids compromises mitochondrial integrity, increases oxidative stress, and leads to cardiac electrophysiological toxicity.
Exp Physiol
September 2025
Unit of Cardiac Physiology, Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Sciences Centre, 3.24 Core Technology Facility, University of Manchester, Manchester, UK.
The phosphodiesterase-5 inhibitor sildenafil suppresses ventricular arrhythmias in a sheep model of drug-induced long QT. In that study, ventricular arrhythmias were abolished by reducing premature ventricular complexes (PVCs) and delaying PVC onset, thus preventing 'R-on-T' ventricular tachycardia. Evidence for effects in humans with arrhythmias is lacking.
View Article and Find Full Text PDFEur J Case Rep Intern Med
August 2025
Internal Medicine and Hypertension Center, Sant'Anna Hospital Castelnovo ne' monti, Azienda USL-IRCCS di Reggio Emilia, Reggio Emilia, Italy.
Unlabelled: Brugada syndrome (BrS) is a disorder leading to potentially life-threatening ventricular arrhythmias in patients with an apparently normal heart. It mostly affects men of Asian descent, and the prevalence varies between ethnicities. Typical ECG abnormalities with no symptoms are referred to as the Brugada pattern, and hypothyroidism is a potential trigger of this.
View Article and Find Full Text PDFRev Cardiovasc Med
August 2025
The Heart Institute, Department of Pediatrics, University of Tennessee Health and Science Center, Memphis, TN 38103, USA.
Left ventricular noncompaction (LVNC), also called noncompaction cardiomyopathy (NCM), is a myocardial disease that affects children and adults. Morphological features of LVNC include a noncompacted spongiform myocardium due to the presence of excessive trabeculations and deep recesses between prominent trabeculae. Incidence and prevalence rates of this disease remain contentious due to varying clinical phenotypes, ranging from an asymptomatic phenotype to fulminant heart failure, cardiac dysrhythmias, and sudden death.
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