Key result
Propranolol (0.1 and 1 microm) suppressed all early afterdepolarizations in LQT3 murine hearts, while 0.1 microm reduced VT triggering to 12.5% compared to 50% at baseline.
Why the study?
Does propranolol suppress early afterdepolarizations and alter transmural repolarization gradients in a murine model of long QT 3 syndrome?
Population
Isolated wild type (WT) and Scn5a+/Delta murine hearts modelling human long QT 3 syndrome
Comparison
Perfusion with 0.1 and 1 microm propranolol vs 0 microm propranolol and wild type hearts
Design
Preclinical
Authors
Loading...
Should not yet change LQT3 practice; leaves open whether EAD suppression prevents arrhythmias in patients.
Does propranolol suppress early afterdepolarizations and alter transmural repolarization gradients in a murine model of long QT 3 syndrome?
Absolute Event Rate: 12.5% vs 50%
Propranolol suppresses early afterdepolarizations but has dose-dependent effects on transmural repolarization gradients in a murine model of LQT3, implicating EADs in initiating spontaneous arrhythmias.
Thomas et al. (2007) studied Long QT 3 syndrome (murine model) (n=17). Propranolol vs. 0 microm propranolol (baseline) and wild type hearts was evaluated on Triggering of ventricular tachycardia following programmed electrical stimulation. Propranolol (0.1 and 1 microm) suppressed all early afterdepolarizations in LQT3 murine hearts, while 0.1 microm reduced VT triggering to 12.5% compared to 50% at baseline.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: