Key result
Fever significantly increased QTc duration by 15 ms/°C in LQT-2 patients with the A558P HERG mutation, contrasting with a 6 ms/°C decrease in control patients, triggering life-threatening arrhythmias.
Why the study?
Does fever induce QTc prolongation and ventricular arrhythmias in individuals with type 2 congenital long QT syndrome?
Population
2 patients with type 2 congenital long QT syndrome carrying the A558P missense mutation in HERG, 9 control…
Comparison
Fever / hyperthermia. vs Normothermia.
Design
Preclinical
Authors
Loading...
Fever may trigger arrhythmias via QTc prolongation in A558P LQT-2; hypothesis-generating from animal data, needs clinical confirmation.
Does fever induce QTc prolongation and ventricular arrhythmias in individuals with type 2 congenital long QT syndrome?
Absolute Event Rate: 15% vs -6%
p-value: p=<0.001
Fever is a potential trigger for life-threatening arrhythmias in LQT-2 patients because the mutant HERG channels fail to increase current density appropriately at febrile temperatures, leading to QTc prolongation.
Amin et al. (2008) studied Type 2 congenital long QT syndrome (LQT-2) (n=11). Fever (elevated body temperature) vs. Normothermia (body temperature below 38°C) was evaluated on QTc duration change per °C increase in body temperature (p=<0.001). Fever significantly increased QTc duration by 15 ms/°C in LQT-2 patients with the A558P HERG mutation, contrasting with a 6 ms/°C decrease in control patients, triggering life-threatening arrhythmias.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: