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QT dispersion in patients with chronic heart failure: beta blockers are associated with a reduction in QT dispersion
C E Bonnar1, A P Davie, L Caruana
1Department of Clinical Pharmacology and Therapeutics, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK. c.e.bonnar@clinpharm.dundee.ac.uk
Insights
QT dispersion is elevated in patients with systolic heart failure. Beta blockers may reduce this dispersion, suggesting an antiarrhythmic effect by improving ventricular repolarization.
Area of Science:
- Cardiology
- Electrophysiology
- Heart Failure Research
Background:
- Left ventricular systolic dysfunction is associated with increased risk of arrhythmias.
- QT dispersion is a measure of repolarization variability, and increased dispersion is linked to arrhythmogenesis.
Purpose of the Study:
- To compare QT dispersion in patients with impaired left ventricular systolic function versus matched controls with normal function.
- To investigate the effect of beta blockers on QT dispersion in these patient groups.
Main Methods:
- A retrospective, case-control study involving 25 patients with impaired left ventricular systolic function and 100 controls.
- QT and QTc dispersion were measured using three distinct methods.
- Patients were matched for age, sex, prior myocardial infarction, and medication use (diuretics, beta blockers).
Main Results:
- All measures of QT and QTc dispersion were significantly increased in patients with impaired left ventricular systolic function compared to controls (p < 0.001).
- Beta blocker use was associated with a significant reduction in both QT and QTc dispersion (p < 0.05), irrespective of left ventricular function status.
Conclusions:
- Increased QT and QTc dispersion are present in systolic heart failure patients, independent of measurement method or confounding factors.
- Beta blockers demonstrate a potential antiarrhythmic mechanism by reducing ventricular repolarization dispersion.
Objective:
To compare QT dispersion in patients with impaired left ventricular systolic function and in matched control patients with normal left ventricular systolic function.
Design:
A retrospective, case-control study with controls matched 4:1 for age, sex, previous myocardial infarction, and diuretic and beta blocker treatment.
Setting:
A regional cardiology centre and a university teaching hospital.
Patients:
25 patients with impaired left ventricular systolic function and 100 patients with normal left ventricular systolic function.
Main Outcome Measures:
QT and QTc dispersion measured by three methods: the difference between maximum and minimum QT and QTc intervals, the standard deviation of QT and QTc intervals, and the "lead adjusted" QT and QTc dispersion.
Results:
All measures of QT/QTc dispersion were closely interrelated (r values 0.86 to 0.99; all p < 0.001). All measures of QT and QTc dispersion were significantly increased in the patients with impaired left ventricular systolic function v controls (p < 0.001): 71.9 (6.5) (mean (SEM)) v 46.9 (1.7) ms for QT dispersion, and 83.6 (7.6) v 54.3 (2.1) ms(-1-2) for QTc dispersion. All six dispersion parameters were reduced in patients taking beta blockers (p < 0.05), regardless of whether left ventricular function was normal or impaired-by 9.4 (4.6) ms for QT dispersion (p < 0.05) and by 13.8 (6. 5) ms(-1-2) for QTc dispersion (p = 0.01).
Conclusions:
QT and QTc dispersion are increased in patients with systolic heart failure in comparison with matched controls, regardless of the method of measurement and independently of possible confounding factors. beta Blockers are associated with a reduction in both QT and QTc dispersion, raising the possibility that a reduction in dispersion of ventricular repolarisation may be an important antiarrhythmic mechanism of beta blockade.