CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 4, May 2012
AFRICA
193
of heart failure patients, QT dispersion has been shown to be
a marker of electrical instability and increased risk of sudden
death.
12
In patients with known repolarisation abnormalities, the
QTcd has been demonstrated to be a better prognostic indicator
of arrhythmic risk than the QT itself.
13
Unstable ventricular
repolarisation may contribute to the development of ventricular
tachycardia and fibrillation.
It is well known that
β
-blockers are the only anti-arrhythmic
drug class effectively reducing mortality and arrhythmic sudden
death in patients with heart failure.
14
These drugs have been also
shown to improve QT dynamics.
15-17
It has been demonstrated that nebivolol therapy reduced
the composite risk of all-cause mortality or cardiovascular
hospital admission compared with placebo in patients with
heart failure.
4
Nebivolol therapy as an antihypertensive drug
has been extensively studied and approved. Its effect on QT
dynamics in hypertensive patients has shown that nebivolol
significantly reduced QTcd in hypertensive subjects without
affecting left ventricular mass.
7
In our study, no statistically
significant difference was found between hypertensive and
non-hypertensive patients according to QTc and QTcd at
baseline and in the first and third months of follow up (
p
>
0.05
for all).
Statin therapy has also been found to be associated with
improved QT dynamics in heart failure patients.
18
In our study
there was no significant difference between patients on statin
therapy and those without statins, according to QTc and QTcd
parameters at baseline (
p
>
0.05 for all). We found that in female
subjects, neither QT dynamic significantly decreased in the
first month compared to baseline. The reason for this could be
the small number of females, which did not reach statistical
significance.
Although ACE inhibitor therapy has been shown to decrease
QTd,
19
in our study no significant difference was found between
patients on ACE inhibitors and those not on them at baseline (
p
>
0.05). Also, no significant difference was found between those
on digoxin and those not on digoxin at baseline (
p
>
0.05).
Neither QTc nor QTcd were different among NHYA functional
classes at baseline and in the first and third months of follow up.
This demonstrates that QT dynamics were impaired regardless of
NYHA functional class. Since there were no significant changes
in the left ventricular ejection fraction and NYHA functional
class, this indicates that the QT changes were the result of the
drug’s effect on the heart rate and blood pressure and not due to
improvement in the heart failure.
A limitation of this study was that this was a case–control
observational study without primary end-points such as
hospitalisation for heart failure, cardiac and total mortality.
Therefore, randomised blinded studies with longer follow-up
periods are needed. In addition, we only studied heart failure
patients with systolic dysfunction and normal coronary arteries.
Similar studies should be performed in heart failure patients with
preserved systolic function and coronary heart disease.
Conclusion
Similar to other older-generation
β
-blockers, nebivolol is a
selective
β
1
-blocker with vasodilator properties that have the
potential to improve QT dynamics in patients with heart failure.
Therefore the good clinical results obtained in the heart failure
patients in our study can partly be attributed to improvement in
their QT dynamics.
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