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Although the negative effect of an irregular
ventricular rhythm on cardiac performance was proved long ago, mainly by experimental
animal studies3 but also by clinical studies in humans1,2, only recently has been any investigation into the
effects of regularisation of the ventricular rhythm on ventricular function and the
patient's quality of life. In 1993 Naito et al3
reported their findings concerning the effects of an abnormal ventricular rhythm on
cardiac output in dogs with complete atrioventricular block. They found that ventricular
pacing which caused an abnormal ventricular rhythm led to a 9% reduction in cardiac
output, compared with ventricular pacing at the same rate but with equal R-R intervals.
Moreover, they demonstrated angiographically that mitral regurgitation appeared during
pacing with the irregular rhythm but disappeared during pacing with regular beat to beat
intervals. Daoud et al5 were the first to examine the
haemodynamic effect of regular and irregular ventricular pacing at identical average heart
rates in patients with atrial fibrillation and complete atrioventricular block. After
radiofrequency ablation of the atrioventricular junction they measured the cardiac output
(Fick method), pulmonary artery pressure and wedge pressure during regular and irregular
ventricular pacing from the right ventricular apex with the same mean pacing rate. They
found that at mean cycle lengths of both 750 ms (80 bpm) and 500 ms (120 bpm) irregular
pacing caused a 12% reduction in cardiac output. The results of this study suggest that an
irregular ventricular rhythm, independently of rate, has deleterious effects on myocardial
function. Natale et al4, in a recent prospective study,
examined the impact on ventricular function and quality of life of atrioventricular nodal
ablation in chronic atrial fibrillation with a normal ventricular response. They concluded
that a chronic irregular heart rate alone could produce an overall reduction in cardiac
function that can be reversed by atrioventricular nodal ablation and pacemaker
implantation. This procedure could represent a more appropriate therapeutic modality over
treatments targeting rate control, particularly in patients with left ventricular
dysfunction. In a recent presentation by Natale et al at the 1997 ACC meeting6 the authors reported that, in patients with chronic
atrial fibrillation, discontinuation of "effective" therapy for rate control (b-blockers, Ca++ antagonists, digoxin) followed by
atrioventricular nodal ablation and pacing seems to improve the quality of life and
symptom severity, as well as left ventricular function. In this study the authors did not
find any difference between the exercise duration and VO2 max before and after
ablation.
The results from a recent study (still in progress) in our own department confirm the
findings of the above investigators, while also establishing the importance of the
restoration of the patients' chronotropy during exercise. This study so far involves 14
patients, aged 72 ± 6 years, with NYHA Class II or III heart failure and chronic atrial
fibrillation with resting heart rate between 60 and 100 bpm. The patients were taking no
antiarrhythmic medication apart from digitalis. All patients underwent radiofrequency
catheter ablation of the atrioventricular junction and implantation of a permanent VVIR
pacemaker. One day before and one and six months after the ablation ejection fraction was
measured echocardiographically and a symptom limited exercise test (Naughton) with
breath-by-breath gas exchange analysis was carried out to determine oxygen consumption at
peak exercise and at the anaerobic threshold. The importance of the procedure to the
patients' quality of life was evaluated using a special questionnaire. We found that
ejection fraction increased significantly, from 34 ± 8% before to 41 ± 9% six months
after the procedure (p < 0.01). The ergospirometric parameters also improved after the
atrioventricular junctional ablation. Oxygen consumption showed a trend to increase from
15.4 ± 0.8 to 17.8 ± 0.6 ml/kg/min (p = 0.06) at peak exercise and from 12.1 ± 0.6 to
14.8 ± 1 ml/kg/min (p = 0.06) at the aerobic threshold. According to the questionnaires
there was a significant improvement in quality of life and a decrease in the severity of
symptoms.
It should be noted that our findings regarding the improvement in the patients'
exercise performance differ from those of Natale et al. However, it is not clear whether
the patient populations in the two studies are comparable: further studies with larger
numbers of patients are needed to clarify this matter.
Although the precise underlying mechanism for the reduction in cardiac output
associated with an irregular rhythm has not been well established various mechanisms have
been implicated. The beat-to-beat variation in ventricular filling which results from an
irregular rhythm influences the intensity of cardiac systole via the Frank-Starling
mechanism and the interval-force relation12.
Neurohormonal and vasculokinetic changes13, as well as
inefficient ventricular mechanics2 may also cause a
reduction in cardiac output. Lastly, mitral regurgitation caused by the irregular rhythm
may contribute to the adverse haemodynamics3.
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