The Deleterious Effect of Atrial Fibrillation and Its Association with Mortality in Non-Responders to Cardiac Resynchronization Therapy-Juniper Publishers
The well known complexity of the mechanism for
developing atrial fibrillation (AF) accounts for the failure and
relative success of the different therapeutic maneuvers in the
management of AF. Despite medical improvements made in recent years,
patients with heart failure (HF) are at increased risk of developing AF
[1-3]. AF is known to worsen the clinical course of HF through multiple
mechanisms including rapid ventricular response, irregularity of
ventricular rhythm, loss of organized atrial contribution to cardiac
output, and in some cases, tachycardia-induced cardiomyopathy. The
prevalence of AF, in patients with HF, increases with the severity of
the disease reaching up to 50% in advanced cases. In these patients with
HF, AF is an independent predictor of morbidity and mortality
increasing the risk of death and hospitalization in 76% [4-7].
As a result of more successful recognition and
treatment of cardiovascular risk factors and diseases, mortality
continues to decrease favoring an increase in the proportion of elderly
population. It has been observed that normal histological changes in the
atrial muscle occur with advancing age. These changes include a
reduction in the number of myocardial cells within the sinus node, a
generalized loss of atrial myocardial fibers in the nearness of the
internodal tracts, as well as an increase in the quantity of connective
tissue which leads to an apparent loss of myocardial fiber continuity,
atrial electrophysiological changes, and increased incidence of AF
[8-14]. Despite the excellent results obtained with some of the
pharmacological agents in the treatment of HF and AF, the optimal
medical treatment failed in the intention to improve symptoms and
quality of life in certain patients with severe HF. Thus, the necessity
to utilize cardiac devices emerges facing the failure of optimal medical
treatment in order to achieve hemodynamic improvement and correction of
the physio pathological alterations. In these patients, cardiac
resynchronization therapy (CRT) can reduce the interventricular and
intraventricular mechanical dissynchrony produced by left bundle branch
block. Indeed, the simultaneous electric stimulation of both ventricles
with CRT results in a significant hemodynamic improvement restoring a
more homogeneous contraction pattern. It has been shown that CRT
increases the left ventricular filling time, decreases septal
disquinesia and mitral regurgitation, allowing a hemodynamic improvement
[15-17]. These beneficial effects are, apparently dependent on
continuous bi-ventricular stimulation since interruption of electric
stimulation produce a progressive but not immediate loss of effect.
Therefore, CRT reverts the ventricular reverse remodeling produced by
chronic heart failure, and it is suggested that improvement in
mechanical synchrony is the predominant mechanism. However, not all
patients respond well to CRT. There are 30 to 40% of non-responders
after successful implantation of a CRT device, and the most common
reasons for interruption of CRT are the development of AF (18%) and loss
of left ventricular capture (10%). Nevertheless, CRT can be
re-instituted in a high proportion of patients so that only 5% of
patients who successfully undergo implantation of a CRT device
permanently lose CRT. Almost one fifth of patients who undergo
successful implantation of a defibrillator capable of delivering CRT
experience an AF with a rapid ventricular response, which at least
temporarily results in the inability to deliver CRT.
Predictors of interruption of CRT as the result of
the development of AF in the HF population include a previous history of
AF, a relatively slow resting heart rate, and the absence of therapy
with both beta-blockers and angiotensin converting enzyme (ACE)
inhibitors [17]. These findings are consistent with the analysis of the
SOLVD study which found that treatment with enalapril markedly reduces
the risk of development of AF in patients with left ventricular
dysfunction [18]. Therefore, although it is not clear whether the use of
both beta-blockers and ACE inhibitors directly influence the
effectiveness of CRT,
their use appears to improve the ability to deliver CRT. Similar
finding were reported with angiotensin receptor antagonists. In
the LIFE study, it was demonstrated that losartan reduced the
incidence of new onset AF in 33% compared to atenolol despite
a similar blood pressure control in both treated groups [19].
The goal should be to eliminate AF since it will improve the
ability to deliver CRT. In this regard, it is very useful the atrial
fibrillation suppression algorithm in dual-chamber permanent
pacemakers. It promotes an atrial stimulation with adequate
rates for the patient. It dynamically adjusts the stimulation rates
in manner that stimulates the heart slightly over the intrinsic
atrial rate regardless of the activity status [20-24]. Because
patients with slower heart rates are more likely to develop
AF, a dual-chamber rate-modulated pacing mode may reduce
interruptions of CRT. The search for better pharmacological
maneuvers should continue to provide the help needed to
cardiac devices. The incorporation of the AF suppression
algorithm to CRT devices may be very useful in eliminating
AF, allowing a better performance of the CRT device without
interruption. It has been clearly demonstrated that sinus rhythm
is associated with a long-term improvement in left ventricular
systolic function after AF ablation [25]. Therefore, AF catheter
ablation may have a primary role as a rhythm control strategy in
the definite treatment of AF in patients with HF [25-27]. There
should always be a strong effort to convert and maintain to
sinus rhythm by all means, after all, sinus rhythm is a God given
rhythm.
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