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• W2007120265 abstract "Cardiac pump function depends on ordered mechanical events that are precisely orchestrated by electrical timing. This ordering of mechanical events occurs at multiple anatomic levels: between chambers, within chambers, and of particular importance, at the left ventricular level, within myocardial segments. A reasonably accurate first-order assessment of atrioventricular (AV) coupling, which is easiest to understand, can be made at the bedside using the jugular venous waves and heart sounds. Assessment of ventricular electromechanical coupling is considerably more complex and requires higher resolution. The ventricular conduction pattern on the surface ECG offers some insights, but is potentially misleading; greater precision at the global and segmental level is possible using sophisticated imaging techniques.1-3 The sequence of contraction at the chamber level proceeds in a descending fashion, but the relative contribution at the chamber level to overall cardiac performance is in the reverse order: ventricular pump function matters most of all. A word applied to this electromechanical ordering is “synchrony.” Disruptions to electrical timing result in disordered mechanical events (desynchronization, or “dyssynchrony”), can occur spontaneously or be induced at any level, and may reduce pump function. Atrial fibrillation (AF) disrupts atrial coupling (atrial desynchronization) and eliminates AV coupling (AV desynchronization), whereas ventricular synchrony is maintained, though rapid ventricular rates may occur. So in the context of permanent AF, where atrial and AV synchrony have already been lost but undesirable rapid ventricular rates remain, resides an interesting physiologic experiment: removal of the last remaining and most important contributing element to pump function, ventricular synchrony, by interrupting AV conduction and inducing ventricular desynchronization with continuous right ventricular apical (RVA) pacing. Therefore, it is important to ask what might happen to patients in whom total cardiac desynchronization has occurred due to disease (AF) and, subsequently, treatment for the disease (AV junction ablation and RVA pacing). Permanent destruction of the AV junction (AVJ) ablation for definitive rate control in atrial arrhythmias was first described using endocardial catheters and direct current energy in 1982.4 Acceptance and widespread application of the technique was rapid with the emergence of radio frequency energy.5 Voluntary surveys of catheter ablation practice in the United States reported that AVJ ablation accounted for 18.9% of all ablations in 2001 where notably 51% of patients were age >70 years.6 In this issue of the Journal, Chen et al.7 present a single-center, observational experience with AVJ ablation and permanent RVA pacing for definitive ventricular rate control in AF. Single-center reports have a few virtues and many potential deficiencies. The principal virtue is the possibility of systematic follow-up (post-hoc bias, but done the same way most of the time). A major deficiency is that there is always residual uncertainty as to why some patients were treated and others were not. This is the underpinning of an enrollment bias complaint. This problem is immediately evident in the present report, where in the second sentence of Results (Demographics), we learn that only 286 of 748 (38.2%) patients who underwent AVJ ablation over a 12-year span at the Mayo Clinic had follow-up echocardiograms, which was the primary endpoint of the analysis. This introduces a second level of bias since diagnostic tests are more likely to be obtained in patients for whom greater clinical concern exists. Not unexpectedly, these 286 patients were sicker (more hypertension, myocardial infarction-MI, mitral regurgitation-MR, and heart failure) than the 462 patients who did not have echocardiograms. Therefore, the opportunity to generalize the results is immediately jeopardized since more than 60% of patients who were exposed to continuous RVA pacing after AVJ ablation did not have follow-up echocardiograms for review. This amount of missing data would completely doom a prospective randomized clinical trial. In order to proceed with evaluation of this manuscript, one must be willing to suspend disbelief at this point in the process. The authors basically have one conclusion: EF did not change significantly in most patients in whom it was measured after AVJ ablation and “long-term” exposure to RVA pacing. While this conclusion is statistically correct when applied to the whole study population, what lies beneath merits emphasizing. Among patients with baseline EF < 40%, further declines were rare (1%). However, 19% of patients with EF > 40% prior to AVJ ablation had a > 10% absolute reduction in EF during follow-up. The most likely explanation for these findings is that atrial tachycardiomyopathy8 was the cause of low EF that improved after rate control and regularization, counterbalancing the penalty of continuous ventricular desynchronization. The authors hint at this possibility in reporting that preablation ECG-determined mean ventricular rate > 100 beats/minute was a univariate predictor of improvement in EF. It is somewhat surprising that more detailed evidence for atrial tachycardiomyopathy, such as duration of low EF, higher resolution measures of nominal ventricular rates, and absence of other causes of cardiomyopathy, is not presented. In contrast, for nearly 20% of patients with EF > 40% where AVJ ablation was done presumably to palliate symptoms rather than relieve rate-related cardiomyopathy, the penalty of ventricular desynchronization was a reduction in systolic function (>10% decline in EF). A relatively recent meta-analysis of 21 studies involving 1,181 patients concluded that AVJ ablation and RVA pacing is safe and effective for reducing symptoms, improving quality of life, and reducing health care utilization when uncontrolled ventricular rates during AF persist despite maximally tolerated medical therapy.9 Ejection fraction improves modestly and sometimes dramatically among patients with preceding atrial tachycardiomyopathy, whereas a slight or modest decline in EF is typically observed among patients with normal baseline EF, long-standing observations that were basically duplicated by Chen et al.7 in a much smaller data set. It was argued in 1998 on the basis of the already 16-year cumulative clinical experience with AVJ ablation and RVA pacing that “…further outcome studies, randomized or not, using this most recalcitrant population are not warranted,”10 and AVJ ablation and RVA pacing still meet Class II b level of evidence in updated consensus criteria for the treatment of AF.11 So, why are we hearing about this now from Chen et al.?7 One reason may be to provide reassurance that condemnation to “long-term” RVA pacing is not all so bad. This counterargument is important and timely because more recent clinical evidence has implicated RVA pacing with increased risks of AF and heart failure hospitalization in typical pacemaker patients12-14 and ventricular arrhythmias and death among implantable cardioverter defibrillators (ICDs) patients.15-17 These adverse effects of RVA pacing are attributed to left ventricular desynchronization, similar to left bundle branch block, although left-sided AV desynchronization induced by RVA pacing may be relevant as well. The notion that pacemakers might do harm has received a lot of attention lately, but the idea is not new. Earlier literature on RVA pacing, with or without AVJ ablation, includes many startling reports of new onset heart failure due to functional MR,18-21 in some instances requiring mitral valve replacement.22 Interestingly, there was some erroneous speculation that the appearance of MR after AVJ ablation was related to undetermined effects of the application of radio frequency energy itself rather than RVA pacing.21 The mechanism of functional MR after RVA pacing has multiple components. The immediate cause is papillary muscle desynchronization, which has been recently demonstrated using strain rate imaging.23 In apparently rare patients who develop dilated cardiomyopathy due to ventricular desynchronization during RVA pacing, volumetric remodeling probably contributes to functional MR by increasing papillary muscle tethering forces24 and reducing the transmitral pressure gradient. 25 Does the report of Chen et al.7 provide reassurance? These data should be interpreted carefully and in a mechanistic context. It should not be concluded that the absence of a population-scale reduction in EF means that significant morbidity does not occur with continuous RVA pacing. None of the pacemaker or ICD trials linking RVA pacing with heart failure and AF provided evidence in either direction that RVA pacing-induced decline in EF was the explanation for these observations. In these trials, evidence for heart failure worsening was based on clinical signs and symptoms, sometimes supplemented by simple diagnostic testing such as chest radiography, but unaccompanied by systematic reassessment of EF. It is far more likely that the relationship between RVA pacing and worsening heart failure and AF, at least in typical pacemaker patients with normal ventricular function, is due to increased left atrial pressure caused by functional MR and left-sided AV desynchronization rather than a precipitous decline in EF. Therefore, it is notable that Chen et al. observed new onset of mild-moderate MR in 49% of patients with no MR at baseline, and worsening of MR in 14% of patients with baseline MR.7 Additionally, the mean duration of follow-up in the “long-term” group was 36 months, but with a huge standard deviation (18 months). Certainly, in practical terms, among patients who have been condemned to continuous RVA pacing, “long-term” should be measured at least by the lifetime of the pulse generator, or even better, the patient's life. This is important because the complex relationship between RVA pacing and heart failure appears to have two primary elements: (1) substrate and (2) time. The risk of heart failure increases with increasing paced QRS duration, and this risk relationship is greatest among patients with low EF, preexisting ventricular conduction delay (left bundle branch block), heart failure, and MI.13 These substrate conditions interact with cumulative percent RVA pacing, which also has an increasing risk relationship with heart failure.12, 13 The total burden of ventricular desynchronization can be conceptualized as a function of the paced QRS duration, which is a measure of “potency per dose” and the cumulative percent RVA pacing, which is the frequency at which the dose is delivered.13 The standard practice of RVA pacing over the past 40 years has not triggered an epidemic of pacing-induced low EF heart failure. In the Mode Selection Trial, only 10% of patients over a median follow-up of 33 months had heart failure that could be linked to RVA pacing.12 This is because most typical pacemaker patients are elderly, have normal ventricular function, and no preexisting ventricular conduction delay, heart failure or MI (low risk substrate). These patients tolerate chronic RVA pacing reasonably well, and the 2-year probability of heart failure that can be linked to pacing is approximately 1.4%.13 This likely explains the relative insensitivity of clinical outcomes to cumulative percent RVA pacing in pacemaker trials. Importantly, approximately 90% of pacemaker recipients are >60 years old, and 30% or more are >80 years old in many nations.26 Advanced age and a high comorbidity rate in typical pacemaker patients also means that most will not live long enough to be harmed by their pacemaker (insufficient time). On the other hand, typical ICD patients have most or all of these substrate conditions, and the relative risk of heart failure associated with RVA pacing rises to approximately 52% over 2 years.13 This provides some explanation for the observation that it took 3–5 years before heart failure attributed to RVA pacing became manifest in pacemaker trials, but <1 year in ICD trials. It should also not be assumed that absence of baseline substrate risk factors confers freedom from adverse effects of RVA pacing-induced ventricular desynchronization. Given enough time, younger patients exposed to chronic RVA pacing develop significant LV remodeling and, in some instances, dilated cardiomyopathy.27-31 The difference in this situation is the total duration of exposure. Of much greater interest will be the outcome of relatively younger patients 10–20 years after AVJ ablation and continuous RVA pacing. The particular challenge this poses is that the physician who implanted the pacemaker may have long since left the care of the patient and another generation of physicians will have to manage the consequences of long-term RVA pacing exposure. Whether alternative ventricular pacing strategies,32-35 should be considered in these patients at the time of AVJ ablation and pacemaker insertion, we cannot be sure." @default.
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• W2007120265 date "2007-10-25" @default.
• W2007120265 modified "2023-10-16" @default.
• W2007120265 title "The World Is Not Black and White. More Like Black and Gray" @default.
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