Author + information
- Evan Adelstein, MD⁎ ( and )
- Samir Saba, MD
- ↵⁎Cardiovascular Institute, University of Pittsburgh, 200 Lothrop Street, PUH B535, Pittsburgh, Pennsylvania 15213
It is with great interest that we read the article in the September 25, 2007, issue of the Journal by Yannopoulos et al. (1). The finding of reduced atrial tachyarrhythmia (AT) burden after cardiac resynchronization therapy (CRT) implantation is indeed an intriguing finding that is pleasing from a pathophysiological and clinical perspective. However, in reviewing the literature on this topic, we feel that a contribution from our laboratory has been neglected. We performed a retrospective analysis of 27 patients who failed CRT implantation at our institution and did not go on to have an epicardial left ventricular (LV) lead surgically implanted (2). These patients were then matched, by gender, age, heart failure etiology, and history of atrial fibrillation (AF) with 2 CRT patients, 1 responder, and 1 nonresponder. We found no difference in AF burden between the CRT and non-CRT cohorts, using device-based diagnostics as the means of detecting ATs, although CRT patients with no history of AF did have a longer time to their first AF event. Our findings contradict those of the present study and are in agreement with those of Fung et al. (3).
The present study, while well performed, has certain flaws worth mention. First, the exact method of determining the number of AT episodes was not described. For example, would 2 4-s mode-switch episodes occurring within 1 min be classified as separate events? It is more likely that this reflects a single AT event that is undersensed by the device, which then records separate events. For this reason, quantification of AT burden by mode-switching episodes may be inaccurate. A second weakness is the means by which AT was quantified. The number of episodes, their rates, and the longest and shortest AT episodes are less clinically relevant than the total AT duration burden, especially given the propensity for devices to undersense AT. Thromboembolic risk and hemodynamic stress would seem to depend more upon duration and total burden of AT, not the number of episodes. The percentage of AT episodes with saved electrograms is also an important piece of omitted data. The atrial rates during AT episodes, in particular, are largely irrelevant. Whereas AF should register as a faster rate than an atrial tachycardia or flutter, undersensing of fibrillatory waves by the device (as graphically illustrated in the printed electrograms) may paradoxically create the opposite effect. Furthermore, ventricular response during atrial tachycardia and flutter is oftentimes more difficult to control than AF, making AT episodes with slower atrial rates potentially more clinically symptomatic. Finally, it would appear that AT episodes before CRT were quantified strictly from device counters without review, whereas episodes after CRT, when electrograms were available, were reviewed. This may have led to overreporting of events before CRT, again, because of the propensity of devices to undersense ATs.
We do agree with the authors that studies examining AT burden without implanted devices present in both groups (e.g., the CARE-HF [Cardiac Resynchronization Heart Failure Study] analysis in patients with and without CRT ) are of little benefit. Determining AF burden by random electrocardiograms has been demonstrated to be of little clinical import, and Yannopoulos et al. (1) rightly emphasize that the presence of a device in only 1 group will invariably lead to inequities in detection.
Currently, the role of CRT in reducing atrial arrhythmias remains speculative, as the only data come from retrospective or uncontrolled studies. Unfortunately, in the present clinical climate, the prospect of a prospective study examining this question is grim, as are any studies with a true control group examining the effects of CRT in selected populations. This is unfortunate, in that AT burden may provide important objective evidence for a direct effect of CRT upon improving left-sided filling pressures and cardiac hemodynamics, which, after all, should be the mechanism by which pulmonary congestion, dyspnea on exertion, and fatigue are alleviated by CRT.
- American College of Cardiology Foundation
- Yannopoulos D.,
- Lurie K.G.,
- Sakaguchi S.,
- et al.
- Hoppe U.C.,
- Casares J.M.,
- Eiskjaer H.,
- et al.