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J Am Coll Cardiol, 2008; 51:1722-1723, doi:10.1016/j.jacc.2008.02.027 © 2008 by the American College of Cardiology Foundation |
* University of California, San Diego, Box 111A, 3350 La Jolla Village Drive, San Diego, California 92161 (Email: snarayan{at}ucsd.edu).
The slope of the APD restitution relationship at any point relates the change in APD to change in DI. Therefore, slope cannot be influenced by whether the shortest DI is negative (1,2) or zero (3), which would simply translate the restitution curve along the DI axis. We actually used the same method as Selvaraj and Chauhan (2), and many patients did have negative minimum DI.
It is thus intriguing why we could not confirm the authors' finding that ventricular APD restitution is steeper in "high-risk" patients (2). One likely explanation is that minimum DI in their study was significantly shorter in high- than in low-risk patients (by 
14 ms) (2). As a result, the earliest restitution points in low-risk patients commenced at longer DI that, as the authors note, curtailed the steepest portion of restitution (Fig. 2 in Selvaraj and Chauhan [2]). Notably, minimum DI did not differ between groups in our study (1).
This raises the issue of what may alter minimum DI. The authors used activation recovery intervals (ARI) in unipolar electrograms to estimate APD, which, though validated (4), are less accurate at short DI. Even using the modified Wyatt method, ARI is more likely to underestimate than overestimate APD at short DI (see Fig. 4 in reference 4) and therefore overestimate maximum slope and contribute to an inverse relationship with minimum DI (2). The authors also paced from only 1 right ventricle site, which leads to differing actual DIs at some sites owing to conduction delay. Shorter DI in high-risk patients may also reflect greater "triangulation" of action potential phase 3 (5), potentially explaining different effective refractory period to APD ratios between groups (2), although this is not testable using ARIs.
Our results agree with reports that maximum APD restitution slope exceeds 1 in subjects without left ventricular dysfunction (6,7) and does not differ in mild left ventricular dysfunction patients (8). Although Selvaraj and Chauhan note similarities in restitution slope between historical controls and "low-risk" patients, they do not confirm that this group was arrhythmia free on follow-up (2).
Selvaraj and Chauhan also raise the important issue of spatial heterogeneity in APD restitution. Although restitution slope in our study did not differ between sites in patients with dual-site recordings (1), we agree that greater spatial sampling is necessary to explain spatial nonuniformities in TWA (9) and to define the relative importance of repolarization dispersion and restitution slope to arrhythmogenesis.
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