Response to Letter Regarding Article, “Longitudinal Strain Delay Index by Speckle Tracking Imaging: A New Marker of Response to Cardiac Resynchronization Therapy”
We thank Dr Jeilan and colleagues for their interest and comments on our investigation of the strain delay index using speckle tracking imaging. Before addressing Dr Jeilan’s comments directly, it is important to clarify that the mechanism of cardiac resynchronization therapy effect is speculative. To our knowledge, little, if any, definitive data are available to support the premise that specifically targeting electrical or mechanical delay consistently results in resynchronization and reverse remodeling. Some studies have refuted that premise.1 Relative to the question on the presystolic segments, time unfortunately precludes the possibility of reanalyzing the strain delay index without inclusion of the presystolic segments for this response. However, it should be noted that we did include a standard deviation calculation in our study of the peak minus the end-systolic strain data over 12 (rather than 16) segments primarily to contrast with the 12-segment tissue Doppler imaging convention reported by Yu and colleagues.2 The 12-segment standard deviation of strain delay did not favorably compare with the 16-segment strain delay index. These data are represented by a receiver-operator curve in Figure 5.3
A possible explanation as to why cardiac resynchronization therapy may favorably impact pre- and postsystolic segments may relate to the generation of a new electrical (and, in turn, electrical-mechanical) activation pathway created by an optimally positioned right and left ventricular stimulation. In this model, both early and late activating (by electrical or mechanical means or by a combination of both) segments would be resynchronized relative to an early activating segment. The end result is a change of the end-systolic timing, which will also move the early segment nearer to the end of systole.
With regard to Dr Jeilan’s interest in seeing data relating to the effect of cardiac resynchronization therapy on the strain delay index, it is unfortunate that we were unable to acquire those data with this cohort. However, we recognize the importance of these data, and they are the subject of an ongoing investigation.
Dr Buakhamsri is currently affiliated with the Department of Medicine, Faculty of Medicine, Thammasat University Rangsit, Klongluang, Pathumthani, Thailand. Dr Patel is currently affiliated with the Texas Cardiac Arrhythmia Institute, St. David’s Medical Center, Austin, Tex.
Dr Grimm has received consulting fees and honoraria from GE (modest); consulting fees, honoraria, and grant support from Medtronic (modest); and consulting fees from St. Jude Medical (minimal). Dr Thomas has received consulting fees (modest) and research support from GE.
Kocovic DZ, Rothman S, Miske G, Musco S, Britton N, Heiman M, Cox S. Lack of concordance between late activated sites as determined by TDI and the optimal LV site using pressure-volume loops in cardiac resynchronization patients. Heart Rhythm. 2008; 5: S29.
Lim P, Buakhamsri A, Popovic ZB, Greenberg NL, Patel D, Thomas JD, Grimm RA. Longitudinal strain delay index by speckle tracking imaging: a new marker of response to cardiac resynchronization therapy. Circulation. 2008; 118: 1130–1137.