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Internal Medicine (East Africa)


We read with interest the recent article by Lim et al.1 This article demonstrated a strong correlation between a novel longitudinal strain delay index and left ventricular end-systolic volume reduction in both ischemic and nonischemic patients.

The principle outlined by the authors is that an increased longitudinal strain delay index requires both dyssynchrony (defined in their article as a discrepancy between the time of end-systolic contraction and the time to peak strain) and residual contractility. Their concept elegantly considers the problem of cardiac resynchronization therapy (CRT) nonresponse in heart failure patients who have myocardial segments with delayed contraction due to scarred or akinetic segments. The index appears to address some of the limitations of time delay indices that do not take account of residual myocardial contractility. Patients with a high longitudinal strain delay index (dyssynchronous and contractile) are more likely to respond to CRT than are patients with a lower index (synchronous, akinetic, or both).

In the authors’ model, an absolute discrepancy between the time of end-systolic contraction and the time to peak strain is 2 sided. Broadly speaking, resynchronization therapy works by preexciting the areas of latest activation in the dyssynchronous left ventricle. This traditional understanding of CRT-responsive dyssynchrony would suggest that peak strain in the dyssynchronous target segments should be delayed and occur after aortic valve closure (postsystolic segments).2–3 However, the proposed strain delay index also includes “presystolic segments” (peak strain occurring in segments before aortic valve closure) within an averaging calculation. Intuitively, it is difficult to understand why CRT may address this type of presystolic dyssynchrony.

It would be useful to see whether data that eliminate these presystolic, earlier-contracting segments from the analysis or incorporate a measure of the variability of delay (eg, standard deviation) across the 16 segments studied within the data set might affect or improve the index’s performance. Also, the authors did not describe the effect of CRT on this index. Although CRT’s effect was not the remit of their article, it would be interesting to use these data to evaluate the differences in changes (pre- and post-CRT) to the longitudinal strain delay index score among responders and nonresponders.


This work was published before the author joined Aga Khan University.

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