Background: Recent in-vitro observations suggest that left ventricular (LV) contraction is powered by ‘stretch
activation’, an intrinsic mechanism by which the stretching of an activated cardiomyocyte causes delayed force redevelopment.
We hypothesized that mechanical dyssynchrony is related to prolonged early systolic stretch that
delays the timing of peak segmental shortening.
Methods and Results: The time intervals from R wave to segmental longitudinal stretch in early systole (Tstretch)
and peak shortening (Tpeak) and the respective standard deviations (σTstretch and σTpeak) were measured by speckletracking
echocardiography in 57 patients undergoing cardiac resynchronization therapy (CRT). The percentage of
time spent in shortening, normalized to Tpeak duration [corrected ΔT=(Tpeak – Tstretch)/Tpeak] correlated with LV reverse
remodeling (reduction in end-systolic volume ≥15%). Of the 57 patients, 40 (70.2%) demonstrated LV reverse remodeling
at an average follow-up of 263±125 days after CRT. At baseline, Tstretch and σTstretch correlated with Tpeak
and σTpeak, respectively. Though there was no difference in Tstretch, Tpeak, σTstretch and σTpeak between responders and
non-responders, corrected ΔT in the mid-lateral and mid-septal segments was shorter in the responders (P<0.05 for
both) and the average of the 2 independently predicted LV reverse remodeling (area under the curve: 0.77, P=0.001).
Conclusions: Mapping LV segmental shortening in relation to early systolic stretch may aid dyssynchrony assessment
in patients undergoing CRT.
