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 speckle-tracking 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.
- Cardiac resynchronization therapy
- Heart failure
- Left ventricular function
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine