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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.

Myocardial Stretch in Early Systole is a Key Determinant of the Synchrony of Left Ventricular Mechanical Activity in vivo