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Effect on Obstruction on Longitudinal Left Ventricular Shortening in Hypertrophic Cardiomyopathy

Barac et al. ( 1 ) performed an elegant echocardiographic study to investigate the previously described midsystolic drop (MSD) in left ventricular (LV) cavity pressure that is frequently observed in patients with clinically relevant obstructive hypertrophic cardiomyopathy. In their intriguing paper, the authors conclude that “the MSD in ejection velocities and flow are caused by premature termination of LV longitudinal segmental shortening.” This conclusion is based on longitudinal pulsed-wave tissue Doppler [imaging] (PW-TDI) data, which showed premature termination of longitudinal shortening in patients with LV outflow gradients of >60 mm Hg and normalization of the PW-TDI profiles after medical abolition of the gradient.</P>We have made similar observations in the past and firmly agree with the authors’ conclusions about the significant impact of dynamic LV outflow tract obstruction on mechanical LV function. However, the PW-TDI technique may not be the most sensitive clinical tool to document the effects of dynamic outflow tract obstruction on longitudinal septal shortening. In our experience with high-frame-rate color-coded TDI, we did not observe complete premature termination of LV longitudinal shortening as described by Barac et al. ( 1 ), but rather a distinct pattern with an early systolic velocity spike followed by a sudden midsystolic septal deceleration and a second, late systolic, velocity peak ( 2,3 ). This pattern identified patients with a clinically significant resting gradient <30 mm Hg with a 93% sensitivity and 91% specificity and was always abolished by successful transcoronary ablation of septal hypertrophy.</P> http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of the American College of Cardiology Elsevier
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