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J Am Coll Cardiol, 2007; 50:1006, doi:10.1016/j.jacc.2007.04.083 (Published online 20 August 2007).
© 2007 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

Effect on Obstruction on Longitudinal Left Ventricular Shortening in Hypertrophic Cardiomyopathy

Ole-A. Breithardt, MD*, Berit Stolle, MD and Horst Kuhn, MD, FESC

* Medizinische Klinik 2, Universitätsklinikum Erlangen, Ulmenweg 18, DE-91054 Erlangen, Germany (Email: olebreithardt{at}gmx.de).


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.

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.


    References
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 References
 

  1. Barac I, Upadya S, Pilchik R, et al. Effect of obstruction on longitudinal left ventricular shortening in hypertrophic cardiomyopathy J Am Coll Cardiol 2007;49:1203-1211.[Abstract/Free Full Text]
  2. Breithardt OA, Stolle B, Franke A, Janssens U, Hanrath P, Kuhn H. Mid-systolic septal deceleration—a new sign of left ventricular outflow tract obstruction obtained by color-coded tissue Doppler echocardiography Z Kardiol 2003;92:1003-1007.[CrossRef][ISI][Medline]
  3. Breithardt OA, Beer G, Stolle B, et al. Mid-systolic septal deceleration in hypertrophic cardiomyopathy: clinical value and insights into the pathophysiology of outflow tract obstruction by tissue Doppler echocardiography Heart 2005;91:379-380.[Free Full Text]

Related Articles

Effect on Obstruction on Longitudinal Left Ventricular Shortening in Hypertrophic Cardiomyopathy
Ole-A. Breithardt, Berit Stolle, and Horst Kuhn
J. Am. Coll. Cardiol. 2007 50: 1006. [Full Text] [PDF]

Reply
Ivan Barac and Mark V. Sherrid
J. Am. Coll. Cardiol. 2007 50: 1006-1007. [Full Text] [PDF]




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