CORRESPONDENCE
Letters to the Editor
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 cardio-
myopathy. 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 con-
clusion 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
Ͼ60 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 com-
plete 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 Ͻ30 mm Hg with a 93% sensitivity and 91% specificity
and was always abolished by successful transcoronary ablation of
septal hypertrophy.
*Ole-A. Breithardt, MD
Berit Stolle, MD
Horst Kuhn, MD, FESC
*Medizinische Klinik 2
Universitätsklinikum Erlangen
Ulmenweg 18
DE-91054 Erlangen
Germany
E-mail: olebreithardt@gmx.de
doi:10.1016/j.jacc.2007.04.083
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;49:1203–11.
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 echocar-
diography. Z Kardiol 2003;92:1003–7.
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 echo-
cardiography. Heart 2005;91:379 –80.
Reply
We appreciate the comments of Drs. Breithardt, Stolle, and Kuhn
on our paper concerning premature termination of systolic left
ventricular contraction in hypertrophic cardiomyopathy (HCM)
with severe obstruction (1). Their results are in a similar group of
patients, acquired by color-coded tissue Doppler imaging (TDI).
Although the data on timing of events recorded by TDI are not
available in their reports (2,3), we agree that they have described
the same phenomenon: an abnormal drop in left ventricular
longitudinal shortening velocities in obstructive HCM. This ab-
normality was not observed in nonobstructed patients. The fact
that it was abolished by reduction of the gradient either with
pharmacologic intervention (1) or with alcohol ablation (2,3)
confirms that the drop is caused by the acute imposition of
afterload.
Breithardt et al. (2,3) observed a second late systolic velocity
peak of TDI velocities after the midsystolic drop. We observed
premature termination of contraction. We offer 2 possible expla-
nations for the differences between our findings:
1. Our group included only patients with very severe left ventric-
ular outflow track gradients: All of the patients had gradients
of Ͻ60 mm Hg, with a mean gradient of 132 mm Hg.
Dr. Breithardt’s obstructed group included patients with gra-
dients Ͻ30 mm Hg, with a mean gradient of 71 mm Hg (2).
We believe that more severe obstruction among our patients
produced the more pronounced abnormality: premature termi-
nation of septal longitudinal shortening. We also found these
abnormalities in the lateral wall, which was not reported by
Breithardt et al.
2. We used spectral TDI, in contrast to Breithardt et al., who
used color-coded TDI. The differences between techniques
have been described (4) and may have contributed to the
differences observed. Comparisons in the same patients of peak
spectral versus mean color-coded TDI tracings would be of
interest, particularly with respect to the timing of contraction
abnormalities.
Ivan Barac, MD
*Mark V. Sherrid, MD
*St. Luke’s-Roosevelt Hospital Center
Columbia University College of Physicians and Surgeons
1000 10th Avenue, 3B-30
New York, New York 10019
E-mail: msherrid@chpnet.org
doi:10.1016/j.jacc.2007.05.027
Journal of the American College of Cardiology Vol. 50, No. 10, 2007
© 2007 by the American College of Cardiology Foundation ISSN 0735-1097/07/$32.00
Published by Elsevier Inc.