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Am J Physiol Heart Circ Physiol 291: H2551-H2552, 2006; doi:10.1152/ajpheart.00618.2006
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LETTERS TO THE EDITOR

REPLY

C. Carlhäll, L. Wigström, and E. Heiberg

Department of Medicine and Care
Division of Clinical Physiology
and Center for Medical Image Science and Visualization
Linköping University
Linköping, Sweden
e-mail: carca{at}imv.liu.se

M. Karlsson

Department of Biomedical Engineering
and Center for Medical Image Science and Visualization
Linköping University
Linköping, Sweden

A. F. Bolger

Department of Medicine
Division of Cardiology
University of California
San Francisco, California

E. Nylander

Department of Medicine and Care
Division of Clinical Physiology
and Center for Medical Image Science and Visualization
Linköping University
Linköping, Sweden

To the Editor: We appreciate this opportunity to respond to the comments by Dr. Wandt and colleagues regarding the contribution of long-axis motion to left ventricular (LV) volume change. First, and most importantly, we do not claim to have studied the contribution of the systolic LV long-axis shortening to the total LV stroke volume. Our aim was to study the contribution of the mitral annular (MA) excursion and shape variation to LV filling and emptying throughout the cardiac cycle, using three-dimensional (3-D) echocardiography. As reported in the first paragraph of RESULTS (1), we found that the mitral annular excursion volume represented 19 ± 3% of the total LV volume change. The source of the residual portion of the total systolic LV stroke volume was not the subject of this study, although we did discuss this volume (Ref. 1, last sentence of paragraphs 2 and 3 of DISCUSSION).

The annular excursion volume in our study is accurately calculated, and the finding of 19% contribution of MA dynamics to total LV volume change is consistent with earlier studies. Toumanidis et al. (8) computed the mitral annular excursion volume as the volume of a truncated cone using 2-D echocardiography. When correcting the equation of the truncated cone by adding the denominator, the contribution of MA dynamics to total LV filling would be ~18%. Tibayan et al. (6) used a slightly different method than ours, which considered both the MA dynamics as well as the dynamics of the basal part of the LV myocardium in assessing regional LV filling. They observed a contribution of ~25% in ovine hearts, which closely corresponds to our current findings in humans.

The concept that Wandt and colleagues are emphasizing is a distinct and more global way of illustrating the relative contribution of the atrioventricular plane displacement to the total LV stroke volume. They claim that the relative contribution of the systolic LV long-axis shortening to the total stroke volume is ~80%, citing two different articles, Carlsson et al. (2) and Emilsson et al. (3). This claim however, appears to be difficult to substantiate, as discussed below.

Wandt and colleagues state that the results from the MRI study by Carlsson et al. (2) show that the relative contribution of the LV systolic shortening to the total stroke volume is 75%. Surprisingly, this result is not mentioned in the cited paper. The only related finding was that the percentage of the stroke volume from both ventricles that is filled into the atria during ventricular systole appeared to be 64 ± 2%, and that this amount would be lower on the left side because of the assumed greater reservoir function of the right atrium compared with the left (2).

In the other reference cited by Wandt and colleagues, Emilsson et al. (3) used 2-D echocardiography to compute the LV stroke volume according to a cylinder model. This stroke volume approximation represented 82% of the total LV stroke volume, using the modified biplane Simpson's rule as the reference method. The cylinder model was based on the LV epicardial cross-sectional area at the onset of systole, assuming constant outer diameter during the cardiac cycle, multiplied by the MA systolic longitudinal motion. The authors themselves point out the technical difficulties with lateral resolution and placing the LV short-axis image plane perpendicular to the long axis. These limitations most likely promote overestimation of the cross-sectional area.

Of note, Rodriguez et al. (5) have shown that the longitudinal motion of the LV apex represented 22% of the total LV long-axis motion in ovine hearts, implying that MA systolic shortening cannot be assumed to be equal to LV systolic shortening.

Moreover, the concept heralded by Wandt and colleagues has not been described in the context of the well-established theory of the coupling between the double helix myocardial fiber architecture and LV function (4, 7). The helically oriented fibers contribute to shortening both in the long- and short-axis dimension. According to Torrent-Guasp et al. (7), shortening in the short-axis diameter is actually believed to precede the long-axis shortening in systole.

In summary, it appears that Wandt and colleagues have misinterpreted the message of our original article to which they refer. It is clear that none of the different approaches to describing the contribution of the atrioventricular plane displacement to total LV volume change should presently be described as incorrect, but instead they illustrate the need for further research in this important area of LV pumping mechanics.

REFERENCES

  1. Carlhäll C, Wigström L, Heiberg E, Karlsson M, Bolger AF, and Nylander E. Contribution of mitral annular excursion and shape dynamics to total left ventricular volume change. Am J Physiol Heart Circ Physiol 287: H1836–H1841, 2004.[Abstract/Free Full Text]
  2. Carlsson M, Cain P, Holmqvist C, Stahlberg F, Lundback S, and Arheden H. Total heart volume variation throughout the cardiac cycle in humans. Am J Physiol Heart Circ Physiol 287: H243–H250, 2004.[Abstract/Free Full Text]
  3. Emilsson K, Brudin L, and Wandt B. The mode of left ventricular pumping: is there an outer contour change in addition to the atrioventricular plane displacement? Clin Physiol 21: 437–446, 2001.[CrossRef][ISI][Medline]
  4. Ingels NB Jr. Myocardial fiber architecture and left ventricular function. Technol Health Care 5: 45–52, 1997.[Medline]
  5. Rodriguez F, Tibayan FA, Glasson JR, Liang D, Daughters GT, Ingels NB Jr, and Miller DC. Fixed-apex mitral annular descent correlates better with left ventricular systolic function than does free-apex left ventricular long-axis shortening. J Am Soc Echocardiogr 17: 101–107, 2004.[CrossRef][ISI][Medline]
  6. Tibayan FA, Karlsson M, Glasson JR, Rodriguez F, Daughters GT, Miller DC, and Ingels NB Jr. Mitral annular regional contribution to filling after ring annuloplasty (Abstract). Circulation 106: II-687, 2002.
  7. Torrent-Guasp F, Buckberg GD, Clemente C, Cox JL, Coghlan HC, and Gharib M. The structure and function of the helical heart and its buttress wrapping. I. The normal macroscopic structure of the heart. Semin Thorac Cardiovasc Surg 13: 301–319, 2001.[Medline]
  8. Toumanidis ST, Sideris DA, Papamichael CM, and Moulopoulos SD. The role of mitral annulus motion in left ventricular function. Acta Cardiol 47: 331–348, 1992.[ISI][Medline]



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This Article
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