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J Am Coll Cardiol, 2010; 55:504-505, doi:10.1016/j.jacc.2009.08.066
© 2010 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

Aortic Stiffness in Hypertrophic Cardiomyopathy

Michael F. O'Rourke, MD, DSc*, Thomas Weber, MD and Audrey Adji, MB, MBiomedE

* St. Vincent's Clinic, 438 Victoria Street, Suite 810, Darlinghurst, Sydney, NSW 2010, Australia (Email: m.orourke{at}unsw.edu.au).


In the paper by Boonyasirinant et al. (1) in a recent issue of the Journal, there are serious problems in the use of pulse wave velocity (PWV) data as an index of aortic stiffness in hypertrophic cardiomyopathy (HCM).

The major technical problem is that whereas magnetic resonance imaging (MRI) can measure dimensions accurately, it can only measure flow at intervals of around 30 ms (Fig. 1 from Boonyasirinant et al. [1]), so that PWV, as distance travelled divided by time between wave feet, is likely to be less accurate, especially over very short distances (typically 12 to 13 cm in this report [1]) than when measured invasively or noninvasively by high fidelity manometry (2,3). This may account for unusually high variability of PWV measurements, especially in the HCM groups.

The most curious issue in this MRI report (1) is that normal subjects had lower values of aortic PWV (3.7 m/s, SD 0.9 m/s) than previously published for any normal group using invasive or noninvasive techniques (2,3). A previous MRI study (4) in normal (but obese) subjects of similar age gave PWV values of 6.8 m/s (SD 2.2 m/s), which is similar to that reported for HCM patients in the recent MRI report (1). Further, normal subjects (Fig. 5 from Boonyasirinant et al. [1]) had a blunted wave foot for the distal aortic wave, which is quite different from normal flow and pressure waves, from which PWV is usually calculated. High variability of PWV in HCM (mean 9.66 m/s, SD 6.43 m/s in 1 group and 6.51 m/s, SD 3.2 m/s in another) is not correctly represented in Figure 2 of Boonyasirinant et al. (1), nor are the confidence intervals, whose long "whiskers" do not appear at all. Data in the text and legend of Figure 2 (1) do not correspond to that shown in the figure.

These issues ought to be considered before the confident assertions of Boonyasirinant et al. (1) or Kuhl (5) are accepted that the MRI technique reveals "novel insights in vascular function from MRI" (1) or "an unidentified association unraveled by MRI" (5).


    Footnotes
 
Please note: Dr. O'Rourke is a founding director of AtCor Medical Pty. Ltd., manufacturer of systems for analyzing arterial pulse.


    References
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 References
 
1. Boonyasirinant T, Rajiah P, Setser RM, et al. Aortic stiffness is increased in hypertrophic cardiomyopathy with myocardial fibrosis: novel insights in vascular function from magnetic resonance imaging J Am Coll Cardiol 2009;54:255-262.[Abstract/Free Full Text]

2. Weber T, Ammer M, Rammer M, et al. Noninvasive determination of carotid-femoral pulse wave velocity depends critically on assessment of travel distance: a comparison with invasive measurement J Hypertens 2009;27:1624-1630.[CrossRef][Web of Science][Medline]

3. Laurent S, Cockcroft J, Van Bortel L, et al. European Network for Noninvasive Investigation of Large Arteries Expert consensus document on arterial stiffness: methodological issues and clinical applications Eur Heart J 2006;27:2588-2605.[Abstract/Free Full Text]

4. Joly L, Perret-Guillaume C, Kearney-Schwartz A, et al. Pulse wave velocity assessment by external non-invasive devices and phase-contrast magnetic resonance imaging in the obese Hypertension 2009;54:421-506.[Abstract/Free Full Text]

5. Kuhl HP. Hypertrophic cardiomyopathy, fibrosis, and aortic stiffness: an unidentified association unraveled by magnetic resonance imaging J Am Coll Cardiol 2009;54:263-264.[Free Full Text]


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