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• Re. Long axis excursion in aortic stenosis
  Fatih Yalcin
  Published on: 26 April 2002
• Previous experience with long axis shortening in aortic stenosis
  J G Dumesnil
  Published on: 19 July 2001

• Published on: 26 April 2002

  Re. Long axis excursion in aortic stenosis

  • Fatih Yalcin

  Dear Editor

  Takeda et al. have observed that degree of mitral lateral annular excursion in mild to moderate aortic stenosis is very close to that in control group. In this study, both lateral and septal side of mitral annulus have shown a consistent decrease in long axis excursion with disease progression. Aortic stenosis may lead to physiological hypertrophy in early stages of the disease as discussed in hy...

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  Dear Editor

  Takeda et al. have observed that degree of mitral lateral annular excursion in mild to moderate aortic stenosis is very close to that in control group. In this study, both lateral and septal side of mitral annulus have shown a consistent decrease in long axis excursion with disease progression. Aortic stenosis may lead to physiological hypertrophy in early stages of the disease as discussed in hypertrophy session at the 4th annual meeting of the working group on echocardiography of the ESC.[1] In a similar way, we have observed that mitral annular circumferential and longitudinal axis functions are in normal limits as compared to much lower function in cardiomyopathic patients using real-time 3-dimensional echocardiography and complex reconstruction methodology in patients with secondary LV hypertrophy caused by aortic stenosis.[2] In those patients, left ventricular systolic function had been preserved. Takeda et al. have shown that long axis excursion is independently related to both LV mass index and the grade of aortic stenosis. They have explained that both pathophysiological changes as a result of LV hypertrophy and increased afterload as a result of aortic stenosis may together contribute to changes in systolic function in aortic stenosis. These observations can support that aortic stenosis possibly results in physiological hypertrophy before existing LV dysfunction. On the other hand, it is well known that hypertension and cardiomyopathy are associated with pathological hypertrophy.[3] I believe, this comprehensive study by Takeda et al. is an important step to predict the stages of the disease process and aortic stenosis may be the unique example of physiological hypertrophy conversion to pathological one with development of LV dysfunction.

  Note: I noticed that there may be a discordance between a sentence and the referred number. In the discussion part, the second sentence is about wall stress relief in patients with aortic stenosis after the valve replacement, while marked reference (19th) is related to left ventricular dysfunction after MI.

  References

  (1) 4th Annual and plenary meeting of the working group on echocardiography of the European Society of Cardiology, 2000.

  (2) Yalçin F, Tsujino H, Greenberg N, Bauer F, Farias CA, Shiota T, Lever H, Thomas JD. Real-time three-dimensional echocardiographic evaluation of mitral annular characteristics in myocardial hypertrophy. Europ Heart J 1999:291;P1599.

  (3) Vinereanu D, Florescu N, Sculthorpe N,. Tweddel AC, Stephens MR, Fraser AG. Differentiation between pathologic and physiologic left ventricular hypertrophy by tissue doppler assessment of lon-axis function in patients with hypertrophic cardiomyopathy or systemic hypertension and in athletes. Am J Cardiol 2001; 88:53-8.

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  Conflict of Interest:
  None declared.

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• Published on: 19 July 2001

  Previous experience with long axis shortening in aortic stenosis

  • J G Dumesnil, Professors
  • Other Contributors:
    • P Pibarot

  Editor,

  We have read with interest the article by Takeda et al.[1]. Our group has previously observed that patients with aortic stenosis often have selective decreases in ventricular longitudinal shortening and wall thickening concomitant with normal fractional shortening and ejection fraction [2-4]. In the same studies, we also postulated that since subendocardial fibres are oriented longitudinally, this selective dec...

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  Editor,

  We have read with interest the article by Takeda et al.[1]. Our group has previously observed that patients with aortic stenosis often have selective decreases in ventricular longitudinal shortening and wall thickening concomitant with normal fractional shortening and ejection fraction [2-4]. In the same studies, we also postulated that since subendocardial fibres are oriented longitudinally, this selective decrease in longitudinal shortening may be the result of an increase in subendocardial wall stress and the associated subendocardial abnormalities that are often observed in patients with aortic stenosis. Moreover, the potential interest of longitudinal shortening in patients with aortic stenosis is also confirmed by our recent observation [5] that the main change in left ventricular function occurring after aortic valve replacement is a selective improvement of the left ventricular longitudinal shortening. These previously reported data are thus highly consistent with the data of Takeda et al and we fully agree with their interpretation that these observations are likely due to changes in subendocardial myocardial function. In this context, the relation they found between long axis excursion and symptoms is particularly interesting and coherent.

  On the other hand, Takeda et al measured the absolute change in longitudinal shortening using M-mode echocardiography whereas we have evaluated relative longitudinal shortening using M-mode echocardiography and a validated mathematical model of the dynamic geometry of the left ventricle. We would like to submit that relative shortening is probably more sensitive to intrinsic changes in function since absolute shortening is also influenced by the size of the ventricle, irrespective of function. For the same reason, it could also better correlate with the appearance of symptoms but this remains to be demonstrated. From a practical standpoint, it should also be emphasized that newer methods such as analysis of strain using Doppler tissue imaging [6] will probably render the evaluation of relative left ventricular longitudinal shortening much easier compared to the M-mode method. The use of the latter in the context of aortic stenosis however needs to be validated.

  References

  (1). Takeda S, Rimington H, Smeeton N, Chambers J. Long axis excursion in aortic stenosis. Heart 2001;86(1):52-6
  (2). Dumesnil J G, Shoucri R M, Laurenceau J L, Turcot J. A mathematical model of the dynamic geometry of the intact left ventricle and its application to clinical data. Circulation 1979;59(5):1024-34.
  (3). Dumesnil J G, Shoucri R M. Effect of the geometry of the left ventricle on the calculation of ejection fraction. Circulation 1982;65(1):91-8.
  (4). Dumesnil J G, Shoucri R M. Quantitative relationships between left ventricular ejection and wall thickening and geometry. J Appl Physiol 1991;70(1):48-54.
  (5). Pibarot P, Dumesnil J G, LeBlanc M H, Cartier P, Métras J. Changes in left ventricular mass and function after aortic valve replacement: A comparison between stentless and stented bioprosthetic valves. J Am Soc Echocardiogr 1999;12(11):981-7.
  (6). Voigt J-U, Arnold M F, Karlsson M, Hübbert L, Kukulski T, Hatle L, Sutherland G R. Assessment of regional longitudinal myocardial stain rate derived from Doppler myocardial imaging indexes in normal and infarcted myocardium. J Am Soc Echocardiogr 2000;13:588-98.

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  Conflict of Interest:
  None declared.

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