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European Heart Journal Advance Access published online on July 10, 2008

European Heart Journal, doi:10.1093/eurheartj/ehn330
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Assessment and relevance of ventricular wall stress in heart failure

Peter Alter

Internal Medicine – Cardiology
Philipps University
Baldingerstrasse
D-35033 Marburg
Germany
Tel: +49 6421 5866462
Fax: +49 6421 5868954
Email: alter{at}staff.uni-marburg.de

Heinz Rupp

Internal Medicine – Cardiology
Philipps University
Baldingerstrasse
D-35033 Marburg
Germany

Bernhard Maisch

Internal Medicine – Cardiology
Philipps University
Baldingerstrasse
D-35033 Marburg
Germany

We read with great interest the article by De Simone et al.1, published in the European Heart Journal. By using M-mode echocardiography, the authors examined the relationship between left ventricular (LV) mass and incident heart failure not attributable to myocardial infarction. LV hypertrophy (LVH) or ‘excess’ of LV mass was found to be an independent predictor of incident heart failure. To quantify this so-called ‘excess’ of LV mass, expected normal values were calculated based on body height, gender, and stroke work. The latter was defined by the authors as systolic blood pressure times Teichholz-based stroke volume. In contrast to the used method, we prefer to assess stroke work in accordance with its physiological definition as the area within the pressure–volume loop, which is the standard method in experimental studies and is also feasible in patients.2 In the present study, systolic cuff blood pressure was obtained,3 which appears to be a further limitation since only LV pressure is decisive for LV wall stress.

In addition, an M-mode-based echocardiographic approach was used to assess LV wall stress. In a recent study on patients with non-ischaemic LV dysfunction, we compared an echocardiography-based method with a thick-walled sphere model,4 using parameters derived from cardiac magnetic resonance (CMR) imaging,5 which is the generally accepted reference method for assessing cardiac volumes and mass. The echocardiography-based method systematically underestimated LV wall stress.6 The extent of underestimation was proportional to the wall stress.7

As regards the present manuscript, a moderately (<5%) increased LV end-systolic wall stress was found in patients with increased ‘excess’ of LV mass as stratified into quartiles. Potentially, the increase in LV wall stress has been underestimated because of the methods used.

Noteworthy, LV dimensions were increased in patients with ‘excess’ of LV mass. LV pressure, volume, and myocardial mass are crucial determinants of wall stress. LV dilatation implies an increase in radius (of the sphere model of the LV) and, therefore, raises LV wall stress by square. An increased wall stress occurs, if the myocardial growth is not adequate for coping with the expanding ventricular volume.

It appears likely that calculation of CMR- based wall stress would have revealed greater differences. LV wall stress might thus also emerge as a stronger predictor of incident heart failure. In conclusion, we agree with the authors that it is necessary to assess myocardial mass, a vital parameter in heart failure. However, it also appears crucial to monitor an increased wall stress that has various adverse consequences for energy metabolism, gene expression, and arrhythmia risk. In particular, one should be aware of an increase in myocardial wall stress during progression of heart failure.

References

  1. De Simone G, Gottdiener JS, Chinali M, Maurer MS. Left ventricular mass predicts heart failure not related to previous myocardial infarction: the Cardiovascular Health Study. Eur Heart J (2008) 29:741–747.[Abstract/Free Full Text]
  2. Alter P, Rupp H, Rominger MB, Klose KJ, Maisch B. A new methodological approach to assess cardiac work by pressure–volume and stress–length relations in patients with aortic valve stenosis and dilated cardiomyopathy. Pflugers Arch (2008) 455:627–636.[CrossRef][Web of Science][Medline]
  3. Aurigemma GP, Devereux RB, De Simone G, Roman MJ, O'Grady MJ, Koren M, Alderman M, Laragh J. Myocardial function and geometry in hypertensive subjects with low levels of afterload. Am Heart J (2002) 143:546–551.[CrossRef][Web of Science][Medline]
  4. Turcani M, Rupp H. Etomoxir improves left ventricular performance of pressure-overloaded rat heart. Circulation (1997) 96:3681–3686.[Abstract/Free Full Text]
  5. Alter P, Rupp H, Czerny F, Vollrath A, Rominger MB, Maisch B. Relation of ventricular wall stress and autonomic tone in patients with dilated cardiomyopathy assessed by cardiac magnetic resonance imaging. Eur Heart J (2006) 27(Supp):P4039.
  6. Alter P, Rupp H, Rominger MB, Vollrath A, Czerny F, Klose KJ, Maisch B. Relation of B-type natriuretic peptide to left ventricular wall stress as assessed by cardiac magnetic resonance imaging in patients with dilated cardiomyopathy. Can J Physiol Pharmacol (2007) 85:790–799.[CrossRef][Web of Science][Medline]
  7. Alter P, Rupp H, Rominger MB, Vollrath A, Czerny F, Figiel JH, Adams P, Stoll F, Klose KJ, Maisch B. B-type natriuretic peptide and wall stress in dilated human heart. Mol Cell Biochem (2008) 314:179–191.[CrossRef][Web of Science][Medline]

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