4.5 Article

Towards a re-definition of 'cardiac hypertrophy' through a rational characterization of left ventricular phenotypes: a position paper of the Working Group 'Myocardial Function' of the ESC

Journal

EUROPEAN JOURNAL OF HEART FAILURE
Volume 13, Issue 8, Pages 811-819

Publisher

WILEY
DOI: 10.1093/eurjhf/hfr071

Keywords

Hypertrophy; Heart failure; Myocardial function

Funding

  1. Deutsche Forschungsgemeinschaft (DFG) [Kn448/9-1, 2, Kn448/10]
  2. Fritz Thyssen Stiftung
  3. British Heart Foundation (BHF)
  4. FP6-I.P. 'EUGeneHeart'
  5. Fondation Leducq
  6. Belgian Politique Scientifique Federale
  7. Communaute Francaise de Belgique
  8. Portuguese FCT [PIC/IC/82943/2007]
  9. Cardiovascular RD Unit [51/94]
  10. Italy Health Ministry
  11. Fundação para a Ciência e a Tecnologia [PIC/IC/82943/2007] Funding Source: FCT

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Many primary or secondary diseases of the myocardium are accompanied with complex remodelling of the cardiac tissue that results in increased heart mass, often identified as cardiac 'hypertrophy'. Although there have been numerous attempts at defining such 'hypertrophy', the present paper delineates the reasons as to why current definitions of cardiac hypertrophy remain unsatisfying. Based on a brief review of the underlying pathophysiology and tissue and cellular events driving myocardial remodelling with or without changes in heart dimensions, as well as current techniques to detect such changes, we propose to restrict the use of the currently popular term 'hypertrophy' to cardiac myocytes that may or may not accompany the more complex tissue rearrangements leading to changes in shape or size of the ventricles, more broadly referred to as 'remodelling'. We also discuss the great potential of genetically modified (mouse) models as tools to define the molecular pathways leading to the different forms of left ventricle remodelling. Finally, we present an algorithm for the stepwise assessment of myocardial phenotypes applicable to animal models using well-established imaging techniques and propose a list of parameters most suited for a critical evaluation of such pathophysiological phenomena in mouse models. We believe that this effort is the first step towards a much auspicated unification of the terminology between the experimental and the clinical cardiologists.

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