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The European Society of Cardiology (ESC) Working Group on Myocardial Function is calling for a redefinition of the term cardiac hypertrophy as ‘myocardial remodelling’, in a report published recently in the European Journal of Heart Failure.1

The term hypertrophy, say the working group, lacks specificity, precision, and resolution due to the complexity of the underlying biological phenomena it is applied to.  First author of the paper, Ralph Knöll, National Heart & Lung Institute, Imperial College London, said: “The advantage of the term cardiac remodelling is that it simply defines reorganisation of the different cardiac tissue components, and can be used to describe an increase, or decrease in the size of the left ventricle, as well as a change to the cellular components”.

The term ‘hypertrophy’, propose the working group, should in future be restricted to cardiac myocytes rather than the whole heart.  In the paper the authors challenge the widely held view that any form of cardiac remodelling is ultimately malign, and stress that there are fundamental differences between maladaptive remodelling that leads to heart failure and adaptive remodelling that does not result in heart failure.

“One of the major research tasks is to understand more about these two types of remodelling and to find ways of translating maladaptive remodelling into  adaptive remodelling so we can prevent or reverse the course towards this adverse phenotype ,” says Knöll.

The potential of experimental models to help investigators gain information on the genetic and molecular events controlling cardiac remodelling is acknowledged by the position paper. Animal models of haemodynamic overload, infarction, and heart failure are helping to define the processes that result in cardiac remodeling, they say.

Non-invasive imaging techniques, such as echocardiography and magnetic resonance imaging as well as invasive techniques such as heart catheterisation, are now allowing investigators to closely follow the development of the pathological phenotype.  The paper outlines proposed parameters that need to be evaluated to ensure accurate evaluation of the experimental cardiac phenotypes.

“The aim is to encourage common standards that will allow a more uniform analysis of animal models,” says Balligand. “This should help scientists and clinicians to better communicate and compare results, a pre-requisite for a faster and easier translation of experimental results into the clinical arena.”

The paper concludes with suggestions for an algorithm to define a pathway for investigation of cardiac remodelling in both animal models and patients.  The algorithm takes into account whether left ventricular (LV) internal size is changed, LV wall thickness altered, LV basal function altered and whether the patient experiences stress intolerance. “The algorithm is intended to help investigators and clinicians accurately evaluate heart failure phenotypes for better risk stratification and tailored treatment” explains Knöll. “The working group believes that this could be an important tool in future prospective studies for the establishment of new treatment protocols”.

“We hope that clarifying the terminology will help foster communication between different investigators in the field and act as an impetus to increase research in cardiac remodelling,” says Jean-Luc Balligand, previous chair of the Myocardial Function working group.


1 R Knöll, G Iaccarino, G Tarone, et al. 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. Euro J Heart Fail. Doi:10.1093/eurjhf/hfr071.

Published on: July 6, 2011

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