In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

We use cookies to optimise the design of this website and make continuous improvement. By continuing your visit, you consent to the use of cookies. Learn more

The enigma of cardiac remodelling: new viewpoints

Top researchers in this field presented their latest results to the nearly 100 people who attended this session. Lively discussions took place after each presentation, enriching the session.

Myocardial Disease

de Windt from Utrech, the Netherlands, presented the topic : “ Calcium regulation in the cardiac myocyte as a signal for cellular remodeling”. After a short review of the intracellular calcium signaling pathway, he showed data supporting that Mir-199b antagomir delivery reduces calcineurin-induced hypertrophy in vivo. Dyrk1a regulates NFAT and is involved in heart failure in animal models, and in humans as well. Mir-199 antagomir delivery restores functional Dyrk1a expression in vivo.

Kranias, a researcher from Cincinnati, USA, addressed the topic: “Phospholamban binding partners and myocyte survival”. She started her presentation describing the role of phospholamban (Pho) in the SRCa++ transport. In fact, when overexpressed Pho reduces cardiac contractitlity. HAX-1 has demonstrated to interact with Pho in cardiac extracts, and it has been localized to mitochondria. HAX-1 prevents cell death and its action is enhanced in the presence of Pho, by a mechanism involving caspase 3. HAX-1 down regulation leads to an increase in contractility both in vitro and in vivo. HAX-1 attenuates cardiomyocyte calcium transients through the inhibition of SR calcium uptake. Overexpression of HAX-1 reduces infarct size. The inducible expression of I-1c influences Pho phosporilation and reduces infarct size in ischemia/reperfusion models. This mechanism is mediated by ER stress responses during ischemia/reperfusion. Moreover, she showed data supporting the view that gene therapy with Ad-I-1c restores Emax in failing rat hearts.

Sipido, from Leuven, Belgium, presented data on myocardial remodeling in atrial fibrillation. A review on excitation-contraction and calcium handling in chronic atrial fibrillation was provided by her at the beginning of her presentation. Sheeps with atrial fibrillation were studied . The myocytes in these animals showed a smaller and slower contraction, associated with myocyte hypertrophy. Calcium transients are also reduced in this animal model. These animals also showed a reduction in T-tubule density in the atrium, but not in the ventricle. In this model it was also observed a reduction of calcium release in both the longitudinal and transversal axis.

Ertl, from Wurzburg, Germany, addressed the topic: “Post-infarct remodeling: the heart as a wound”. He reviewed the mechanisms involved in the post-infarct remodeling process as well as the interventions which can potentially interfere with wound healing post-Mi. There are several conditions associated with impaired wound healing, such as male gender, post-menopause female, age, diabetes, clotting factor XIII deficiency, among others. In Factor XIII homozygote knock-out mices show a reduced survival after MI. When the factor XIII is administered to these animals they show an intermediate survival. These results can be explained by an inadequate inflammation, inadequate fibrosis, and apoptosis. In a mice model of osteogenesis imperfecta an impairment of healing can also be observed after MI.




The enigma of cardiac remodelling: new viewpoints

Notes to editor

This congress report accompanies a presentation given at the ESC Congress 2009. Written by the author himself/herself, this report does not necessarily reflect the opinion of the European Society of Cardiology.

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.