Molecular Biology of Heart Failure

  • B. Swynghedauw


Myocardial dysfunction is no more functional in nature and recent progress in molecular biology have allowed a better understanding of the process. The new myocardial phenotype is not only quantitatively, but also qualitatively different from the normal heart. The first evidence that qualitative changes occur after chronic overload was published by our laboratory in 1979 [1]. We were indeed able to show in the rat ventricles, after aortic stenosis or aortic insufficiency, an isomyosin shift resulting in the reexpression of a foetal isoform with a low ATPase specific activity. Further investigations in the rat and in other animal species, have shown that such a shift was responsible for the diminution of the shortening velocity and, partly, for the improvement of the economy of contraction [2,3]. Several other changes in genetic expression were further reported, including those encoding sarcomeric proteins, membrane proteins, receptors, proteins responsible for energy metabolism and also several pathways in charge of the transduction process [4]. The puzzle is now more or less complete and it is now possible to establish a rational link between the aforementioned modifications and the well-documented physiological alterations which characterise the failing myocardium.


Heart Rate Variability Sarcoplasmic Reticulum Diastolic Dysfunction Cardiac Hypertrophy Action Potential Duration 
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© Springer-Verlag Italia 1998

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  • B. Swynghedauw

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