[Plasticity of myocardial phenotype during cardiac hypertrophy and failure].

Cardiac hypertrophy and failure frequently cause complications in some cardiovascular diseases. Both conditions are associated with important modifications of the heart's contractile and endocrine functions, induced by various changes in gene expression, which in turn are attributable to chronic hemodynamic overload. Differential expression of the myosin heavy chain family leads to a disproportionate accumulation of the alpha form relative to the beta, which in turn causes slower but more efficient myocardial contraction. This transition occurs in the rodent ventricle and human atrium. In the sarcomeric actin family, both the alpha-cardiac and alpha-skeletal isoforms are expressed in the mammalian ventricle in utero. After birth, the latter transiently accumulates in the rodent ventricle at the acute phase of an experimental overload. In humans, alpha-skeletal actin accounts for over half of total actin; this ratio remains the same during heart failure. In experimental models of hemodynamic overload, and during heart failure in humans, expression of Ca(2+)-ATPase in the sarcoplasmic reticulum is reduced. This decrease may partly account for the changes in cardiac relaxation observed in these circumstances. The atrial natriuretic factor gene in the ventricular myocardium is also activated, permitting the ventricle to participate in the regulation of its loading conditions. Several mechanical and neurohumoral factors have been proposed as triggers for this gene reprogramming. Research is currently focussed on signal transduction mechanisms, and in particular identification of the transcription factors involved.