[Abnormalities of ion movements in cardiac hypertrophy and failure]

Main sources of transmembrane ionic current that lead to cellular electrical activity are described. In hypertrophied myocardium, action potentials are usually markedly prolonged. Current modifications that could be responsible for this are not well established. However, despite divergent observations, one can postulate that calcium current density (current per area unit) is maintained to its normal level and that action potential lengthening can be related to a prolonged Na-Ca exchange current, a prolongation due to the lengthening of the calcium transient (systolic increase of intracellular calcium). In heart failure, calcium current appears reduced. It is markedly depressed in dilated human atria which greatly shortens action potential plateau. In cat, during the initial overload phase which triggers right ventricle hypertrophy, action potential plateau is also transiently reduced, which could correspond to an initial reduction of calcium current before its normalisation. Several effects are probably related to fiber stretch and appear to involve different types of stretch sensitive ionic channels.