L’allongement acquis de l’espace QT dans l’hypertrophie ventriculaire. Origine, fréquence, signification

Abstract

Long QT is not only inherited or drug-induced. It reflects the degree of myocardial adaptation to mechanical overload In normal conditions, in isolated cells, the action potential (AP) duration depends on the activity of several ion channels. On body-surface ECG, the QT interval depends on two additional factors, namely transmural gradients and the spatial 3D projection of the electrical wave vectors. AP lengthening is a well-documented feature of cardiac hypertrophy and failure. The ion current most frequently involved, especially in humans, is an outward potassium current, I(tO), whose density is reduced as a consequence of a reduction in the corresponding gene density. In vivo, cardiac hypertrophy can modify and even reverse the transmural gradients. In humans and rats, hypertensive cardiopathy is associated with a reversible prolongation of the QT interval. The reduction in the density of l(tO )is adaptative, participates in the slowing of the cardiac cycle, and reflects fetal reprogramming. The ECG counterpart of this cellular mechanism is frequently attenuated or even masked by associated myocardial ischemia or by remodelling of the cardiac anatomic structure. Prolongation of the QT interval is a crucial component of the adaptative response to mechanical overload. As such, it has prognostic significance in heart failure of purely mechanical origin, such as hypertensive cardiopathy.