[Physiopathology of heart failure: experimental model and therapeutic effects]

Studies have shown the importance of heart rate variability alterations as a marker of neurohumoral dysregulation and haemodynamic derangements in experimental heart failure. Other studies have also revealed the importance of enhanced sympathetic nerve traffic and chemoreflex dysregulation in patients with pulmonary hypertension. Furthermore, the lack of favorable effects of beta mimetic agents on long term survival in heart failure patients may implicate an absence of sympathoinhibition, possibly related to a sensitization of the peripheral chemoreceptors. Sympathetic hyperactivity is however reduced by cardiac resynchronisation therapy. Last, a comparison of sympathetic nerve traffic during normoxia and hyperoxia in heart transplant recipients, essential hypertensive patients and control subjects has revealed that transplantation does not normalize peripheral chemoreflex hyperactivity and hypersensitivity. This mechanism contributes to blood pressure elevation and exercise hyperpnea in cardiac transplant recipients.