Rapid fall in sympathetic nerve hyperactivity in patients with heart failure after cardiac transplantation

Severe heart failure is associated with an intense sympathetic nerve hyperactivity. After cardiac transplantation, neurochemical studies have indicated a normalization of sympathetic outflow. Intraneural recordings have, however, yielded varying results; both a normalization and a remaining hyperactivity have been obtained in cardiac transplant recipients, the latter being attributed to cyclosporine treatment.

To circumvent the methodologic variation associated with different patient groups in cross-sectional studies, a longitudinal study design was employed in this study. Intraneural recordings of muscle sympathetic nerve activity in 21 heart failure patients were performed before, and repeatedly during the first year after, heart transplantation. Before surgery, muscle sympathetic nerve activity was augmented in all patients (78 +/- 4 bursts/min, 90 +/- 2 bursts/100 heartbeats). Both muscle sympathetic nerve activity burst frequency (burst/minute) and burst incidence (bursts/100 heartbeats) decreased rapidly following surgery. One month after surgery, burst frequency was reduced by 35% (51 +/- 5 bursts/min P < .05), whereas burst incidence decreased by 32% (61 +/- 5 bursts/100 heartbeats, P < .05). This decrease remained unchanged up to 1 year after surgery. The fall in posttransplant muscle sympathetic nerve activity was similar in transplant recipients who developed hypertension during the course of the study (n = 12) and those who remained normotensive (n = 9).

The sympathoexcitation recorded in patients with heart failure was rapidly and substantially reduced after cardiac transplantation despite cyclosporine treatment, most likely reflecting improved central and peripheral hemodynamics.