The human transplanted heart is a model of denervated heart, hence any fluctuation present in thc RR interval variability can be either due to reaquired innervation, or to represent the effect of some non autonomic activity, such as a direct effect of respiration on atrial stretch. Various physical and pharmacological manoeuvres on the respiratory and non-respiratory components of heart rate variability are used to assess the occurrence of reinnervation.

So far reinnervation was limited to the sympathetic branch. This could be due to the “standard” type of surgery that Ieaves most of vagal fibers intact. Our first observation of vagal reinnervation assessed by sinusoidal modulation of arterial baroreceptors by neck suction was obtained in a transplant patient (TX) who underwent a new type of surgery called “bi-caval”, characterised by a more extensive removal of the recipient atria. In a further study in “bi-caval” TX the probability of observing vagal reinnervation was similar to that of sympathetic reinnervation; in contrast, this probability with the “standard” technique is very low or zero regardless of time since transplantation, unless more extensive cutting of the recipient atria is performed. Similar to sympathetic reinnervation, vagal reinnervation progresses over time.

In conclusion, there is the possibility to increase vagal reinnervation in patients undergoing heart transplantation, namely by extensive resection of ihe recipient atria. This observation has high clinical relevance because a better control of the cardiovascular system would improve adaptation to various stimuli and to physical exercise.