Background. Recipient pulmonary hypertension due to chronic congestive hear
t failure is a major cause of right ventricular (RV) dysfunction after hear
t transplantation. We hypothesized that inhaled nitric oxide (NO), in the p
ostoperative period, would a) selectively reduce pulmonary vascular resista
nce and improve RV hemodynamics and b) reduce the incidence of RV dysfuncti
on compared with a matched historical group.
Methods. Sixteen consecutive adult heart transplant recipients with lowest
mean pulmonary artery (PA) pressures > 25 mmHg were prospectively enrolled.
Inhaled NO at 20 parts per million (ppm) was initiated before termination
of cardiopulmonary bypass (CPB). At 6 and 12 hours after CPB, NO was stoppe
d for 15 minutes and systemic and pulmonary hemodynamics were measured. RV
dysfunction was defined as central venous pressure > 15 mmHg and consistent
echocardiographic findings. The incidence of RV dysfunction and 30-day sur
vival in this group was compared with a historical cohort of 16 patients ma
tched for pulmonary hypertension.
Results. Discontinuation of NO for 15 minutes at 6 hours after transplantat
ion resulted in a significant rise in mean PA pressure, pulmonary vascular
resistance (PVR), and RV stroke work index. Systemic hemodynamics were not
affected by NO therapy. One patient in the NO-treated group, compared with
6 patients in the historical cohort group, developed RV dysfunction (P < .0
5). The 30-day survival in the NO-treated group and the historical cohort g
roup were 100% and 81%, respectively (P > .05).
Conclusion. In heart transplant recipients with pulmonary hypertension, inh
aled NO in the postoperative period selectively reduces PVR and enhances RV
stroke work. Furthermore, NO reduces the incidence of RV dysfunction in th
is group of patients when compared with a historical cohort matched for pul
monary hypertension. Inhaled NO is a useful adjunct to the postoperative tr
eatment protocol of heart transplant patients with pulmonary hypertension.