RANDOMIZED, DOUBLE-BLIND TRIAL OF INHALED NITRIC-OXIDE IN LVAD RECIPIENTS WITH PULMONARY-HYPERTENSION

Background. Pulmonary vascular resistance is often elevated in patient s with congestive heart failure, and in those undergoing left ventricu lar assist device (LVAD) insertion, it may precipitate right ventricul ar failure and hemodynamic collapse. Because the effectiveness of inot ropic and vasodilatory agents is limited by systemic effects, right ve ntricular assist devices are often required. Inhaled nitric oxide (NO) is an effective, specific pulmonary vasodilator that has been used su ccessfully in the management of pulmonary hypertension. Methods. Eleve n of 23 patients undergoing LVAD insertion met criteria for elevated p ulmonary vascular resistance on weaning from cardiopulmonary bypass (m ean pulmonary artery pressure >25 mm Hg and LVAD flow rate <2.5 L . mi n(-1) . m(-2)) and were randomized to receive either inhaled NO at 20 ppm (n = 6) or nitrogen (n = 5). Patients not manifesting a clinical r esponse after 15 minutes were given the alternative agent. Results. He modynamics for the group at randomization were as follows: mean arteri al pressure, 72 +/- 6 mm Hg; mean pulmonary artery pressure, 32 +/- 4 mm Hg; and LVAD flow, 2.0 +/- 0.3 L . min(-1) . m(-2). Patients receiv ing inhaled NO exhibited significant reductions in mean pulmonary arte ry pressure and increases in LVAD now, whereas none of the patients re ceiving nitrogen showed hemodynamic improvement. Further, when the nit rogen group was subsequently given inhaled NO, significant hemodynamic improvements ensued. There were no significant changes in mean arteri al pressure in either group. Conclusions. Inhaled NO induces significa nt reductions in mean pulmonary artery pressure and increases in LVAD flow in LVAD recipients with elevated pulmonary vascular resistance. W e conclude that inhaled NO is a useful intraoperative adjunct in patie nts undergoing LVAD insertion in whom pulmonary hypertension limits de vice filling and output.