NITRIC-OXIDE INHALATION IN THE TREATMENT OF RIGHT-VENTRICULAR DYSFUNCTION FOLLOWING LEFT-VENTRICULAR ASSIST DEVICE IMPLANTATION

Background Following left ventricular assist device (LVAD) implantatio n in end-stage heart failure, the management of right ventricular dysf unction presents a therapeutic problem unresolved by conventional drug therapy (catecholamines, nitrates, and prostacyclin). This study was performed to investigate the effects of supplemental inhalation of nit ric oxide (NO), a selective pulmonary vasodilator, postoperatively and prospectively. Methods and Results Intraindividual dose titration of NO was performed (0 to 40 ppm) according to a standardized protocol. T hereafter treatment was continued with the individually most effective dose of NO (25 to 40 ppm). In 8 consecutive male patients presenting with right ventricular dysfunction postoperatively, a significant dose -dependent improvement in hemodynamic function was observed: pulmonary vascular resistance decreased from 336 +/- 110 to 210 +/- 59 dynes.s. cm(-5) (P < .0001), cardiac index rose from 2.0 +/- 0.4 to 2.7 +/- 0.4 L.min(-1).m(-2) (P < .003) at 40 ppm; doses of > 20 ppm were effectiv e in increasing cardiac index (P < .05). With continuous NO inhalation up to 48 hours, pulmonary vascular resistance decreased further to 15 5 +/- 33 dynes.s.cm(-5) (P < .0001) as the cardiac index increased to 3.3 +/- 0.6 L.min(-1).m(-2) (P < .003). Pulmonary artery pressure decr eased (P < .0001) as did systemic vascular resistance with hemodynamic improvement (P < .01). Central venous pressure and mean arterial pres sure remained unchanged. Right ventricular ejection fraction at transe sophageal echocardiography increased from 24 +/- 7% to 44 +/- 7% (P < .01) at the end of the study, and right ventricular end-diastolic volu me decreased (P < .05). Weaning from NO therapy was successful at 2 to 8 days, and all patients were extubated. Right ventricular function r emained stable thereafter. Conclusions In the treatment of right ventr icular dysfunction following LVAD implantation, inhalation of NO marke dly decreased right ventricular afterload by its selective vasodilatin g effects on the pulmonary circulation without producing systemic hypo tension; this merits further evaluation.