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Ann Thorac Surg 1998;65:340-345
© 1998 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Randomized, Double-Blind Trial of Inhaled Nitric Oxide in LVAD Recipients With Pulmonary Hypertension

Department of Surgery, Columbia University College of Physicians and Surgeons, New York, New York, USA,
Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA,
Department of Anesthesiology, Columbia University College of Physicians and Surgeons, New York, New York, USA

Dr Argenziano, Division of Cardiothoracic Surgery, Milstein Hospital, Rm 7-435, 177 Fort Washington Ave, New York, NY 10032 (e-mail: ma66@columbia.edu).

Presented at the Thirty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Feb 3–5, 1997.

Background. Pulmonary vascular resistance is often elevated in patients with congestive heart failure, and in those undergoing left ventricular assist device (LVAD) insertion, it may precipitate right ventricular failure and hemodynamic collapse. Because the effectiveness of inotropic and vasodilatory agents is limited by systemic effects, right ventricular assist devices are often required. Inhaled nitric oxide (NO) is an effective, specific pulmonary vasodilator that has been used successfully in the management of pulmonary hypertension.

Methods. Eleven of 23 patients undergoing LVAD insertion met criteria for elevated pulmonary vascular resistance on weaning from cardiopulmonary bypass (mean pulmonary artery pressure >25 mm Hg and LVAD flow rate <2.5 L · min^-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 response after 15 minutes were given the alternative agent.

Results. Hemodynamics for the group at randomization were as follows: mean arterial 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 receiving inhaled NO exhibited significant reductions in mean pulmonary artery pressure and increases in LVAD flow, whereas none of the patients receiving nitrogen showed hemodynamic improvement. Further, when the nitrogen group was subsequently given inhaled NO, significant hemodynamic improvements ensued. There were no significant changes in mean arterial pressure in either group.

Conclusions. Inhaled NO induces significant reductions in mean pulmonary artery pressure and increases in LVAD flow in LVAD recipients with elevated pulmonary vascular resistance. We conclude that inhaled NO is a useful intraoperative adjunct in patients undergoing LVAD insertion in whom pulmonary hypertension limits device filling and output.