Randomized, double-blind trial of inhaled nitric oxide in LVAD recipients with pulmonary hypertension

Michael Argenziano, Asim Choudhri, Nader Moazami, Eric A. Rose, Craig R. Smith, Howard R. Levin, Arthur J. Smerling, Mehmet C. Oz

Research output: Contribution to journalArticle

158 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)340-345
Number of pages6
JournalAnnals of Thoracic Surgery
Volume65
Issue number2
DOIs
StatePublished - Feb 1 1998
Externally publishedYes

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Heart-Assist Devices
Pulmonary Hypertension
Nitric Oxide
Pulmonary Artery
Hemodynamics
Vascular Resistance
Pressure
Nitrogen
Arterial Pressure
Random Allocation
Cardiopulmonary Bypass
Vasodilator Agents
Heart Failure
Equipment and Supplies
Lung

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Surgery

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Randomized, double-blind trial of inhaled nitric oxide in LVAD recipients with pulmonary hypertension. / Argenziano, Michael; Choudhri, Asim; Moazami, Nader; Rose, Eric A.; Smith, Craig R.; Levin, Howard R.; Smerling, Arthur J.; Oz, Mehmet C.

In: Annals of Thoracic Surgery, Vol. 65, No. 2, 01.02.1998, p. 340-345.

Research output: Contribution to journalArticle

Argenziano, Michael ; Choudhri, Asim ; Moazami, Nader ; Rose, Eric A. ; Smith, Craig R. ; Levin, Howard R. ; Smerling, Arthur J. ; Oz, Mehmet C. / Randomized, double-blind trial of inhaled nitric oxide in LVAD recipients with pulmonary hypertension. In: Annals of Thoracic Surgery. 1998 ; Vol. 65, No. 2. pp. 340-345.
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abstract = "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.",
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AU - Rose, Eric A.

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AU - Levin, Howard R.

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AU - Oz, Mehmet C.

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