Chest
Volume 114, Issue 3, September 1998, Pages 780-786
Journal home page for Chest

Comparison of Inhaled Nitric Oxide and Inhaled Aerosolized Prostacyclin in the Evaluation of Heart Transplant Candidates With Elevated Pulmonary Vascular Resistance

https://doi.org/10.1378/chest.114.3.780Get rights and content

Study objective: Elevated pulmonary vascular resistance is a risk factor in heart transplantation and reversibility of high pulmonary vascular resistance is evaluated preoperatively in potential recipients using IV vasodilators or inhaled nitric oxide. Prostacyclin is a potent vasodilator, which when inhaled, has selective pulmonary vasodilatory properties. The aim of this study was to compare the central hemodynamic effects of inhaled prostacyclin with those of inhaled nitric oxide in heart transplant candidates.

Design: A pharmacodynamic comparative study.

Setting: Cardiothoracic ICU or laboratory for diagnostic heart catheterization at a university hospital.

Patients: Ten heart transplant candidates with elevated pulmonary vascular resistance (>200 dynes o s o cm−5 and/or a transpulmonary pressure gradient > 10 mm Hg) were included in the study.

Interventions: Nitric oxide (40 ppm) and aerosolized prostacyclin (10 μg/mL) were administered by inhalation in two subsequent 10-min periods. Hemodynamic measurements preceeded and followed inhalation of each agent.

Measurements and results: Both inhaled nitric oxide and inhaled prostacyclin reduced mean pulmonary artery pressure (–7% vs −7%), pulmonary vascular resistance (–43% vs −49%), and the transpulmonary gradient (–44% vs −38%). With inhaled prostacyclin, an 11% increase in cardiac output was observed. Other hemodynamic variables, including the systemic BP, remained unaffected by each of the agents.

Conclusions: Inhaled prostacyclin induces a selective pulmonary vasodilation that is comparable to the effect of inhaled nitric oxide. Major advantages with inhaled prostacyclin are its lack of toxic reactions and easy administration as compared with the potentially toxic nitric oxide requiring more complicated delivery systems.

(CHEST 1998; 114:780–786)

Abbreviations: CO=cardiac output; CVP=central venous pressure; HR=heart rate; LV=left ventricle; MAP=mean arterial BP; MPAP=mean pulmonary artery pressure; NO=nitric oxide; NO2=nitrogen dioxide; PCWP=pulmonary capillary wedge pressure; PGI2=prostacyclin; PVR=pulmonary vascular resistance; SaO2= arterial oxygen saturation; SV=stroke volume; SvO2=mixed venous oxygen saturation; SVR = systemic vascular resistance; TPG=transpulmonary pressure gradient

Section snippets

MATERIALS AND METHODS

The study was performed at Sahlgrenska University Hospital, Göteborg, Sweden, and approved by the Human Ethics Committee of the Medical Faculty, University of Göteborg. Ten patients, 4 female and 6 male (24 to 59 years of age, mean 49 years) with elevated PVR (PVR >200 dyne o s o cm−5 and/or TPG >10 mm Hg) were included after informed consent. The patients were scheduled for diagnostic right heart catheterization. The diagnoses were ischemic (n=5) or dilated (n=5) cardiomyopathy (Table 1).

RESULTS

Patient characteristics prior to inclusion are shown in Table 1. Mean values for central hemodynamic variables during control and during PGI2 and NO inhalation are given in Table 2. No CO values were obtained for patient 7 due to a severe tricuspid valve insufficiency. Individual data on the effects of inhalation on MPAP, PCWP, TPG, and PVR are shown in Figure 2.

DISCUSSION

In the present study, we have compared the effects of inhaled aerosolized PGI2 (concentration in solution 10 μg/mL) with those of inhaled NO (40 ppm) on central hemodynamics in heart transplant candidates with congestive heart failure and elevated PVR. The main findings were that inhaled PGI2 induced a pulmonary vasodilation, with a decrease in PVR, MPAP, and TPG, comparable to that induced by inhaled NO. Furthermore, inhaled PGI2 caused no significant effect on SVR. It is not immediately

REFERENCES (41)

  • EricksonKW et al.

    Influence of preoperative transpulmonary gradient on late mortality after orthotopic heart transplantation.

    J Heart Lung Transplant

    (1990)
  • Costard-JäckleA et al.

    The influence of preoperative patient characteristics on early and late survival following cardiac transplantation.

    Circulation

    (1991)
  • Kieler-JensenN et al.

    Pulmonary vasodilation after heart transplantation: a comparison among prostacyclin, sodium nitroprusside and nitroglycerin on right ventricular function and pulmonary selectivity.

    J Heart Lung Transplant

    (1993)
  • Kieler-JensenN et al.

    Inhaled nitric oxide in the evaluation of heart-transplant candidates with elevated pulmonary vascular resistance.

    J Heart Lung Transplant

    (1994)
  • MoncadaS et al.

    Nitric oxide: physiology, pathophysiology and pharmacology.

    Pharmacol Rev

    (1991)
  • GirardC et al.

    Inhaled nitric oxide after mitral valve replacement in patients with chronic pulmonary artery hypertension.

    Anesthesiology

    (1992)
  • RichGF et al.

    Inhaled nitric oxide: selective pulmonary vasodilation in cardiac surgical patients.

    Anesthesiology

    (1993)
  • PowellM

    Toxic fumes from shotfireing in coal mines.

    Ann Occup Hyg

    (1961)
  • StenquistO et al.

    Evaluation of a new system for ventilatory administration of nitric oxide.

    Acta Anaesthesiol Scand

    (1993)
  • FerreiraSH et al.

    Prostaglandins: their disappearance from and release into the circulation.

    Nature

    (1967)
  • Cited by (141)

    View all citing articles on Scopus

    Manuscript received November 19, 1997; revision accepted March 2, 1998.

    Supported by the Swedish Medical Research Council (No. 8682 and 4341), The Medical Faculty of Göteborg (LUA), Göteborg Medical Association, and Sahlgrenska University Hospital Foundations.

    Presented in part at the International Society for Heart and Lung Transplantations 17th annual meeting and scientific sessions, April 2-5, 1997, London, England.

    View full text