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CLINICAL STUDY: PULMONARY HYPERTENSION

Inhaled nitric oxide selectively dilates pulmonary vasculature in adult patients with pulmonary hypertension, irrespective of etiology

Richard A. Krasuski, MD^*, John J. Warner, MD^*, Andrew Wang, MD^*, J. Kevin Harrison, MD^*, Victor F. Tapson, MD and Thomas M. Bashore, MD^*

^* Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
Division of Pulmonary and Critical Care, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA

Manuscript received December 30, 1999; revised manuscript received June 1, 2000, accepted July 14, 2000.

Reprint requests and correspondence: Dr. Thomas M. Bashore, Box 3012, Duke University Medical Center, Durham, North Carolina 27710
thomas.bashore{at}duke.edu

OBJECTIVES

We sought to compare the responses of patients with pulmonary hypertension from primary and secondary causes (PPH and SPH, respectively) to inhaled nitric oxide (iNO) in the cardiac catheterization laboratory.

BACKGROUND

Pulmonary hypertension can lead to right ventricular pressure overload and failure. Although vasodilators are effective as therapy in patients with PPH, less is known about their role in adults with SPH. Inhaled nitric oxide can accurately predict the response to other vasodilators in PPH and could be similarly utilized in SPH.

METHODS

Forty-two patients (26 to 77 years old) with pulmonary hypertension during cardiac catheterization received iNO. Demographic and hemodynamic data were collected. Their response to iNO was defined by a decrease of 20% in mean pulmonary artery (PA) pressure or pulmonary vascular resistance (PVR).

RESULTS

Mean PA pressures and PVR were lower during nitric oxide (NO) inhalation in all patients with pulmonary hypertension. Seventy-eight percent of patients with PPH and 83% of patients with SPH were responders to iNO. A trend was seen toward a greater response with larger doses of NO in patients with SPH. Nitric oxide was a more sensitive predictor of response (79%), compared with inhaled oxygen (64%), and was well tolerated, with no evidence of systemic effects. Elevation in right ventricular end-diastolic pressure appeared to predict poor vasodilatory response to iNO.

CONCLUSIONS

Nitric oxide is a safe and effective screening agent for pulmonary vasoreactivity. Regardless of etiology of pulmonary hypertension, pulmonary vasoreactivity is frequently demonstrated with the use of NO. Right ventricular diastolic dysfunction may predict a poor vasodilator response.

Abbreviations and Acronyms   iNO = inhaled nitric oxide   NO = nitric oxide   NO2 = nitric dioxide   NYHA = New York Heart Association   PA = pulmonary artery   PPH = primary pulmonary hypertension   PVR = pulmonary vascular resistance   RVEDP = right ventricular end-diastolic pressure   SPH = secondary pulmonary hypertension   SVR = systemic vascular resistance

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