SESSION TYPE: DVT/PE/Pulmonary Hypertension Posters II
PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM
PURPOSE: The unique lung anatomy with the close proximity of the airways to the blood vessels allows nitric oxide (NO) that is produced in high levels in the airways to affect the pulmonary vascular tone in concert with the NO produced in the vascular endothelium. Impaired endogenous NO production has long been speculated as a potential mechanism in pulmonary hypertension. The aim of this study was to investigate the relationship between exhaled NO, lung function and pulmonary artery pressure in consecutive patients undergoing cardiac catheterization for the assessment of heart disease.
METHODS: All the patients underwent transthoracic echocardiography, right and left heart catheterization, lung function tests, arterial blood gas analysis and exhaled NO at multiple flow-rates. Alveolar NO (CalvNO) and bronchial flux (JawNO) were calculated using the slope-intercept model.
RESULTS: Patients were 26 men and 24 women, mean age 65 years (SEM 2), 5 current smokers. Pulmonary hypertension (PH) was found in 33 (65%), 26 with PH WHO groups II-IV and 7 with pulmonary artery hypertension A significant inverse relationship was found between the values of JawNO and those of systolic pulmonary artery pressure (r=0.316, p=0.05) and of transpulmonary gradient (r=0.424, p=0.009). CalvNO was not related to pulmonary pressure. The comparison between patients with and those without pulmonary hypertension, showed that PH was associated with significantly lower FEF25-75 ( 57% vs 78%, p=0.023), lung diffusing capacity (TLCO 49% vs 91%, p=0.025) and PaO2 (75 vs 81 mmHg, p=0.036). No significant difference in the six minutes walking distance was found between the two groups.
CONCLUSIONS: Our findings indicate that bronchial NO flux is related to pulmonary artery pressure and to transpulmonary gradient. Patients with PH have decreased aiflow rates, lung diffusing capacity and PaO2.
CLINICAL IMPLICATIONS: These findings suggest that measurement of exhaled nitric oxide might be used as a marker of increased pulmonary artery pressure in patients with heart disease.
DISCLOSURE: The following authors have nothing to disclose: Caterina Bucca, Corrado Magnino, Walter Grosso Marra, Arianna Vaudano, Irene Parisi, Monica Masoero, Luisa Brussino, Alberto Milan
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