Aims: It is controversial whether or not pulmonary nitric oxide (NO) production, reflected in the end-tidal alveolar NO concentration, is diminished in patients with heart failure. Since pulmonary perfusion is regulated by NO production, decreased NO production in the pulmonary vasculature is assumed to result in diminished lung perfusion and further increases in ventilation-perfusion mismatch. The aim of this study is to investigate whether exhaled NO correlates with both exercise-induced hyperpnea and exercise tolerance in patients with heart disease.
Methods and results: Forty-two patients with heart disease were enrolled (history of prior myocardial infarction (n=19), dilated cardiomyopathy (n=2), hypertensive heart disease (n=5) and prior open-heart surgery (n=16)). During cardiopulmonary exercise testing, exhaled air was collected and end-tidal NO (ETNO) was measured using a chemiluminescent method. Peak ETNO was found to correlate positively with both ventilatory anaerobic threshold (r=0.468) and peak VO(2) (r=0.562). The VE-CO(2) slope, which reflects the ventilatory response to exercise, correlated negatively with peak ETNO (r=-0.588).
Conclusion: These data indicate that NO exhalation correlates, inversely, with the ventilatory response to exercise and directly with exercise intolerance, although the weakness of the correlation coefficient suggests there may be other possible mechanisms.