Author + information
- Marius M Hoeper, MDa
We appreciate Dr. Gorenflo’s interest in our manuscript. We do not, however, share his concerns regarding the interpretation of our results. In our study in patients with primary pulmonary hypertension, inhaled nitric oxide caused a fall in the pulmonary artery pressure by a mean of 7% from baseline, while the systemic arterial pressure remained stable, clearly indicating selective pulmonary vasodilation. Aerosolized iloprost resulted in a fall of the pulmonary artery pressure by a mean of 13%, whereas the systemic artery pressure declined by 3%. The mean decline in pulmonary vascular resistance with aerosolized iloprost was 33%, and the mean decline in systemic vascular resistance was 21%, also suggesting real pulmonary vasodilation. As we stated in our manuscript, aerosolized iloprost exerted preferential, but not selective, pulmonary vasodilatory effects in patients with pulmonary hypertension.
Whenever an increase in cardiac output is accompanied by stable or decreased pulmonary artery pressures, there must be some degree of pulmonary vasodilation (or recruitment of pulmonary vessels). Back in time, when we used to test oral calcium channel blockers in almost every patient with primary pulmonary hypertension (1), we observed several patients in whom the systemic arterial pressure decreased, the cardiac output increased and the pulmonary artery pressure also increased. In these patients, the pulmonary vascular resistance remained constant. This is what happens when there is systemic vasodilation accompanied by reflectory increase in cardiac output but lack of pulmonary vasodilation.
- American College of Cardiology