Pulmonary hypertension in high-altitude chronic hypoxia: response to nifedipine

Permanent residents at high altitude may develop excessive polycythaemia (H -Hb) and pulmonary hypertension, which often leads to cardiac failure. Inhi bitors of calcium channels have been shown to reverse pulmonary hypertensio n in respiratory diseases and in primary pulmonary hypertension, but their efficiency has not been evaluated in high-altitude-induced pulmonary hypert ension. Systolic pulmonary arterial pressure (Ppa) was studied by Doppler echocardi ography, at rest and after sublingual nifedipine, in 31 asymptomatic reside nts at 3,600 France m. Individuals were separated into two groups according to resting Ppa: a group with low Ppa (less than or equal to 4.7 kPa, n=17) and a group with high Ppa (>4.7 kPa, n=14), Individuals were also split in to two groups according to haemoglobin (Hb) concentration: a normocythaemic (L-Hb) group ([Hb] less than or equal to 180 g.L-1, n=17) and a H-Hb group ([Hb] >180 g.L-1, n=14), No significant difference in Ppa was observed between the L-Hb and H-Hb gro ups. There was no correlation between [Hb] and Ppa, Nifedipine induced a de crease of >20% in Ppa in two-thirds of the subjects. This response was corr elated with higher levels of basal Ppa (p<0.001) and was inversely correlat ed with age in the L-Hb group (p<0.05). Pulmonary vasoreactivity to nifedipine was independent of the degree of H-H b Pulmonary hypertension secondary to chronic altitude hypoxia may be rever sible, despite a possible remodelling of the pulmonary arterioles.