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

Abstract

Permanent residents at high altitude may develop excessive polycythaemia (H-Hb) and pulmonary hypertension, which often leads to cardiac failure. Inhibitors of calcium channels have been shown to reverse pulmonary hypertension in respiratory diseases and in primary pulmonary hypertension, but their efficiency has not been evaluated in high-altitude-induced pulmonary hypertension. Systolic pulmonary arterial pressure (Ppa) was studied by Doppler echocardiography, at rest and after sublingual nifedipine, in 31 asymptomatic residents at 3,600 m. Individuals were separated into two groups according to resting Ppa: a group with low Ppa (< or =4.7 kPa, n=17) and a group with high Ppa (>4.7 kPa, n=14). Individuals were also split into two groups according to haemoglobin (Hb) concentration: a normocythaemic (L-Hb) group ([Hb] < or =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 groups. There was no correlation between [Hb] and Ppa. Nifedipine induced a decrease of >20% in Ppa in two-thirds of the subjects. This response was correlated with higher levels of basal Ppa (p<0.001) and was inversely correlated with age in the L-Hb group (p<0.05). Pulmonary vasoreactivity to nifedipine was independent of the degree of H-Hb. Pulmonary hypertension secondary to chronic altitude hypoxia may be reversible, despite a possible remodelling of the pulmonary arterioles.