Exaggerated exercise‐induced pulmonary hypertension in Chronic Mountain Sickness

Abstract

Excessive erythrocytosis is a hallmark of Chronic Mountain Sickness (CMS). By scavenging nitric oxide (NO), erythrocytosis may impair NO bioavailability, and, in turn, increase pulmonary artery tone. Little is known, however, about pulmonary vasoregulation at rest and during exercise in CMS. We measured systolic pulmonary artery pressure (echocardiography) at rest and during exercise (bicycle ergometer) in 20 male subjects with CMS (primary erythrocytosis, Hb level >20g/dl) and 40 healthy controls in La Paz (3600 m). All subjects were Bolivian high‐altitude natives. Hemoglobin levels, as expected, were markedly higher in CMS than in control subjects (22.1±2.0 vs. 16.7±0.8, mean±SD, p<0.001), and were associated with an increased resting systolic pulmonary artery pressure (35.5±8.7 vs. 29.5±4.9 mm Hg, p<0.002). Most importantly, the exercise‐induced increase in pulmonary artery pressure was roughly twice as large in patients with CMS than in control subjects: at 50 Watts systolic‐pulmonary artery pressure increased to 59.3±14.5 mm Hg in the patients, but to only 43.3±8.3 mm Hg in the control subjects (P<0.001). These data provide the first evidence for a strikingly exaggerated pulmonary artery pressure response to mild exercise in CMS. This exaggerated pulmonary vasoconstrictor response, which is possibly related to impaired NO biodisponibility, may contribute to impaired exercise tolerance in CMS.