PAH Patients Can Take High Altitudes Without Heart Problems, Tests Show

Patients with pulmonary arterial hypertension (PAH) who took an altitude-simulation test were able to tolerate a short-term decrease in oxygen without it impacting the right side of their heart, according to a new study.

The research addressed the question of whether patients with PAH can travel safely at high altitudes without supplemental oxygen.

The study, “Right heart function during simulated altitude in patients with pulmonary arterial hypertension,” was published in the journal Open Heart.

Scientists have known that a decrease in oxygen increases pulmonary arterial pressure. What they didn’t know was whether a decrease could affect the functioning of the heart’s right ventricle (RV), including triggering an adverse medical event.

The researchers recruited 14 PAH patients whose condition was stable (WHO functional class II and III) from a pulmonary hypertension clinic. They also examined seven controls with no history of heart or lung problems.

All 21 participants were given electrocardiography and gas-exchange tests, or measures of gases inhaled and exhaled.

The research team considered the baseline, or normal situation, as a patient being at rest and breathing room air. In that scenario, the oxygen level was 21%.

Researchers then measured patient response to a 15.1% oxygen concentration, or hypoxia state, during a 20-minute resting period and five-minute mild exercise stage that involved leg lifts. Hypoxia is oxygen deprivation.

While there was a significant difference in measures of RV size and function between the PAH patients and controls at baseline, the PAH group showed the same values from baseline to hypoxia at rest or during mild exercise.

Pulmonary arterial systolic pressure (PASP), as determined by electrocardiography, increased in both groups during hypoxia and correlated with baseline measures. One reason researchers considered that meaningful is that electrocardiography is non-invasive as opposed to catheterization, and can “simultaneously assess both RV function and PASP under hypoxic conditions.”

The team said the “postulated deleterious effects on RV function from hypoxic pulmonary vasoconstriction and/or RV ischaemia in patients with PAH were not apparent in this study.” They noted, however, that the time and oxygen concentration they used may not have been sufficient to detect such effects.

Another interesting observation was that an RV-function measurement called the tricuspid annular plane systolic excursion (TAPSE) value increased in the control group — which was expected — but not in PAH patients. The lack of change in PAH patients could have reflected early signs of hypoxic decompensation or reduced RV reserve, the team said.

“It is acknowledged that our study population included mainly WHO FC [functional class] II patients who were stabilised on PAH-specific therapies,” the researchers wrote. “Thus, our study findings pertain strictly to this population which had well compensated disease. It is unknown whether a more prolonged period of hypoxia (beyond our protocol duration) will lead to deleterious effects on RV function, particularly considering the observed non-changing TAPSE.

“Thus, our study findings do not contradict current recommended guidelines regarding the use of supplemental oxygen in flight,” the team concluded, emphasizing that “duration and extent of hypoxia in this study was tolerated well despite a mild increase in symptoms of breathlessness.”

The authors wrote that “further studies are needed to determine the effect of simulated altitude in patients with PAH with more advanced FC status.”