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This editorial refers to ‘Exercise training improves peak oxygen consumption and haemodynamics in patients with severe pulmonary arterial hypertension and inoperable chronic thrombo-embolic pulmonary hypertension: a prospective, randomized, controlled trial’†, by N. Ehlken et al., on page 35.

Introduction

Pulmonary hypertension is a pathophysiological condition characterized by an increase of mean pulmonary arterial pressure ≥25 mmHg at rest.1 Pulmonary hypertension may complicate multiple clinical disorders and invariably it reduces exercise and functional capacity and represents a risk factor for morbidity and mortality.2 Although important progress in the pharmacotherapy of pulmonary arterial hypertension has been achieved in the past 15 years,3,4 limited functional capacity and reduced survival still characterize patient outcome. Further advances are needed in this area to improve the clinical results of a comprehensive treatment strategy.

Effects of exercise training

Ehlken and colleagues now present the data of a randomized controlled trial on the impact of exercise training on peak oxygen consumption and haemodynamics in 87 patients with pulmonary arterial hypertension or inoperable chronic thrombo-embolic pulmonary hypertension.5 The majority of subjects (91%) were on background approved pulmonary arterial hypertension therapies. The exercise training started with an in-hospital 3-week programme and was continued at home with at least 15 min/day for 5 days a week for the following 12 weeks.

Issue Section:
Clinical Research > Editorial
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Comments (1)
Re:"Exercise training in pulmonary hypertension: improving performance but waiting for outcome"Galie, et al., 37 (1): 45-48 doi:10.1093/eurheartj/ehv440
22 February 2016
Jason S. Fritz, Pulmonologist
University of Pennsylvania
With regards to Ehlken & colleagues' speculation concerning the physiologic underpinnings of their findings with training, some additional data might provide some clarity. First, did the authors compare maximal arterio-venous oxygen content differences between the trained and untrained groups? A training-induced increase in A-V O2 difference would suggest increased peripheral muscle oxygen utilization. Second, were there differences between groups in measures of ventilatory efficiency (Ve/VCO2 slope, Ve/VCO2 nadir value, and/or end-tidal CO2)? An improved ventilatory efficiency with training would support the notion of improved ventilation-perfusion relationships. Lastly, it is also worth pointing out that maximal heart rate was significantly improved with training which will account for a portion of the observed effect on cardiac output.
Submitted on 22/02/2016 12:00 AM GMT