Purpose: To characterize the hemodynamic and ventilatory responses to exercise in a group of patients with unexplained dyspnea, increased risk for pulmonary arterial hypertension (PAH), and an elevated mean pulmonary artery pressure (mPAP; >30 mm Hg) on exercise.
Methods: A total of 37 symptomatic patients at risk of PAH and 20 healthy controls underwent a cardiopulmonary exercise test and were assessed for quality of life (QOL). Patients had a pulmonary artery catheter in situ during the exercise test.
Results: Seventeen subjects had exercise-induced PAH (EIPAH), which we defined as mPAP ≤ 25 mm Hg at rest, and mPAP > 30 mm Hg and pulmonary artery wedge pressure <20 mm Hg on exercise. These subjects had reduced peak exercise cardiac output (72% ± 19% predicted). Further, compared with matched controls, subjects with EIPAH had reduced peak oxygen consumption (1.2 ± 0.4 vs 1.7 ± 0.5 L·min−1, P < 0.05), an elevated ventilatory equivalent for carbon dioxide (41.0 ± 7.3 vs 31.0 ± 2.9, P < 0.05) and reduced end-tidal carbon dioxide tension (32.6 ± 3.6 vs 39.4 ± 2.7 mm Hg, P < 0.05) at the anaerobic threshold. These exercise abnormalities were associated with impaired QOL (P < 0.05).
Conclusions: Elevated pulmonary artery pressure on exercise can be associated with hemodynamic and ventilatory abnormalities typical of PAH, along with impaired exercise capacity and reduced QOL.
1Advanced Lung Disease Program, Royal Perth Hospital, Perth, AUSTRALIA; 2School of Physiotherapy and Curtin Health Innovation Research Institute, Curtin University, Perth, AUSTRALIA; 3Lung Institute of Western Australia, Centre for Asthma, Allergy and Respiratory Research, University of Western Australia, Perth, AUSTRALIA; 4Advanced Heart Failure and Cardiac Transplant Service, Royal Perth Hospital, Perth, AUSTRALIA; 5Physiotherapy Department, Sir Charles Gairdner Hospital, Perth, AUSTRALIA; 6Respiratory Medicine Department, Royal Perth Hospital, Perth, AUSTRALIA; 7School of Medicine, University of Western Australia, Perth, AUSTRALIA; 8School of Medicine, University of Notre Dame, Perth, AUSTRALIA; and 9Heart and Lung Transplant Foundation of Western Australia, Perth, AUSTRALIA
Address for correspondence: Eli Gabbay, MBBS, FRACP, Advanced Lung Disease Program, Royal Perth Hospital, Level 3 Ainslie House, Murray St., Perth, Western Australia 6000; Box 2213 GPO, Perth, Western Australia 6847; E-mail: firstname.lastname@example.org.
Submitted for publication September 2010.
Accepted for publication November 2010.