Key result
Exercise raises mean pulmonary arterial pressure by ~18 mmHg despite resting improvements on combination therapy.
Why the study?
PAH-specific combination therapy improves resting pulmonary haemodynamics, but exertional dyspnoea remains.
Does cardiopulmonary exercise testing reveal persistently impaired pulmonary haemodynamic response to exercise in PAH patients treated with combination therapy despite improved resting haemodynamics?
Observational (n=32)
No
Does cardiopulmonary exercise testing reveal persistently impaired pulmonary haemodynamic response to exercise in PAH patients treated with combination therapy despite improved resting haemodynamics?
Despite remarkable resting haemodynamic improvement on combination therapy, most PAH patients retain a steep mPAP/CO slope during exercise, which correlates with ventilatory inefficiency and hypoxaemia.
Normal resting pressures may mask residual vascular dysfunction in treated PAH; leaves open whether targeting exercise hemod.
Pulmonary arterial hypertension (PAH)-specific combination therapy improves pulmonary haemodynamics at rest in patients with PAH; nevertheless, exertional dyspnoea remains. We investigated pulmonary haemodynamic response to exercise, and the relationship to ventilatory efficiency and hypoxaemia in patients with PAH treated with combination therapy. 32 clinically stable patients with PAH undergoing combination therapy underwent cardiopulmonary exercise testing with right heart catheterisation. Haemodynamic impairment was moderate to severe before treatment. However, after treatment it was significantly improved, and the mean pulmonary arterial pressure (mPAP) at rest was <25 mmHg in 13 patients. The mPAP increased significantly from 27.9±10.7 to 45.9±16.7 mmHg (p<0.01) during exercise. The cardiac index increased inadequately, and the total pulmonary resistance (TPR) increased significantly from 5.74±3.42 to 6.58±3.82 Wood units (p<0.01). The mPAP/cardiac output (CO) slope was steep (10.0±6.7 mmHg·min·L −1 ). It significantly correlated with both the minute ventilation/carbon dioxide output slope (r=0.51, p<0.01) and peripheral arterial oxygen saturation/workload slope (r=−0.41, p=0.02). In addition, the mPAP/CO slope correlated significantly with mPAP at rest (r=0.73, p<0.01) and TPR at rest (r=0.64, p<0.01). Even after pulmonary haemodynamics at rest was significantly improved in PAH patients with PAH-specific combination therapy, the mPAP/CO slope was steep and the steep mPAP/CO slope related to decreased ventilatory efficiency and the severity of hypoxaemia. The mPAP/CO slope was steeper in patients with higher mPAP and TPR at rest.
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Nishizaki et al. (2020) conducted an observational in Pulmonary arterial hypertension (n=32). Exercise during cardiopulmonary exercise testing vs. Resting baseline was evaluated on Mean pulmonary arterial pressure (mPAP) (p=<0.01). Even after resting pulmonary haemodynamics improved with combination therapy, exercise significantly increased mean pulmonary arterial pressure from 27.9 to 45.9 mmHg (p<0.01), indicating persistently impaired haemodynamic response.
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