Key result
Post-PEA patients exhibited abnormal pulmonary vascular reserve during exercise, characterized by a steeper mPAP-cardiac output slope compared to controls (4.7 vs 1.0 mm Hg/L/min, P<0.0001).
Why the study?
Does incremental exercise unmask abnormal pulmonary vascular and right ventricular reserve in post-pulmonary endarterectomy patients with normalized resting hemodynamics, and can sildenafil attenuate this?
Cross-Sectional (n=36)
No
Does incremental exercise unmask abnormal pulmonary vascular and right ventricular reserve in post-pulmonary endarterectomy patients with normalized resting hemodynamics, and can sildenafil attenuate this?
Despite normalized resting hemodynamics after pulmonary endarterectomy, patients continue to exhibit abnormal pulmonary vascular reserve and right ventricular function during exercise, which can be partially attenuated by sildenafil.
Answers are grounded in this paper and cite their sources.
May unmask residual pulmonary vascular dysfunction post-PEA; hypothesis-generating for sildenafil and requires prospective validation.
BACKGROUND: Patients with normalized mean pulmonary artery pressure (mPAP) after pulmonary endarterectomy (PEA) for chronic thromboembolic pulmonary hypertension (CTEPH) do not always regain normal exercise capacity. We evaluated right ventricular function, its interaction with both pulsatile and resistive afterload, and the effect of sildenafil during exercise in these patients. METHODS AND RESULTS: Fourteen healthy controls, 15 CTEPH patients, and 7 patients with normalized resting mPAP (≤25 mm Hg) post-PEA underwent cardiopulmonary exercise testing, followed by cardiac magnetic resonance imaging with simultaneous invasive mPAP measurement during incremental supine cycling exercise. Peak oxygen consumption and peak heart rate were significantly reduced in post-PEA and CTEPH patients compared to controls. The mPAP-cardiac output slope was steeper in post-PEA patients than in controls and similar to CTEPH. Relative to controls, resting right ventricular ejection fraction was reduced in CTEPH, but not in post-PEA patients. In contrast, peak exercise right ventricular ejection fraction was reduced both in post-PEA and CTEPH patients. Exercise led to reduction of pulmonary arterial compliance in all groups. Nevertheless, resting pulmonary arterial compliance values in CTEPH and post-PEA patients were even lower than those in controls at peak exercise. In post-PEA patients, sildenafil did not affect resting hemodynamics nor right ventricular function, but decreased the mPAP/cardiac output slope and increased peak exercise right ventricular ejection fraction. CONCLUSIONS: Exercise intolerance in post-PEA patients is explained by abnormal pulmonary vascular reserve and chronotropic incompetence. The mPAP/cardiac output slope and pulmonary arterial compliance are sensitive measures demonstrating abnormal resistive and pulsatile pulmonary vascular function in post-PEA patients. These abnormalities are partially attenuated with sildenafil.
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Claessen et al. (2015) conducted a cross-sectional in Chronic thromboembolic pulmonary hypertension (CTEPH) and post-pulmonary endarterectomy (PEA) (n=36). Post-pulmonary endarterectomy (PEA) status vs. Healthy controls and CTEPH patients was evaluated on mPAP-cardiac output slope during incremental supine cycling exercise (p=<0.0001). Post-PEA patients exhibited abnormal pulmonary vascular reserve during exercise, characterized by a steeper mPAP-cardiac output slope compared to controls (4.7 vs 1.0 mm Hg/L/min, P<0.0001).
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