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editorial

. 2015 Mar 23;4(3):e001895. doi: 10.1161/JAHA.115.001895

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© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 1. — Model pressure‐volume loops derived from Claessen et al⁵ at rest (blue box) and exercise (red dashed box) for normal control patients (A), post‐PEA patients (B), CTEPH patients (C), and post‐PEA patients after sildenafil (D). Green lines denote end‐systolic elastance (Ees, RV contractility) for each state (solid=rest; dashed=exercise). Ratio of Ees/Ea is assumed for each group based on prior studies.^17–20 Increasing slope of Ees denotes increasing contractility in this model. Note the control patients’ ability to augment Ees with exercise, which is largely lost in the post‐PEA and CTEPH patients. Sildenafil improves the ability of post‐PEA patients to augment their contractility with exercise, and reduces overall RV load. CTEPH indicates chronic thromboembolic pulmonary hypertension; PEA, pulmonary endarterectomy; RV, right ventricle.