Author + information
- Received March 9, 2018
- Revision received July 20, 2018
- Accepted July 23, 2018
- Published online September 12, 2018.
- Mathias Claeys, MDa,b,∗ (, )@ClaeysMathias,
- Guido Claessen, MD, PhDa,b,
- Andre La Gerche, MD, PhDa,c,
- Thibault Petit, MDa,b,
- Catharina Belge, MD, PhDd,e,
- Bart Meyns, MD, PhDa,f,
- Jan Bogaert, MD, PhDg,h,
- Rik Willems, MD, PhDa,b,
- Piet Claus, MSc, PhDa and
- Marion Delcroix, MD, PhDd,e
- aDepartment of Cardiovascular Sciences, Katholieke Universiteit (KU) Leuven, Leuven, Belgium
- bDepartment of Cardiology, University Hospitals Leuven, Leuven, Belgium
- cBaker IDI Heart and Diabetes Institute, Melbourne, Australia
- dDepartment of Pneumology, University Hospitals Leuven, Leuven, Belgium
- eDivision of Pneumology, Department of Chronic Diseases, Metabolism and Aging, Katholieke Universiteit (KU) Leuven, Leuven, Belgium
- fDepartment of Cardiac Surgery, University Hospitals Leuven, Leuven, Belgium
- gDepartment of Radiology, University Hospitals Leuven, Leuven, Belgium
- hDepartment of Imaging and Pathology, Katholieke Universiteit (KU) Leuven, Leuven, Belgium
- ↵∗Address for correspondence:
Dr. Mathias Claeys, Department of Cardiovascular Medicine, University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium.
Objectives This study was a comprehensive evaluation of cardiopulmonary function in patients with chronic thromboembolic (pulmonary vascular) disease (CTED) during exercise.
Background Exertional dyspnea is frequent following pulmonary embolism, but only a minority of patients eventually develops chronic thromboembolic pulmonary hypertension (CTEPH). Better understanding of the factors that limit exercise capacity in patients with persistent pulmonary artery obstruction could help to further define the entity of CTED.
Methods Fifty-two subjects (13 healthy control subjects, 14 CTED patients, and 25 CTEPH patients) underwent cardiopulmonary exercise testing and exercise cardiac magnetic resonance with simultaneous invasive pressure registration. Pulmonary vascular function and right ventricular contractile reserve were assessed through combined invasive pressure measurements and magnetic resonance imaging volume measures.
Results Exercise capacity was reduced by 29% and 57% in patients with CTED and CTEPH respectively, compared with control subjects. Both CTED (3.48 [interquartile range: 2.24 to 4.36] mm Hg × l−1 × min−1) and CTEPH patients (8.85 [interquartile range: 7.18 to 10.4] mm Hg × l−1 × min−1) had abnormal total pulmonary vascular resistance. Right ventricular contractile reserve was reduced in CTED patients compared with control subjects (2.23 ± 0.55 vs. 3.72 ± 0.94), but was still higher than that in CTEPH patients (1.34 ± 0.24; p < 0.001). As opposed to patients with CTEPH in whom right ventricular ejection fraction declined with exercise, right ventricular ejection fraction still increased in patients with CTED, albeit to a lesser extent than in healthy control subjects (interaction p < 0.001), which illustrated the distinct patterns of ventricular−arterial coupling.
Conclusions CTED represents an intermediate clinical phenotype. Exercise imaging unmasks cardiovascular dysfunction not evident at rest and identifies hemodynamically significant disease that results from reduced contractile reserve or increased vascular load.
- cardiac magnetic resonance imaging
- chronic thromboembolic pulmonary hypertension
- pulmonary hypertension
- right ventricle
This study was funded by a grant (Project G.0465.10N) from the Fund for Scientific Research Flanders (FWO), Brussels, Belgium.
Dr. La Gerche has received grants from the Fund for Scientific Research Flanders (FWO) and from the National Health and Medical Research Council (NHMRC) of Australia. Dr. Belge has received speaker and consultancy fees from Actelion and GlaxoSmithKline. Dr. Willems has received research funding from Medtronic Belgium and is supported as a postdoctoral clinical researcher by the Fund for Scientific Research Flanders (FWO). Dr. Delcroix has received fees as a speaker, investigator, consultant, or steering committee member for Actelion, Bayer, Bellarophon, Eli Lilly, GlaxoSmithKline, Merck Sharp & Dohme, Pfizer, and Reata; and has received a research grant from Actelion. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received March 9, 2018.
- Revision received July 20, 2018.
- Accepted July 23, 2018.
- 2018 American College of Cardiology Foundation
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