Author + information
- Received July 31, 2018
- Revision received November 16, 2018
- Accepted December 20, 2018
- Published online November 4, 2019.
- Khodr Tello, MDa,∗ (, )
- Antonia Dalmera,
- Rebecca Vanderpool, PhDb,
- Hossein A. Ghofrani, MDa,c,d,
- Robert Naeije, MD, PhDe,
- Fritz Roller, MDf,
- Werner Seeger, MDa,
- Jochen Wilhelm, PhDa,
- Henning Gall, MD, PhDa and
- Manuel J. Richter, MDa
- aDepartment of Internal Medicine, Justus-Liebig-University Giessen, Universities of Giessen and Marburg Lung Center, Giessen, Germany
- bDivision of Translational and Regenerative Medicine, University of Arizona, Tucson, Arizona
- cDepartment of Pneumology, Kerckhoff Heart, Rheuma, and Thoracic Center, Bad Nauheim, Germany
- dDepartment of Medicine, Imperial College London, London, United Kingdom
- eDepartment of Cardiology, Erasme University Hospital, Brussels, Belgium
- fDepartment of Radiology, Justus-Liebig-University Giessen, Universities of Giessen and Marburg Lung Center, Giessen, Germany
- ↵∗Address for correspondence:
Dr. Khodr Tello, Department of Internal Medicine, Justus-Liebig-University Giessen, Klinikstrasse 32, 35392 Giessen, Germany.
Objectives This study sought to compare cardiac magnetic resonance (CMR) imaging-derived right ventricular (RV) strain and invasively measured pressure-volume loop-derived RV contractility, stiffness, and afterload and RV-arterial coupling in pulmonary hypertension (PH).
Background In chronic RV pressure overload, RV-arterial uncoupling is considered the driving cause of RV maladaptation and eventual RV failure. The pathophysiological and clinical value of CMR-derived RV strain relative to that of invasive pressure-volume loop-derived measurements in PH remains incompletely understood.
Methods In 38 patients with PH, global RV CMR strain was measured within 24 h of diagnostic right heart catheterization and conductance (pressure-volume) catheterization. Associations were evaluated by correlation, multivariate logistic binary regression, and receiver operating characteristic analyses.
Results Long-axis RV longitudinal and radial strain and short-axis RV radial and circumferential strain were −18.0 ± 7.0%, 28.9% [interquartile range (IQR): 17.4% to 46.6%]; 15.6 ± 6.2%; and −9.8 ± 3.5%, respectively. RV-arterial coupling (end-systolic [Eds]/arterial elastance [Ea]) was 0.76 (IQR: 0.47 to 1.07). Peak RV strain correlated with Ees/Ea, afterload (Ea), RV diastolic dysfunction (Tau), and stiffness (end-diastolic elastance [Eed]) but not with contractility (Ees). In multivariate analysis, long-axis RV radial strain was associated with RV-arterial uncoupling (Ees/Ea: <0.805; odds ratio [OR]: 5.50; 95% confidence interval [CI]: 1.50 to 20.18), whereas long-axis RV longitudinal strain was associated with increased RV diastolic stiffness (Eed: ≥0.124 mm Hg/ml; OR: 1.23; 95% CI: 1.10 to 1.51). The long-axis RV longitudinal strain-to-RV end-diastolic volume/body surface area ratio strongly predicted RV diastolic stiffness (area under receiver operating characteristic curve: 0.908).
Conclusions In chronic RV overload, CMR-determined RV strain is associated with RV-arterial uncoupling and RV end-diastolic stiffness and represents a promising noninvasive alternative to current invasive methods for assessment of RV-arterial coupling and end-diastolic stiffness in patients with PH. (Right Ventricular Haemodynamic Evaluation and Response to Treatment [Rightheart I]; NCT03403868)
- lusitropic function
- pulmonary hypertension
- right ventricular contractile function
- speckle tracking
Supported by the Excellence Cluster Cardio-Pulmonary System and Collaborative Research Center 1213 Pulmonary Hypertension and Cor Pulmonale grant SFB1213/1, and German Research Foundation project B08. Dr. Tello has received speaker fees from Actelion and Bayer. Dr. Ghofrani is a consultant for Bayer, Actelion, Pfizer, Merck, GlaxoSmithKline, and Novartis; is a compensated advisory board member for Bayer, Pfizer, GlaxoSmithKline, Actelion, and Takeda; has received lecture fees from Bayer HealthCare, GlaxoSmithKline, Actelion, and Encysive/Pfizer; and has received grants from Bayer HealthCare, Aires, Encysive/Pfizer, Novartis, the German Research Foundation, Excellence Cluster Cardiopulmonary Research, and the German Ministry for Education and Research. Dr. Naeije has received research support from, is a consultant for, and sits on scientific advisory boards of AOPOrphan Pharmaceuticals, Actelion, Bayer, Reata, Lung Biotechnology Corporation, and United Therapeutics. Dr. Seeger is a compensated speaker and consultant for Pfizer, Bayer Pharma AG, United Therapeutics, and Liquidia. Dr. Gall has received fees from Actelion, AstraZeneca, Bayer, Bristol-Myers Squibb, GlaxoSmithKline, Janssen-Cilag, Lilly, Merck Sharpe & Dohme, Novartis, Optimal Medical Therapies, Pfizer, and United Therapeutics. Dr. Richter has received support from United Therapeutics and Bayer; has received speaker fees from Actelion, Mundipharma, Roche, and Optimal Medical Therapies; and has received consultant fees from Bayer. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received July 31, 2018.
- Revision received November 16, 2018.
- Accepted December 20, 2018.
- 2019 American College of Cardiology Foundation
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