Farhad Waziri1, Steffen Ringgaard2, Søren Mellemkjær3, Nikolaj Bøgh4, Won Yong Kim5, Tor Skibsted Clemmensen6, Vibeke Elisabeth Hjortdal7, Sten Lyager Nielsen8, Steen Hvitfeldt Poulsen6. 1. Department of Cardiology, Aarhus University Hospital, Denmark; Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Denmark; Department of Clinical Medicine, Aarhus University, Denmark; Department of Internal Medicine, Regional Hospital of Randers, Denmark. Electronic address: farhad@clin.au.dk. 2. Department of Clinical Medicine, Aarhus University, Denmark; Department of MR Research Centre, Aarhus University Hospital, Denmark. 3. Department of Cardiology, Aarhus University Hospital, Denmark. 4. Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Denmark; Department of Clinical Medicine, Aarhus University, Denmark; Department of MR Research Centre, Aarhus University Hospital, Denmark. 5. Department of Cardiology, Aarhus University Hospital, Denmark; Department of Clinical Medicine, Aarhus University, Denmark; Department of MR Research Centre, Aarhus University Hospital, Denmark. 6. Department of Cardiology, Aarhus University Hospital, Denmark; Department of Clinical Medicine, Aarhus University, Denmark. 7. Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Denmark; Department of Clinical Medicine, Aarhus University, Denmark. 8. Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Denmark.
Abstract
BACKGROUND: Right ventricular (RV) afterload in patients with chronic thromboembolic pulmonary hypertension (CTEPH) is associated with reduced myocardial contractility and ventriculoarterial coupling. The impact of increased afterload on RV myocardial deformation was assessed by comparing the characteristics of CTEPH patients to healthy controls at baseline, and by comparing characteristics of CTEPH patients before and 12 months after pulmonary endarterectomy (PEA). METHODS: Cardiac deformation and function of CTEPH patients (n = 20) and healthy controls (n = 20) were assessed by cardiac magnetic resonance (CMR). CTEPH patients were also examined with right heart catheterization before and 12 months after PEA. RESULTS: PEA resulted in significant improvement of invasive hemodynamics and normalization of RV hypertrophy and right atrial, RV and left ventricular dimensions and volumes. RV ejection fraction improved from 30 ± 13% at baseline to 44 ± 10% at 12 months (p < 0.0001) but remained decreased compared with control subjects (54 ± 4%, p < 0.05). RV global circumferential strain (GCS) normalized 12 months after PEA, but RV global longitudinal strain (GLS) remained significantly lower in CTEPH patients than controls (baseline -12.9 ± 3.3% vs. -16.5 ± 3.6% at 12 months p < 0.01, vs. controls -19.3 ± 3.2%, p < 0.05). RV mass changes were significantly correlated with RV-ejection fraction, RV-GLS, and RV-GCS. RV-pulmonary arterial coupling with the volume method improved at 12 months (0.49 ± 0.30 vs. 0.84 ± 0.31, p < 0.0005), but remained significantly reduced compared with healthy controls (1.19 ± 0.20, p < 0.0005). CONCLUSION: RV global longitudinal and circumferential myocardial three-dimensional strain by CMR improved significantly in CTEPH patients 12 months after PEA. Improvements in myocardial deformation were associated with regression of RV hypertrophy and decrease in pulmonary artery pressure.
BACKGROUND: Right ventricular (RV) afterload in patients with chronic thromboembolic pulmonary hypertension (CTEPH) is associated with reduced myocardial contractility and ventriculoarterial coupling. The impact of increased afterload on RV myocardial deformation was assessed by comparing the characteristics of CTEPHpatients to healthy controls at baseline, and by comparing characteristics of CTEPHpatients before and 12 months after pulmonary endarterectomy (PEA). METHODS:Cardiac deformation and function of CTEPHpatients (n = 20) and healthy controls (n = 20) were assessed by cardiac magnetic resonance (CMR). CTEPHpatients were also examined with right heart catheterization before and 12 months after PEA. RESULTS: PEA resulted in significant improvement of invasive hemodynamics and normalization of RV hypertrophy and right atrial, RV and left ventricular dimensions and volumes. RV ejection fraction improved from 30 ± 13% at baseline to 44 ± 10% at 12 months (p < 0.0001) but remained decreased compared with control subjects (54 ± 4%, p < 0.05). RV global circumferential strain (GCS) normalized 12 months after PEA, but RV global longitudinal strain (GLS) remained significantly lower in CTEPHpatients than controls (baseline -12.9 ± 3.3% vs. -16.5 ± 3.6% at 12 months p < 0.01, vs. controls -19.3 ± 3.2%, p < 0.05). RV mass changes were significantly correlated with RV-ejection fraction, RV-GLS, and RV-GCS. RV-pulmonary arterial coupling with the volume method improved at 12 months (0.49 ± 0.30 vs. 0.84 ± 0.31, p < 0.0005), but remained significantly reduced compared with healthy controls (1.19 ± 0.20, p < 0.0005). CONCLUSION: RV global longitudinal and circumferential myocardial three-dimensional strain by CMR improved significantly in CTEPHpatients 12 months after PEA. Improvements in myocardial deformation were associated with regression of RV hypertrophy and decrease in pulmonary artery pressure.
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