Tom Verbelen1, Piet Claus2, Daniel Burkhoff3, Ronald B Driesen4, Chandan Kadur Nagaraju4, Erik Verbeken5, Karin Sipido4, Marion Delcroix6, Filip Rega7, Bart Meyns7. 1. Department of Cardiac Surgery, University Hospitals Leuven, Leuven, Belgium; Division of Experimental Cardiac Surgery, Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium. Electronic address: tom.verbelen@kuleuven.be. 2. Division of Cardiovascular Imaging and Dynamics, Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium. 3. Division of Cardiology, Columbia University College of Physicians and Surgeons, New York, New York, USA. 4. Division of Experimental Cardiology, Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium. 5. Division of Translational Cell & Tissue Research, Department of Imaging & Pathology, University of Leuven, Leuven, Belgium. 6. Respiratory Division, University Hospitals Leuven Leuven, Belgium; Department of Clinical and Experimental Medicine, University of Leuven, Leuven, Belgium. 7. Department of Cardiac Surgery, University Hospitals Leuven, Leuven, Belgium; Division of Experimental Cardiac Surgery, Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium.
Abstract
BACKGROUND: Mechanical right ventricular (RV) support in pulmonary arterial hypertension patients has been feared to cause pulmonary hemorrhage and to be detrimental for the after-load-sensitive RV. Continuous low-flow pumps offer promise but remain insufficiently tested. METHODS: The pulmonary artery was banded in 20 sheep in this study. Eight weeks later, a Synergy micro-pump (HeartWare International, Framingham MA) was inserted in 10 animals, driving blood from the right atrium to the pulmonary artery. After magnetic resonance imaging, hemodynamics and RV pressure-volume loop data were recorded. Eight weeks later, RV function was assessed in the same way, followed by histologic analysis of the ventricular tissue. RESULTS: During the 8 weeks of support, RV volumes and central venous pressure decreased significantly, whereas RV contractility increased. Pulmonary artery pressure increased modestly, particularly its diastolic component. RV contribution to total right-sided cardiac output increased from 12 ± 12% to 41 ± 9% (p < 1 × 10-4). After pump inactivation, and compared with 8 weeks earlier, RV volumes had significantly decreased, tricuspid valve regurgitation had almost disappeared, and RV contractility had significantly increased, resulting in significantly increased RV forward power (0.25 ± 0.05 vs 0.16 ± 0.06 W, p = 0.014). Fulton index and RV myocyte size were significantly smaller, and without changes in fibrosis, when compared with controls. CONCLUSIONS: Prolonged continuous low-flow RV mechanical support significantly unloads the chronic pressure-overloaded RV and improves cardiac output. After 8 weeks, RV hemodynamic recovery and reverse remodeling begin to occur, without increased fibrosis.
BACKGROUND: Mechanical right ventricular (RV) support in pulmonary arterial hypertensionpatients has been feared to cause pulmonary hemorrhage and to be detrimental for the after-load-sensitive RV. Continuous low-flow pumps offer promise but remain insufficiently tested. METHODS: The pulmonary artery was banded in 20 sheep in this study. Eight weeks later, a Synergy micro-pump (HeartWare International, Framingham MA) was inserted in 10 animals, driving blood from the right atrium to the pulmonary artery. After magnetic resonance imaging, hemodynamics and RV pressure-volume loop data were recorded. Eight weeks later, RV function was assessed in the same way, followed by histologic analysis of the ventricular tissue. RESULTS: During the 8 weeks of support, RV volumes and central venous pressure decreased significantly, whereas RV contractility increased. Pulmonary artery pressure increased modestly, particularly its diastolic component. RV contribution to total right-sided cardiac output increased from 12 ± 12% to 41 ± 9% (p < 1 × 10-4). After pump inactivation, and compared with 8 weeks earlier, RV volumes had significantly decreased, tricuspid valve regurgitation had almost disappeared, and RV contractility had significantly increased, resulting in significantly increased RV forward power (0.25 ± 0.05 vs 0.16 ± 0.06 W, p = 0.014). Fulton index and RV myocyte size were significantly smaller, and without changes in fibrosis, when compared with controls. CONCLUSIONS: Prolonged continuous low-flow RV mechanical support significantly unloads the chronic pressure-overloaded RV and improves cardiac output. After 8 weeks, RV hemodynamic recovery and reverse remodeling begin to occur, without increased fibrosis.
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