Daniel McLennan1, Michal Schäfer2, Alex J Barker3,4, Max B Mitchell5, Richard J Ing6, Lorna P Browne3, D Dunbar Ivy1, Gareth J Morgan1. 1. Division of Cardiology, Department of Pediatrics, Heart Institute, Children's Hospital Colorado, University of Colorado Denver | Anschutz Medical Campus, 13123 E 16th Ave, Aurora, CO, 80045-2560, USA. 2. Division of Cardiology, Department of Pediatrics, Heart Institute, Children's Hospital Colorado, University of Colorado Denver | Anschutz Medical Campus, 13123 E 16th Ave, Aurora, CO, 80045-2560, USA. michal.schafer@cuanschutz.edu. 3. Department of Radiology, Children's Hospital Colorado, University of Colorado Denver | Anschutz Medical Campus, Aurora, CO, USA. 4. Department of Bioengineering, University of Colorado Denver | Anschutz Medical Campus, Aurora, CO, USA. 5. Department of Pediatric Heart Surgery, Children's Hospital Colorado, University of Colorado Denver | Anschutz Medical Campus, Aurora, CO, USA. 6. Division of Pediatric Cardiac Anesthesiology, Department of Anesthesiology, Children's Hospital Colorado, University of Colorado Denver | Anschutz Medical Campus, Aurora, CO, USA.
Abstract
OBJECTIVES: Flow through the proximal pulmonary arteries (PAs) of patients with repaired Tetralogy of Fallot (TOF) is known to be highly disordered and associated with significant regurgitation. The purpose of this study was to evaluate 4D-Flow MRI-derived viscous energy loss [Formula: see text])-as a result of non-efficient flow propagation, and relate this parameter to standard right ventricular (RV) size and function markers in patients with repaired TOF. METHODS: Thirty-five patients with TOF and 14 controls underwent comprehensive 4D-Flow MRI evaluation for qualitative flow analysis and to calculate [Formula: see text] in the main and right pulmonary arteries. Sampled [Formula: see text] indices were correlated with the MRI-derived RV size and functional indices. RESULTS: All patients with TOF exhibited abnormal, supra-physiologic helical/vortical formations in the PAs. Patients with TOF had significantly increased peak systolic [Formula: see text] (8.0 vs 0.5 mW, p < 0.001), time-averaged [Formula: see text] (2.5 vs. 0.2 mW, p < 0.001), and peak systolic [Formula: see text] indexed to stroke volume (0.082 vs. 0.012 mW/mL, p < 0.001). [Formula: see text] indexed to stroke volume correlated with the RV end-diastolic volume (R = 0.68, p < 0.001), end-systolic volume (R = 0.62, p < 0.001), ejection fraction (R = -0.45, p = 0.002), and cardiac index (R = 0.45, p = 0.002). The mean estimated energy loss due to [Formula: see text] with regard to input RV mechanical power was 4.7%. CONCLUSION: This study demonstrates that patients with repaired TOF have highly abnormal flow conduction through the PAs which result into extensive viscous energy loss. This significant flow-mediated energy loss is associated with the RV volume and function, and might represent considerable loss of mechanical power generated by each cardiac cycle. Future studies are required to assess whether the abnormal flow conduction adds to the RV afterload and remodeling. KEY POINTS: • Abnormal flow patterns through proximal pulmonary arteries in patients with TOF are associated with excessive viscous energy loss. • Inefficient flow conduction is associated with the RV dilation and reduced function and might contribute to the RV adaptive remodeling.
OBJECTIVES: Flow through the proximal pulmonary arteries (PAs) of patients with repaired Tetralogy of Fallot (TOF) is known to be highly disordered and associated with significant regurgitation. The purpose of this study was to evaluate 4D-Flow MRI-derived viscous energy loss [Formula: see text])-as a result of non-efficient flow propagation, and relate this parameter to standard right ventricular (RV) size and function markers in patients with repaired TOF. METHODS: Thirty-five patients with TOF and 14 controls underwent comprehensive 4D-Flow MRI evaluation for qualitative flow analysis and to calculate [Formula: see text] in the main and right pulmonary arteries. Sampled [Formula: see text] indices were correlated with the MRI-derived RV size and functional indices. RESULTS: All patients with TOF exhibited abnormal, supra-physiologic helical/vortical formations in the PAs. Patients with TOF had significantly increased peak systolic [Formula: see text] (8.0 vs 0.5 mW, p < 0.001), time-averaged [Formula: see text] (2.5 vs. 0.2 mW, p < 0.001), and peak systolic [Formula: see text] indexed to stroke volume (0.082 vs. 0.012 mW/mL, p < 0.001). [Formula: see text] indexed to stroke volume correlated with the RV end-diastolic volume (R = 0.68, p < 0.001), end-systolic volume (R = 0.62, p < 0.001), ejection fraction (R = -0.45, p = 0.002), and cardiac index (R = 0.45, p = 0.002). The mean estimated energy loss due to [Formula: see text] with regard to input RV mechanical power was 4.7%. CONCLUSION: This study demonstrates that patients with repaired TOF have highly abnormal flow conduction through the PAs which result into extensive viscous energy loss. This significant flow-mediated energy loss is associated with the RV volume and function, and might represent considerable loss of mechanical power generated by each cardiac cycle. Future studies are required to assess whether the abnormal flow conduction adds to the RV afterload and remodeling. KEY POINTS: • Abnormal flow patterns through proximal pulmonary arteries in patients with TOF are associated with excessive viscous energy loss. • Inefficient flow conduction is associated with the RV dilation and reduced function and might contribute to the RV adaptive remodeling.
Authors: Alex J Barker; Michael Markl; Jonas Bürk; Ramona Lorenz; Jelena Bock; Simon Bauer; Jeanette Schulz-Menger; Florian von Knobelsdorff-Brenkenhoff Journal: Circ Cardiovasc Imaging Date: 2012-06-22 Impact factor: 7.792
Authors: Richard M Friesen; Michal Schäfer; D Dunbar Ivy; Steven H Abman; Kurt Stenmark; Lorna P Browne; Alex J Barker; Kendall S Hunter; Uyen Truong Journal: Eur Heart J Cardiovasc Imaging Date: 2019-02-01 Impact factor: 6.875
Authors: Vivian P Kamphuis; Mohammed S M Elbaz; Pieter J van den Boogaard; Lucia J M Kroft; Rob J van der Geest; Albert de Roos; Willem A Helbing; Nico A Blom; Jos J M Westenberg; Arno A W Roest Journal: Eur Heart J Cardiovasc Imaging Date: 2019-03-01 Impact factor: 6.875
Authors: Michal Schäfer; Lorna P Browne; Gareth J Morgan; Alex J Barker; Brian Fonseca; D Dunbar Ivy; Max B Mitchell Journal: J Thorac Cardiovasc Surg Date: 2018-09-21 Impact factor: 5.209
Authors: Riti Mahadevia; Alex J Barker; Susanne Schnell; Pegah Entezari; Preeti Kansal; Paul W M Fedak; S Chris Malaisrie; Patrick McCarthy; Jeremy Collins; James Carr; Michael Markl Journal: Circulation Date: 2013-12-17 Impact factor: 29.690
Authors: Jonas Bürk; Philipp Blanke; Zoran Stankovic; Alex Barker; Maximilian Russe; Julia Geiger; Alex Frydrychowicz; Mathias Langer; Michael Markl Journal: J Cardiovasc Magn Reson Date: 2012-12-13 Impact factor: 5.364
Authors: Michal Schäfer; Alex J Barker; Vitaly Kheyfets; Kurt R Stenmark; James Crapo; Michael E Yeager; Uyen Truong; J Kern Buckner; Brett E Fenster; Kendall S Hunter Journal: J Am Heart Assoc Date: 2017-12-20 Impact factor: 5.501
Authors: David G Guzzardi; Alex J Barker; Pim van Ooij; S Chris Malaisrie; Jyothy J Puthumana; Darrell D Belke; Holly E M Mewhort; Daniyil A Svystonyuk; Sean Kang; Subodh Verma; Jeremy Collins; James Carr; Robert O Bonow; Michael Markl; James D Thomas; Patrick M McCarthy; Paul W M Fedak Journal: J Am Coll Cardiol Date: 2015-08-25 Impact factor: 24.094
Authors: Petter Dyverfeldt; Malenka Bissell; Alex J Barker; Ann F Bolger; Carl-Johan Carlhäll; Tino Ebbers; Christopher J Francios; Alex Frydrychowicz; Julia Geiger; Daniel Giese; Michael D Hope; Philip J Kilner; Sebastian Kozerke; Saul Myerson; Stefan Neubauer; Oliver Wieben; Michael Markl Journal: J Cardiovasc Magn Reson Date: 2015-08-10 Impact factor: 5.364