Michal Schäfer1, Vitaly O Kheyfets2, Alex J Barker3, Kurt Stenmark4, Kendall S Hunter2, P Mason McClatchey5, J Kern Buckner6, T Brett Reece7, Omid Jazaeri8, Brett E Fenster6. 1. Department of Cardiology, National Jewish Health, Denver, Colo; Department of Bioengineering, University of Colorado Denver | Anschutz Medical Campus, Aurora, Colo. Electronic address: michal.schafer@ucdenver.edu. 2. Department of Cardiology, National Jewish Health, Denver, Colo; Department of Bioengineering, University of Colorado Denver | Anschutz Medical Campus, Aurora, Colo. 3. Department of Radiology, Feinberg School of Medicine, Northwestern University, Chicago, Ill. 4. Cardiovascular Pulmonary Research Laboratories, Department of Medicine and Pediatrics, University of Colorado Denver | Anschutz Medical Campus, Aurora, Colo. 5. Department of Bioengineering, University of Colorado Denver | Anschutz Medical Campus, Aurora, Colo. 6. Department of Cardiology, National Jewish Health, Denver, Colo. 7. Division of Cardiothoracic Surgery, Department of Surgery, University of Colorado Denver | Anschutz Medical Campus, Aurora, Colo. 8. Division of Vascular and Endovascular Therapy, Department of Surgery, University of Colorado Denver | Anschutz Medical Campus, Aurora, Colo.
Abstract
OBJECTIVE: Central aortic stiffness and chronic obstructive pulmonary disease (COPD) are associated with increased incidence of devastating aortopathies. However, the exact mechanism leading to elevated aortic stiffness in patients with COPD is unknown. The purpose of this study was to quantify flow and shear hemodynamic indices, known markers of vascular remodeling, in the thoracic aorta of patients with mild to moderate COPD (n = 16) and to compare these results with an age-matched control group (n = 10). METHODS: Four-dimensional flow magnetic resonance imaging has been applied to measure hemodynamic wall shear stress (WSS) at four specific planes along the ascending aorta, aortic arch, and proximal descending aorta for all subjects. Peak systolic WSS and time-averaged WSS, which respectively reflect magnitude and temporal shear variability, were calculated at standardized planes. Aortic deformation was measured by means of relative area change (RAC) at the midlevel of the ascending and descending aorta. RESULTS: Compared with controls, patients with COPD had significantly reduced RAC in the mid ascending aorta (9% vs 18%; P < .0001) and descending aorta (15% vs 19%; P = .0206). Peak systolic WSS in COPD patients was significantly reduced in all considered planes, with the most dramatic difference occurring in the descending aorta (0.46 vs 0.86 N/m2; P < .0001). Peak systolic WSS and time-averaged WSS were both significantly correlated with aortic RAC at each evaluated plane. CONCLUSIONS: Reduced flow shear metrics assessed at specific aortic regions correlated with RAC, a marker of aortic stiffness. Reduced hemodynamic WSS may then contribute to central aortic stiffening and perpetuate the risk for development of severe aortopathy.
OBJECTIVE:Central aortic stiffness and chronic obstructive pulmonary disease (COPD) are associated with increased incidence of devastating aortopathies. However, the exact mechanism leading to elevated aortic stiffness in patients with COPD is unknown. The purpose of this study was to quantify flow and shear hemodynamic indices, known markers of vascular remodeling, in the thoracic aorta of patients with mild to moderate COPD (n = 16) and to compare these results with an age-matched control group (n = 10). METHODS: Four-dimensional flow magnetic resonance imaging has been applied to measure hemodynamic wall shear stress (WSS) at four specific planes along the ascending aorta, aortic arch, and proximal descending aorta for all subjects. Peak systolic WSS and time-averaged WSS, which respectively reflect magnitude and temporal shear variability, were calculated at standardized planes. Aortic deformation was measured by means of relative area change (RAC) at the midlevel of the ascending and descending aorta. RESULTS: Compared with controls, patients with COPD had significantly reduced RAC in the mid ascending aorta (9% vs 18%; P < .0001) and descending aorta (15% vs 19%; P = .0206). Peak systolic WSS in COPDpatients was significantly reduced in all considered planes, with the most dramatic difference occurring in the descending aorta (0.46 vs 0.86 N/m2; P < .0001). Peak systolic WSS and time-averaged WSS were both significantly correlated with aortic RAC at each evaluated plane. CONCLUSIONS: Reduced flow shear metrics assessed at specific aortic regions correlated with RAC, a marker of aortic stiffness. Reduced hemodynamic WSS may then contribute to central aortic stiffening and perpetuate the risk for development of severe aortopathy.