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Reduced haemodynamic coupling and exercise are associated with vascular stiffening in pulmonary arterial hypertension
  1. Alessandro Bellofiore1,
  2. Eric Dinges2,
  3. Robert Naeije3,
  4. Hamorabi Mkrdichian4,
  5. Lauren Beussink-Nelson4,
  6. Melissa Bailey5,
  7. Michael J Cuttica6,
  8. Ranya Sweis4,
  9. James R Runo7,
  10. Jon G Keevil8,
  11. Christopher J Francois9,
  12. Sanjiv J Shah4,6,
  13. Naomi C Chesler2,5
  1. 1Department of Biomedical, Chemical and Materials Engineering, San Jose State University, San Jose, California, USA
  2. 2Department of Biomedical Engineering, University of Wisconsin-Madison, Madison, Wisconsin, USA
  3. 3Department of Cardiology, Erasme University Hospital, Brussels, Belgium
  4. 4Division of Cardiology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
  5. 5Department of Medicine, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin, USA
  6. 6Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, Illinois, USA
  7. 7Division of Pulmonary and Critical Care Medicine, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin, USA
  8. 8Department of Cardiology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin, USA
  9. 9Department of Radiology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin, USA
  1. Correspondence to Professor Naomi C Chesler, Department of Biomedical Engineering, University of Wisconsin-Madison, 2146 Engineering Centers Building, 1550 Engineering Drive, Madison WI 53706-1609, USA; naomi.chesler{at}wisc.edu

Abstract

Objective Inadequate right ventricular (RV) and pulmonary arterial (PA) functional responses to exercise are important yet poorly understood features of pulmonary arterial hypertension (PAH). This study combined invasive catheterisation with echocardiography to assess RV afterload, RV function and ventricular–vascular coupling in subjects with PAH.

Methods Twenty-six subjects with PAH were prospectively recruited to undergo right heart catheterisation and Doppler echocardiography at rest and during incremental exercise, and cardiac MRI at rest. Measurements at rest included basic haemodynamics, RV function and coupling efficiency (η). Measurements during incremental exercise included pulmonary vascular resistance (Z0), characteristic impedance (ZC, a measure of proximal PA stiffness) and proximal and distal PA compliance (CPA).

Results In patients with PAH, the proximal PAs were significantly stiffer at maximum exercise (ZC =2.31±0.38 vs 1.33±0.15 WU×m2 at rest; p=0.003) and PA compliance was decreased (CPA=0.88±0.10 vs 1.32±0.17 mL/mm Hg/m2 at rest; p=0.0002). Z0 did not change with exercise. As a result, the resistance–compliance (RC) time decreased with exercise (0.67±0.05 vs 1.00±0.07 s at rest; p<10−6). When patients were grouped according to resting coupling efficiency, those with poorer η exhibited stiffer proximal PAs at rest, a lower maximum exercise level, and more limited CPA reduction at maximum exercise.

Conclusions In PAH, exercise causes proximal and distal PA stiffening, which combined with preserved Z0 results in decreased RC time with exercise. Stiff PAs at rest may also contribute to poor haemodynamic coupling, reflecting reduced pulmonary vascular reserve that contributes to limit the maximum exercise level tolerated.

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