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Stroke volume increase to exercise in COPD is limited by increased pulmonary artery pressure
  1. Sebastiaan Holverda (bholverda{at}vumc.nl)
  1. VU University Medical Center, Netherlands
    1. Heleen Rietema (h.rietema{at}vumc.nl)
    1. VU University Medical Center, Netherlands
      1. Nico Westerhof (n.westerhof{at}vumc.nl)
      1. VU University Medical Center, Netherlands
        1. J Tim Marcus (jt.marcus{at}vumc.nl)
        1. VU University Medical Center, Netherlands
          1. C Tji-Joong Gan (ct.gan{at}vumc.nl)
          1. VU University Medical Center, Netherlands
            1. Pieter E Postmus (pe.postmus{at}vumc.nl)
            1. VU University Medical Center, Netherlands
              1. Anton Vonk-Noordegraaf (a.vonk{at}vum.nl)
              1. VU University Medical Center, Netherlands

                Abstract

                Aim This study was designed to investigate the mechanisms by which the right ventricle is able to increase stroke volume (SV) during exercise in COPD. A second aim was to determine whether resting pulmonary artery pressure (Ppa) is predictive of exercise SV.

                Methods 16 COPD patients (GOLD stages II-IV) underwent right heart catheterization at rest and during exercise. In this group and 8 age-matched controls resting and exercise right ventricular SV, end-diastolic volume (RVEDV) and end-systolic volume (RVESV) were assessed by MRI. The exercise protocol during both measurements consisted of 3 minutes of cycling in supine position at 40% of maximal workload.

                Results In all patients mPpa increased significantly in response to exercise (21±8 versus 33±11 mmHg, p < 0.01), whereas pulmonary vascular resistance did not change. In the patient group, RVEDV (129±42 versus 135±42 mL, p < 0.05) and SV (63±13 versus 69±14 mL, p < 0.05) increased significantly from rest to exercise, but RVESV and RV ejection fraction remained unaltered. In contrast, in healthy controls SV is augmented (81±22 versus 101±28 mL, p < 0.05) by both increased RVEDV (123±33 versus 134±134 mL, p < 0.05) and reduced RVESV (37±9 versus 27±10 mL, p < 0.05). Resting mPpa was related to SV during exercise (r = -0.59, p < 0.02).

                Conclusion As a consequence of unaltered pulmonary vascular resistance to exercise in COPD patients, Ppa increases and SV response to exercise is limited and results from an increased preload only. Ppa at rest predicts exercise SV.

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