Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction

Paul S. Bhella, Anand Prasad, Katja Heinicke, Jeff L. Hastings, Armin Zadeh, Beverley Adams-Huet, Eric L. Pacini, Shigeki Shibata, M. Dean Palmer, Bradley R. Newcomer, Benjamin D. Levine

Research output: Contribution to journalArticle

Abstract

Aims Peak oxygen uptake (VO2) is diminished in patients with heart failure with preserved ejection fraction (HFpEF) suggesting impaired cardiac reserve. To test this hypothesis, we assessed the haemodynamic response to exercise in HFpEF patients. Methods and resultsEleven HFpEF patients (73 ± 7 years, 7 females/4 males) and 13 healthy controls (70 ± 4 years, 6 females/7 males) were studied during submaximal and maximal exercise. The cardiac output (Qc, acetylene rebreathing) response to exercise was determined from linear regression of Qc and VO2 (Douglas bags) at rest, ∼30 and ∼60 of peak VO2, and maximal exercise. Peak VO2 was lower in HFpEF patients than in controls (13.7 ± 3.4 vs. 21.6 ± 3.6 mL/kg/min; P <0.001), while indices of cardiac reserve were not statistically different: peak cardiac power output [CPO Qc × mean arterial pressure (MAP); HFpEF 1790 ± 509 vs. controls 2119 ± 581 L/mmHg/min; P 0.20]; peak stroke work [SW stroke volume (SV) × MAP; HFpEF 13 429 ± 2269 vs. controls 13 200 ± 3610 mL/mmHg; P 0.80]. The ΔQc/ΔVO2 slope was abnormally elevated in HFpEF patients vs. controls (11.2 ±3.6 vs. 8.3 ± 1.5; P 0.015). ConclusionContrary to our hypothesis, cardiac reserve is not significantly impaired in well-compensated outpatients with HFpEF. The abnormal haemodynamic response to exercise (decreased peak VO2, increased ΔQc/ΔVO2 slope) is similar to that observed in patients with mitochondrial myopathies, suggesting an element of impaired skeletal muscle oxidative metabolism. This impairment may limit functional capacity by two mechanisms: (i) premature skeletal muscle fatigue and (ii) metabolic signals to increase the cardiac output response to exercise which may be poorly tolerated by a left ventricle with impaired diastolic function.

Original languageEnglish (US)
Pages (from-to)1296-1304
Number of pages9
JournalEuropean Journal of Heart Failure
Volume13
Issue number12
DOIs
StatePublished - Dec 2011
Externally publishedYes

Fingerprint

Heart Failure
Hemodynamics
Exercise
Cardiac Output
Arterial Pressure
Skeletal Muscle
Mitochondrial Myopathies
Acetylene
Muscle Fatigue
Stroke Volume
Heart Ventricles
Linear Models
Outpatients
Stroke
Oxygen

Keywords

  • Cardiac output response to exercise
  • Exercise capacity
  • Haemodynamic response to exercise
  • Heart failure with preserved ejection fraction
  • Myocardial contractile reserve
  • Oxygen consumption

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Bhella, P. S., Prasad, A., Heinicke, K., Hastings, J. L., Zadeh, A., Adams-Huet, B., ... Levine, B. D. (2011). Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction. European Journal of Heart Failure, 13(12), 1296-1304. https://doi.org/10.1093/eurjhf/hfr133

Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction. / Bhella, Paul S.; Prasad, Anand; Heinicke, Katja; Hastings, Jeff L.; Zadeh, Armin; Adams-Huet, Beverley; Pacini, Eric L.; Shibata, Shigeki; Palmer, M. Dean; Newcomer, Bradley R.; Levine, Benjamin D.

In: European Journal of Heart Failure, Vol. 13, No. 12, 12.2011, p. 1296-1304.

Research output: Contribution to journalArticle

Bhella, PS, Prasad, A, Heinicke, K, Hastings, JL, Zadeh, A, Adams-Huet, B, Pacini, EL, Shibata, S, Palmer, MD, Newcomer, BR & Levine, BD 2011, 'Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction', European Journal of Heart Failure, vol. 13, no. 12, pp. 1296-1304. https://doi.org/10.1093/eurjhf/hfr133
Bhella, Paul S. ; Prasad, Anand ; Heinicke, Katja ; Hastings, Jeff L. ; Zadeh, Armin ; Adams-Huet, Beverley ; Pacini, Eric L. ; Shibata, Shigeki ; Palmer, M. Dean ; Newcomer, Bradley R. ; Levine, Benjamin D. / Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction. In: European Journal of Heart Failure. 2011 ; Vol. 13, No. 12. pp. 1296-1304.
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AU - Pacini, Eric L.

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N2 - Aims Peak oxygen uptake (VO2) is diminished in patients with heart failure with preserved ejection fraction (HFpEF) suggesting impaired cardiac reserve. To test this hypothesis, we assessed the haemodynamic response to exercise in HFpEF patients. Methods and resultsEleven HFpEF patients (73 ± 7 years, 7 females/4 males) and 13 healthy controls (70 ± 4 years, 6 females/7 males) were studied during submaximal and maximal exercise. The cardiac output (Qc, acetylene rebreathing) response to exercise was determined from linear regression of Qc and VO2 (Douglas bags) at rest, ∼30 and ∼60 of peak VO2, and maximal exercise. Peak VO2 was lower in HFpEF patients than in controls (13.7 ± 3.4 vs. 21.6 ± 3.6 mL/kg/min; P <0.001), while indices of cardiac reserve were not statistically different: peak cardiac power output [CPO Qc × mean arterial pressure (MAP); HFpEF 1790 ± 509 vs. controls 2119 ± 581 L/mmHg/min; P 0.20]; peak stroke work [SW stroke volume (SV) × MAP; HFpEF 13 429 ± 2269 vs. controls 13 200 ± 3610 mL/mmHg; P 0.80]. The ΔQc/ΔVO2 slope was abnormally elevated in HFpEF patients vs. controls (11.2 ±3.6 vs. 8.3 ± 1.5; P 0.015). ConclusionContrary to our hypothesis, cardiac reserve is not significantly impaired in well-compensated outpatients with HFpEF. The abnormal haemodynamic response to exercise (decreased peak VO2, increased ΔQc/ΔVO2 slope) is similar to that observed in patients with mitochondrial myopathies, suggesting an element of impaired skeletal muscle oxidative metabolism. This impairment may limit functional capacity by two mechanisms: (i) premature skeletal muscle fatigue and (ii) metabolic signals to increase the cardiac output response to exercise which may be poorly tolerated by a left ventricle with impaired diastolic function.

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KW - Myocardial contractile reserve

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