What is the clinical evidence from this study?

Study design: Review. Population: Heart failure with reduced or preserved ejection fraction.

April 25, 2015

Determinants of exercise intolerance in patients with heart failure and reduced or preserved ejection fraction

Key Result

Exercise intolerance in patients with heart failure is driven by both central and peripheral factors, with peripheral impairments playing a relatively greater role in limiting exercise performance in those with preserved ejection fraction.

Structured PICO

What are the mechanisms of exercise intolerance in patients with HFrEF and HFpEF?

Population

Patients with heart failure and reduced or preserved ejection fraction (HFrEF and HFpEF)

Comparator

Healthy controls

Outcome

Mechanisms of exercise intolerance (peak pulmonary oxygen uptake)surrogate

Exercise intolerance in HFpEF may be more heavily driven by peripheral vascular and skeletal muscle impairments compared to HFrEF, highlighting potential therapeutic targets.

Limitations

Prior studies examining exercise intolerance pathophysiology are largely based on comparisons with controls without HF rather than direct comparisons between HFREF and HFPEF.
Lack of invasive peripheral hemodynamic measures in some studies comparing HF phenotypes.

Abstract

This mini-review summarizes the literature regarding the mechanisms of exercise intolerance in patients with heart failure and reduced or preserved ejection fraction (HFREF and HFPEF, respectively). Evidence to date suggests that the reduced peak pulmonary oxygen uptake (pulm V̇o₂) in patients with HFREF compared with healthy controls is due to both central (reduced convective O₂ transport) and peripheral factors (impaired skeletal muscle blood flow, decreased diffusive O₂ transport coupled with abnormal skeletal morphology, and metabolism). Although central and peripheral impairments also limit peak pulm V̇o₂ in HFPEF patients compared with healthy controls, emerging data suggest that the latter may play a relatively greater role in limiting exercise performance in these patients. Unlike HFREF, currently there is limited evidence-based therapies that improve exercise capacity in HFPEF patients, therefore future studies are required to determine whether interventions targeted to improve peripheral vascular and skeletal muscle function result in favorable improvements in peak pulm and leg V̇o2 and their determinants in HFPEF patients.

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