Key result
Beta-blockers worsen exercise hemodynamics in an ovine HFpEF model lacking elevated resting sympathetic nerve activity.
Why the study?
The role of the sympathetic nervous system in HFpEF is poorly understood, with scant evidence regarding whether cardiac sympathetic nerve activity is heightened or if β-blockers impair exercise hemodynamics.
Does beta-blocker administration impair exercise hemodynamics in an ovine model of hypertensive HFpEF?
Does beta-blocker administration impair exercise hemodynamics in an ovine model of hypertensive HFpEF?
In an ovine model of hypertensive HFpEF, resting cardiac sympathetic nerve activity is not elevated, and beta-blockers impair exercise hemodynamics, providing a mechanistic rationale for avoiding beta-blockers in HFpEF patients.
Answers are grounded in this paper and cite their sources.
Cautions against routine beta-blocker use in hypertensive HFpEF; provides mechanistic evidence that leaves.
BACKGROUND: The sympathetic nervous system is a crucial mediator of cardiovascular variables during exercise. However, its role in heart failure with preserved ejection fraction (HFpEF), where exercise intolerance is a cardinal feature, is poorly understood. Currently, there is scant and no clear evidence of heightened cardiac sympathetic nerve activity (CSNA) in HFpEF, which might explain why β-blockers lack convincing prognostic benefit in this syndrome. Accordingly, we utilized gold standard direct recordings to test the hypothesis that resting levels of CSNA are not elevated in HFpEF. We also tested whether β-blockers in HFpEF cause further impairments in the hemodynamic determinants of exercise capacity. METHODS: Experiments were conducted in a conscious large animal (ovine) model of hypertensive HFpEF that exhibits similarly impaired exercise hemodynamics as patients with HFpEF. Direct recordings of CSNA were made in this model and compared with non-HFpEF sheep. In addition, hemodynamic responses to graded treadmill exercise testing were compared before and after β-blocker administration. RESULTS: Gold standard direct recordings of resting CSNA were not elevated in HFpEF sheep. Inhibition of this activity using a β-blocker further impaired exercise hemodynamics (cardiac output, heart rate and pulmonary capillary wedge pressure) in HFpEF sheep. In addition, non-HFpEF and HFpEF sheep exhibited differential exercise hemodynamic responses to β-blockers. CONCLUSIONS: Our data demonstrates that CSNA is not elevated in an ovine model of hypertensive HFpEF and suggests that favorable exercise hemodynamics in HFpEF are reliant upon β-adrenergic activation. Our findings provide a mechanistic rationale for why β-blockers should be avoided in patients with HFpEF.
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Chang et al. (2025) studied Hypertensive heart failure with preserved ejection fraction (HFpEF). Beta-blocker administration vs. Before beta-blocker administration and non-HFpEF sheep was evaluated on Resting levels of cardiac sympathetic nerve activity (CSNA) and exercise hemodynamics. Beta-blocker administration in an ovine model of hypertensive HFpEF further impaired exercise hemodynamics, while direct recordings showed resting cardiac sympathetic nerve activity was not elevated.
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