Heart failure and movement-induced hemodynamics: Partitioning the impact of central and peripheral dysfunction

INTERNATIONAL JOURNAL OF CARDIOLOGY

卷:178

Article

Witman, Melissa A. H.^1,2  Ives, Stephen J.³  Trinity, Joel D.^1,2  Groot, H. Jonathan^1,4  Stehlik, Josef⁵  Richardson, Russell S.^1,2,4 

[1] George E Whalen VA Med Ctr, Geriatr Res Educ & Clin Ctr, Salt Lake City, UT USA

[2] Univ Utah, Sch Med, Div Geriatr, Dept Internal Med, Salt Lake City, UT USA

[3] Skidmore Coll, Dept Hlth & Exercise Sci, Saratoga Springs, NY 12866 USA

[4] Univ Utah, Dept Exercise & Sport Sci, Salt Lake City, UT USA

[5] Univ Utah, George E Whalen VA Med Ctr, Dept Internal Med, Div Cardiol,Med Ctr,Sch Med, Salt Lake City, UT USA

关键词: Passive exercise;    Blood flow;    Exercise pressor response;    Afferents;    Mechanoreflex;   

DOI  :  10.1016/j.ijcard.2014.10.044

来源: Elsevier

【 摘 要 】

Background: The complex pathophysiology of heart failure (HF) creates a challenging paradigm to differentiate the role of central and peripheral hemodynamic dysfunction during conventional exercise. Adopting a novel reductionist approach with potential clinical relevance, we studied the central and peripheral contributors to both continuous and single passive leg movement (PLM)-induced hyperemia in 14 HF patients with reduced ejection fraction (HFrEF) and 13 controls. Methods: Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and femoral artery blood flow (FBF) were recorded during PLM. Results: The FBF response (area under the curve; AUC) to 60 s of continuous PLM was attenuated in the HFrEF (25 +/- 15 ml AUC) compared to controls (199 +/- 34 ml AUC) as were peak changes from baseline for FBF, leg vascular conductance (LVC), CO, and HR. During single PLM, increases in CO and HR were smaller and no longer different between groups, supporting the use of this modality to assess groups with disparate central hemodynamics. Interestingly, single PLM-induced hyperemia, likely predominantly driven by flow-mediated vasodilation due to minimal vessel deformation, was essentially nonexistent in the HFrEF (-9 +/- 10 ml AUC) in contrast to the controls (43 +/- 25 ml AUC). Conclusions: These data fail to support a HFrEF-associated exaggeration in the mechanoreceptor driven component of the exercise pressor response. In fact, by exhibiting limited central hemodynamic responses compared to the controls, the observed attenuation in movement-induced FBF in HFrEF appears largely due to peripheral vascular dysfunction, particularly flow-mediated vasodilation. Published by Elsevier Ireland Ltd.

【 授权许可】

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