Metaboreceptor activation in heart failure with reduced ejection fraction: Linking cardiac and peripheral vascular haemodynamics.
Metaboreceptor activation in heart failure with reduced ejection fraction: Linking cardiac and peripheral vascular haemodynamics.
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DOI：
10.1113/ep086948
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发表时间：
2018-06
影响因子：
2.7
通讯作者：
Wray DW
中科院分区：
文献类型：
--
作者：
Barrett-O'Keefe Z;Lee JF;Berbert A;Witman MAH;Nativi-Nicolau J;Stehlik J;Richardson RS;Wray DW
本研究旨在评估射血分数降低（HFrEF）的心力衰竭患者的肌肉代谢反射，重点是多水平代谢受体激活中心脏和外周血管血流动力学之间的相互作用。23例HFrEF患者（63 ± 2岁）和15名健康对照者（64 ± 3岁），我们检测了平均动脉压（MAP）、心输出量（CO）、体循环血管传导性（SVC）、有效动脉弹性（Ea）、每搏作功（SW）、和前臂脱氧血红蛋白浓度在代谢受体激活引起的运动后循环闭塞（PECO）以下三个水平的静态-间歇性握力练习（15、30和45%最大自主收缩（MVC））。在不同的工作负荷下，代谢反射诱导的脱氧血红蛋白和MAP的增加在两组之间是相似的。然而，在对照组中，升压反应是由CO的变化驱动的（Δ495 ± 155，Δ564 ± 156，Δ666 ± 217 ml/min），而在HFrEF患者中，这种变化是由SVC的强度依赖性降低完成的（Δ−4.9 ± 1.5，Δ−9.1 ± 1.9，Δ−12.7 ± 1.8 ml/min/mmHg）。与对照组相比，这种差异反应导致HFrEF中Ea的过度增加，以及HFrEF患者SW中的迟钝反应。总之，这些研究结果表明HFrEF中代谢反射诱导的升压反应的保留作用，但表明这种反应受外周循环变化的影响。这种反应的净效应似乎是适应不良的，因为它对左心室施加了大量血液动力学负荷，可能加重左心室收缩功能障碍，并导致该患者人群的运动不耐受。
This study sought to evaluate the muscle metaboreflex in heart failure patients with reduced ejection fraction (HFrEF), with an emphasis on the interaction between cardiac and peripheral vascular hemodynamics across multiple levels of metaboreceptor activation. In 23 HFrEF patients (63 ± 2 yrs) and 15 healthy controls (64 ± 3 yrs), we examined changes in mean arterial pressure (MAP), cardiac output (CO), systemic vascular conductance (SVC), effective arterial elastance (Ea), stroke work (SW), and forearm deoxyhemoglobin concentration during metaboreceptor activation elicited by post-exercise circulatory occlusion (PECO) following three levels of static-intermittent handgrip exercise (15, 30, and 45% maximal voluntary contraction (MVC)). Across workloads, the metaboreflex-induced increase in deoxyhemoglobin and MAP were similar between groups. However, in controls, the pressor response was driven by changes in CO (Δ495 ± 155, Δ564 ± 156, Δ666 ± 217 ml/min), while this change was accomplished by intensity-dependent reductions in SVC in patients with HFrEF (Δ−4.9 ± 1.5, Δ−9.1 ± 1.9, Δ−12.7 ± 1.8 ml/min/mmHg). This differential response contributed to the exaggerated increases in Ea in HFrEF compared to controls, coupled with a blunted response in SW in the HFrEF patients. Together, these findings indicate a preserved role of the metaboreflex-induced pressor response in HFrEF, but suggest that this response is governed by changes in the peripheral circulation. The net effect of this response appears to be maladaptive, as it places a substantial hemodynamic load on the left ventricle that may exacerbate left ventricular systolic dysfunction and contribute to exercise intolerance in this patient population.