Heart failure and movement-induced hemodynamics: partitioning the impact of central and peripheral dysfunction.
Heart failure and movement-induced hemodynamics: partitioning the impact of central and peripheral dysfunction.
复制标题
DOI：
10.1016/j.ijcard.2014.10.044
复制
发表时间：
2015-01-15
影响因子：
3.5
通讯作者：
Richardson, Russell S.
中科院分区：
文献类型：
--
作者：
Witman, Melissa A. H.;Ives, Stephen J.;Trinity, Joel D.;Groot, H. Jonathan;Stehlik, Josef;Richardson, Russell S.
心衰（HF）的复杂病理生理学为区分常规运动中中枢性和外周性血流动力学功能障碍的作用创造了一个具有挑战性的范式。采用一种具有潜在临床相关性的新颖还原方法，我们研究了14例射血分数降低（HFrEF）的HF患者和13例对照组中连续和单次被动腿部运动（PLM）引起的充血的中枢和外周因素。在PLM期间记录心率（HR）、脑卒中量（SV）、心输出量（CO）、平均动脉压（MAP）和股动脉血流（FBF）。与对照组（199±34 ml AUC）相比，HFrEF组对60秒连续PLM的FBF反应（曲线下面积；AUC）（25±15 ml AUC）减弱，FBF、腿部血管传导（LVC）、CO和HR的峰值变化与基线相比也有所减弱。在单次PLM期间，CO和HR的增加较小，各组之间不再存在差异，支持使用这种模式来评估具有不同中枢血流动力学的组。有趣的是，与对照组（43±25 ml AUC）相比，HFrEF组（- 9±10 ml AUC）基本上不存在单次plm诱导的充血，可能主要是由血流介导的血管舒张引起的，因为血管变形很小。这些数据不能支持运动压力反应中机械受体驱动成分与hfref相关的夸大。事实上，与对照组相比，由于表现出有限的中枢血流动力学反应，HFrEF中观察到的运动诱导FBF的衰减主要是由于周围血管功能障碍，特别是血流介导的血管舒张。
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. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and femoral artery blood flow (FBF) were recorded during PLM. The FBF response (area under the curve; AUC) to 60 seconds 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). 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.
登录
查看更多内容
DOI：
10.1152/ajpheart.00532.2012
发表时间：
2013-01-01
影响因子：
4.8
作者：
Ives, Stephen J.;McDaniel, John;Richardson, Russell S.
通讯作者：
Richardson, Russell S.
影响因子：
37.8
作者：
SULLIVAN, MJ;KNIGHT, JD;COBB, FR
通讯作者：
COBB, FR
DOI：
10.1152/ajpheart.00568.2012
发表时间：
2012-11-01
影响因子：
4.8
作者：
Witman, Melissa A. H.;McDaniel, John;Richardson, Russell S.
通讯作者：
Richardson, Russell S.
DOI：
10.1161/hypertensionaha.112.193318
发表时间：
2012-09
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
--
作者：
Witman MA;Fjeldstad AS;McDaniel J;Ives SJ;Zhao J;Barrett-O'Keefe Z;Nativi JN;Stehlik J;Wray DW;Richardson RS
通讯作者：
Richardson RS
影响因子：
37.8
作者：
Smith, SA;Mitchell, JH;Garry, MG
通讯作者：
Garry, MG