Mechanisms of exercise intolerance in heart failure with preserved ejection fraction: the role of abnormal peripheral oxygen extraction.
Mechanisms of exercise intolerance in heart failure with preserved ejection fraction: the role of abnormal peripheral oxygen extraction.
复制标题
射血分数保留的心力衰竭运动不耐受的机制：异常外周氧提取的作用。
DOI：
10.1161/circheartfailure.114.001825
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发表时间：
2015-03
期刊：
影响因子：
--
通讯作者：
Lewis GD
中科院分区：
文献类型：
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作者：
Dhakal BP;Malhotra R;Murphy RM;Pappagianopoulos PP;Baggish AL;Weiner RB;Houstis NE;Eisman AS;Hough SS;Lewis GD
射血分数保留型心力衰竭 (HFpEF) 和射血分数降低型心力衰竭 (HFrEF) 患者的运动能力（以峰值摄氧量 (Vo2) 衡量）同样受到损害。然而，之前尚未定义 HFpEF 与 HFrEF 中 Vo2 的每个组成部分如何响应增量运动而变化的特征。我们假设运动期间异常低的外周 O2 提取量（动脉-混合静脉 O2 含量差异，[C(a-v)o2]）会显着导致 HFpEF 运动能力受损。我们对 104 名有症状 NYHA II 至 IV 心力衰竭患者（HFpEF，n=48，峰值 Vo2=13.9±0.5 mL kg−1 min−1，平均值±SEM，和 HFrEF，n=56，峰值 Vo2=12.1±0.5 mL kg−1 min−1）和 24 名对照受试者（峰值 Vo2 27.0±1.7）进行了最大增量心肺运动测试和侵入性血流动力学监测。 mL kg−1 min−1)。与 HFrEF 相比，HFpEF 的峰值运动 C(a-v)o2 较低（分别为 11.5±0.27 与 13.5±0.34 mL/dL，P<0.0001），尽管年龄、血红蛋白水平、峰值呼吸交换比、Cao2 或心脏充盈压没有差异。峰值 C(a-v)o2 和峰值心率成为 HFpEF 峰值 Vo2 的主要预测因素。外周血氧提取受损是 40% HFpEF 患者运动能力的主要限制因素，并且与运动期间全身血压升高密切相关（r=0.49，P=0.0005）。在第一项直接测量 HFpEF、HFrEF 和正常人运动过程中 C(a-v)o2 的研究中，我们发现峰值 C(a-v)o2 是 HFpEF 运动能力的主要决定因素。氧气提取受损所造成的重要功能限制可能反映了骨骼肌或外周微血管功能的内在异常，并且代表了治疗干预的潜在目标。
Exercise capacity as measured by peak oxygen uptake (Vo2) is similarly impaired in patients with heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). However, characterization of how each component of Vo2 changes in response to incremental exercise in HFpEF versus HFrEF has not been previously defined. We hypothesized that abnormally low peripheral o2 extraction (arterio-mixed venous o2 content difference, [C(a-v)o2]) during exercise significantly contributes to impaired exercise capacity in HFpEF. We performed maximum incremental cardiopulmonary exercise testing with invasive hemodynamic monitoring on 104 patients with symptomatic NYHA II to IV heart failure (HFpEF, n=48, peak Vo2=13.9±0.5 mL kg−1 min−1, mean±SEM, and HFrEF, n=56, peak Vo2=12.1±0.5 mL kg−1 min−1) and 24 control subjects (peak Vo2 27.0±1.7 mL kg−1 min−1). Peak exercise C(a-v)o2 was lower in HFpEF compared with HFrEF (11.5±0.27 versus 13.5±0.34 mL/dL, respectively, P<0.0001), despite no differences in age, hemoglobin level, peak respiratory exchange ratio, Cao2, or cardiac filling pressures. Peak C(a-v)o2 and peak heart rate emerged as the leading predictors of peak Vo2 in HFpEF. Impaired peripheral o2 extraction was the predominant limiting factor to exercise capacity in 40% of patients with HFpEF and was closely related to elevated systemic blood pressure during exercise (r=0.49, P=0.0005). In the first study to directly measure C(a-v)o2 throughout exercise in HFpEF, HFrEF, and normals, we found that peak C(a-v)o2 was a major determinant of exercise capacity in HFpEF. The important functional limitation imposed by impaired o2 extraction may reflect intrinsic abnormalities in skeletal muscle or peripheral microvascular function, and represents a potential target for therapeutic intervention.