Evidence of microvascular dysfunction in heart failure with preserved ejection fraction.
Evidence of microvascular dysfunction in heart failure with preserved ejection fraction.
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DOI：
10.1136/heartjnl-2015-308403
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发表时间：
2016-02-15
期刊：
影响因子：
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通讯作者：
Wray DW
中科院分区：
文献类型：
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作者：
Lee JF;Barrett-O'Keefe Z;Garten RS;Nelson AD;Ryan JJ;Nativi JN;Richardson RS;Wray DW
虽然射血分数降低 (HFrEF) 的心力衰竭患者的血管功能障碍已明确，但射血分数保留 (HFpEF) 的心力衰竭患者的外周血管系统与疾病相关的改变尚未得到很好的表征。因此，我们试图检验以下假设：与对照组相比，HFpEF 患者在导管动脉和微血管水平上表现出血管功能降低。我们对 24 名 II-IV 级 HFpEF 患者和 24 名年龄、性别和肱动脉直径相匹配的健康对照者，通过肱动脉血流介导的扩张（FMD）检查了导管动脉功能，并通过缺血 5 分钟后的反应性充血（RH）检查了微血管功能。与对照组相比，HFpEF 患者的 FMD 降低（HFpEF：3.1 ± 0.7%；对照组：5.1 ± 0.5%；P = 0.03）。然而，与对照组相比，HFpEF 患者肱动脉扩张峰值时的剪切率较低（HFpEF：42,070 ± 4,018 s−1；对照：69,018 ± 9,509 s−1；P = 0.01），并且当肱动脉 FMD 针对剪切刺激、峰值扩张时累积曲线下面积 (AUC) 进行标准化时，组间差异被消除（HFpEF：0.11 ± 0.03 %/AUC；对照：0.09 ± 0.01 %/AUC；P = 0.58）。 HFpEF 患者的 RH（以 AUC 评估）较低（HFpEF：454 ± 35 mL；对照：660 ± 63 mL；P < 0.01）。总的来说，这些数据表明，微血管水平的适应不良导致了 HFpEF 的病理生理学，而导管动脉血管功能的减弱程度并没有超出健康衰老时发生的程度。
While vascular dysfunction is well-defined in HF patients with reduced ejection fraction (HFrEF), disease-related alterations in the peripheral vasculature of HF patients with preserved ejection fraction (HFpEF) are not well characterized. Thus, we sought test the hypothesis that HFpEF patients would demonstrate reduced vascular function, at both the conduit artery and microvascular levels, compared to controls. We examined both conduit artery function via brachial artery flow-mediated dilation (FMD) and microvascular function via reactive hyperemia (RH) following 5 min of ischemia in 24 Class II–IV HFpEF patients and 24 healthy controls matched for age, sex, and brachial artery diameter. FMD was reduced in HFpEF patients compared to controls (HFpEF: 3.1 ± 0.7%; Controls: 5.1 ± 0.5%; P = 0.03). However, shear rate at time of peak brachial artery dilation was lower in HFpEF patients compared to controls (HFpEF: 42,070 ± 4,018 s−1; Controls: 69,018 ± 9,509 s−1; P = 0.01), and when brachial artery FMD was normalized for the shear stimulus, cumulative area-under-the-curve (AUC) at peak dilation, the between-group differences were eliminated (HFpEF: 0.11 ± 0.03 %/AUC; Controls: 0.09 ± 0.01 %/AUC; P = 0.58). RH, assessed as AUC, was lower in HFpEF patients (HFpEF: 454 ± 35 mL; Controls: 660 ± 63 mL; P < 0.01). Collectively, these data suggest that maladaptations at the microvascular level contribute to the pathophysiology of HFpEF, while conduit artery vascular function is not diminished beyond that which occurs with healthy aging.