Sorimachi Hidemi, Burkhoff Daniel, Verbrugge Frederik H, Omote Kazunori, Obokata Masaru, Reddy Yogesh N V, Takahashi Naoki, Sunagawa Kenji, Borlaug Barry A
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Cardiovascular Research Foundation, New York Biomedical Research Institute, New York, NY, USA.
Eur J Heart Fail. 2021 Oct;23(10):1648-1658. doi: 10.1002/ejhf.2254. Epub 2021 Jun 17.
Circulating blood volume is functionally divided between the unstressed volume, which fills the vascular space, and stressed blood volume (SBV), which generates vascular wall tension and intravascular pressure. With decreases in venous capacitance, blood functionally shifts to the SBV, increasing central venous pressure and pulmonary venous pressures. Obesity is associated with both elevated venous pressure and heart failure with preserved ejection fraction (HFpEF). To explore the mechanisms underlying this association, we evaluated relationships between blood volume distribution, venous compliance, and body mass in patients with and without HFpEF.
Subjects with HFpEF (n = 62) and non-cardiac dyspnoea (NCD) (n = 79) underwent invasive haemodynamic exercise testing with echocardiography. SBV was estimated (eSBV) from measured haemodynamic variables fit to a comprehensive cardiovascular model. Compared to NCD, patients with HFpEF displayed a leftward-shifted central venous pressure-dimension relationship, indicating reduced venous compliance. eSBV was 81% higher at rest and 69% higher during exercise in HFpEF than NCD (both P < 0.0001), indicating reduced venous capacitance. Despite greater augmented eSBV with exercise, the increase in cardiac output was reduced in HFpEF, suggesting operation on the plateau of the Starling curve. Exercise eSBV was directly correlated with higher body mass index (r = 0.77, P < 0.0001) and inversely correlated with right ventricular-pulmonary arterial coupling (r = -0.57, all P < 0.0001).
Patients with HFpEF display reductions in systemic venous compliance and increased eSBV related to reduced venous capacitance, abnormalities in right ventricular-pulmonary artery interaction, and increased body fat. These data provide new evidence supporting an important role of venous dysfunction in obesity-related HFpEF and suggest that therapies that improve venous function may hold promise to improve clinical status in this cohort.
循环血容量在功能上分为填充血管空间的非应激容量和产生血管壁张力及血管内压力的应激血容量（SBV）。随着静脉容量的减少，血液在功能上会转移至SBV，从而增加中心静脉压和肺静脉压。肥胖与静脉压升高及射血分数保留的心力衰竭（HFpEF）均有关联。为探究这种关联背后的机制，我们评估了有和没有HFpEF的患者的血容量分布、静脉顺应性和体重之间的关系。
HFpEF患者（n = 62）和非心源性呼吸困难（NCD）患者（n = 79）接受了侵入性血流动力学运动试验及超声心动图检查。根据符合综合心血管模型的测量血流动力学变量估算SBV（eSBV）。与NCD相比，HFpEF患者的中心静脉压-维度关系向左偏移，表明静脉顺应性降低。HFpEF患者静息时的eSBV比NCD高81%，运动时高69%（均P < 0.0001），表明静脉容量减少。尽管运动时eSBV增加幅度更大，但HFpEF患者的心输出量增加减少，提示处于Starling曲线的平台期。运动时的eSBV与较高的体重指数直接相关（r = 0.77，P < 0.0001），与右心室-肺动脉耦合呈负相关（r = -0.57，均P < 0.0001）。
HFpEF患者表现出全身静脉顺应性降低，eSBV增加与静脉容量减少、右心室-肺动脉相互作用异常及体脂增加有关。这些数据提供了新的证据，支持静脉功能障碍在肥胖相关HFpEF中起重要作用，并表明改善静脉功能的疗法可能有望改善该队列患者的临床状况。
