Identifying the Mechanisms of a Peripherally Limited Exercise Phenotype in Patients With Heart Failure With Preserved Ejection Fraction.

IF 7.8 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Circulation: Heart Failure Pub Date : 2024-08-01 Epub Date: 2024-07-25 DOI:10.1161/CIRCHEARTFAILURE.123.011693

Rachel J Skow, Satyam Sarma, James P MacNamara, Miles F Bartlett, Denis J Wakeham, Zachary T Martin, Mitchel Samels, Damsara Nandadeva, Tiffany L Brazile, Jimin Ren, Qi Fu, Tony G Babb, Bryce N Balmain, Michael D Nelson, Linda S Hynan, Benjamin D Levine, Paul J Fadel, Mark J Haykowsky, Christopher M Hearon

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Abstract

Background: We identified peripherally limited patients using cardiopulmonary exercise testing and measured skeletal muscle oxygen transport and utilization during invasive single leg exercise testing to identify the mechanisms of the peripheral limitation.

Methods: Forty-five patients with heart failure with preserved ejection fraction (70±7 years, 27 females) completed seated upright cardiopulmonary exercise testing and were defined as having a (1) peripheral limitation to exercise if cardiac output/oxygen consumption (VO₂) was elevated (≥6) or 5 to 6 with a stroke volume reserve >50% (n=31) or (2) a central limitation to exercise if cardiac output/VO₂ slope was ≤5 or 5 to 6 with stroke volume reserve <50% (n=14). Single leg knee extension exercise was used to quantify peak leg blood flow (Doppler ultrasound), arterial-to-venous oxygen content difference (femoral venous catheter), leg VO₂, and muscle oxygen diffusive conductance. In a subset of participants (n=36), phosphocreatine recovery time was measured by magnetic resonance spectroscopy to determine skeletal muscle oxidative capacity.

Results: Peak VO₂ during cardiopulmonary exercise testing was not different between groups (central: 13.9±5.7 versus peripheral: 12.0±3.1 mL/min per kg; P=0.135); however, the peripheral group had a lower peak arterial-to-venous oxygen content difference (central: 13.5±2.0 versus peripheral: 11.1±1.6 mLO₂/dL blood; P<0.001). During single leg knee extension, there was no difference in peak leg VO₂ (P=0.306), but the peripherally limited group had greater blood flow/VO₂ ratio (P=0.024), lower arterial-to-venous oxygen content difference (central: 12.3±2.5 versus peripheral: 10.3±2.2 mLO₂/dL blood; P=0.013), and lower muscle oxygen diffusive conductance (P=0.021). A difference in magnetic resonance spectroscopy-derived phosphocreatine recovery time was not detected (P=0.199).

Conclusions: Peripherally limited patients with heart failure with preserved ejection fraction identified by cardiopulmonary exercise testing have impairments in oxygen transport and utilization at the level of the skeletal muscle quantified by invasive knee extension exercise testing, which includes an increased blood flow/V̇O₂ ratio and poor muscle diffusive capacity.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04068844.

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识别射血分数保留型心力衰竭患者外周运动受限表型的机制

背景：我们通过心肺运动测试确定了外周受限患者，并在有创单腿运动测试中测量了骨骼肌氧运输和利用情况，以确定外周受限的机制：45名射血分数保留的心力衰竭患者（70±7岁，27名女性）完成了坐位直立心肺运动测试，如果心输出量/耗氧量（VO2）升高（≥6）或5至6，且搏动容积储备>50%，则被定义为（1）外周运动受限（n=31）；如果心输出量/VO2斜率≤5或5至6，且搏动容积储备为2，则被定义为（2）中枢运动受限，且肌肉氧弥散传导受限。在一部分参与者（36 人）中，通过磁共振波谱测量磷酸肌酸恢复时间，以确定骨骼肌氧化能力：心肺运动测试期间的峰值 VO2 在各组之间没有差异（中心组：13.9±5.7 对外周组：12.0±3.1 mL/min/kg；P=0.135）；但是，外周组的峰值动脉-静脉氧含量差异较低（中心组：13.5±2.0 对外周组：11.1±1.6 mLO2/dL 血液；P2（P=0.306），但外周受限组的血流/VO2 比值更大（P=0.024），动静脉氧含量差更低（中心：12.3±2.5 对外周：10.3±2.2 mLO2/dL 血液；P=0.013），肌肉氧弥散传导更低（P=0.021）。磁共振波谱衍生的磷酸肌酸恢复时间未发现差异（P=0.199）：结论：通过心肺运动测试确定的射血分数保留的周围受限型心力衰竭患者通过有创膝关节伸展运动测试量化了骨骼肌水平的氧运输和利用障碍，包括血流/V.M.O.比率增加和肌肉弥散能力差：URL：https://www.clinicaltrials.gov；唯一标识符：NCT04068844。

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来源期刊

Circulation: Heart Failure 医学-心血管系统

CiteScore

12.90

自引率

3.10%

发文量

271

审稿时长

6-12 weeks

期刊介绍： Circulation: Heart Failure focuses on content related to heart failure, mechanical circulatory support, and heart transplant science and medicine. It considers studies conducted in humans or analyses of human data, as well as preclinical studies with direct clinical correlation or relevance. While primarily a clinical journal, it may publish novel basic and preclinical studies that significantly advance the field of heart failure.