Cardiac output response to exercise in relation to metabolic demand in heart failure with preserved ejection fraction
Cardiac output response to exercise in relation to metabolic demand in heart failure with preserved ejection fraction
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DOI：
10.1093/eurjhf/hft026
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发表时间：
2013-07-01
影响因子：
18.2
通讯作者：
Borlaug, Barry A.
中科院分区：
文献类型：
--
作者：
Abudiab, Muaz M.;Redfield, Margaret M.;Borlaug, Barry A.
运动不耐受是射血分数保留性心力衰竭（HFpEF）的标志，但其机制尚不清楚。本研究旨在确定运动期间心输出量（CO）的增加是否与HFpEF.Patients（n 109）和对照组（n 73）的代谢需求相匹配，同时进行有创（n 96）或无创（n 86）血流动力学评估和呼气分析，以确定直立或仰卧运动期间的耗氧量（VO 2）。在休息时，HFpEF患者有较高的LV充盈压，但相似的心率，每搏输出量，EF，和CO。在仰卧和直立运动，HFpEF患者显示较低的峰值VO 2加上钝性增加的心率，每搏输出量，EF，和CO相比，控制。HFpEF患者左室充盈压显著升高，肺动脉压继发性升高。HFpEF患者的峰值VO 2降低主要归因于CO限制，因为HFpEF患者CO相对于VO 2增加的斜率低20（5.9 2.5 vs. 7.4 2.6 L血液/L O-2，P 0.0005）。虽然HFpEF患者和对照组运动时动静脉O-2差的绝对增加相似，但HFpEF患者动静脉O-2差相对于VO 2的增加更大（8.9 3.4 vs. 5.5 2.0 min/dL，P 0.0001）。这些差异在总队列中观察到，当直立和仰卧运动models.While舒张功能障碍促进充血和肺动脉高压与HFpEF的压力，减少运动能力主要是与不足的CO相对于代谢的需要。
Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF.Patients with HFpEF (n 109) and controls (n 73) exercised to volitional fatigue with simultaneous invasive (n 96) or non-invasive (n 86) haemodynamic assessment and expired gas analysis to determine oxygen consumption (VO2) during upright or supine exercise. At rest, HFpEF patients had higher LV filling pressures but similar heart rate, stroke volume, EF, and CO. During supine and upright exercise, HFpEF patients displayed lower peak VO2 coupled with blunted increases in heart rate, stroke volume, EF, and CO compared with controls. LV filling pressures increased dramatically in HFpEF patients, with secondary elevation in pulmonary artery pressures. Reduced peak VO2 in HFpEF patients was predominantly attributable to CO limitation, as the slope of the increase in CO relative to VO2 was 20 lower in HFpEF patients (5.9 2.5 vs. 7.4 2.6 L blood/L O-2, P 0.0005). While absolute increases in arterialvenous O-2 difference with exercise were similar in HFpEF patients and controls, augmentation in arterialvenous O-2 difference relative to VO2 was greater in HFpEF patients (8.9 3.4 vs. 5.5 2.0 min/dL, P 0.0001). These differences were observed in the total cohort and when upright and supine exercise modalities were examined individually.While diastolic dysfunction promotes congestion and pulmonary hypertension with stress in HFpEF, reduction in exercise capacity is predominantly related to inadequate CO relative to metabolic needs.