Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction
Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction
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DOI：
10.1093/eurjhf/hfr133
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发表时间：
2011-12-01
影响因子：
18.2
通讯作者：
Levine, Benjamin D.
中科院分区：
文献类型：
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作者：
Bhella, Paul S.;Prasad, Anand;Levine, Benjamin D.
射血分数保留性心力衰竭（HFpEF）患者的峰值摄氧量（VO 2）降低，提示心脏储备受损。为了验证这一假设，我们评估了血流动力学反应运动在HFpEF patients.Methods和resultsEleven HFpEF患者（73 +/- 7年，7名女性/4名男性）和13名健康对照（70 +/- 4年，6名女性/7名男性）进行了研究，在次最大和最大的运动。通过对安静时的Q（c）和VO 2（道格拉斯袋）（与峰值VO 2的30%和60%相似）以及最大运动时的Q（c）和VO 2（与峰值VO 2相似）进行线性回归，确定心输出量（Q（c），乙炔再呼吸）对运动的反应。HFpEF患者的峰值VO 2低于对照组（13.7 ± 3.4 vs. 21.6 ± 3.6 mL/kg/min; P < 0.001），而心脏储备指数无统计学差异：峰值心输出功率[CPO = Q（c）x平均动脉压（MAP）; HFpEF 1790 +/- 509 vs.对照组2119 +/- 581 L/mmHg/min; P = 0.20];峰搏出功[SW每搏输出量（SV）x MAP; HFpEF 13 429 +/- 2269 vs.对照组13 200 +/- 3610 mL/mmHg; P = 0.80]。HFpEF患者的Δ Q（c）/Δ VO 2斜率异常升高（11.2 ± 3.6 vs.8.3 ± 1.5; P = 0.015）。结论与我们的假设相反，HFpEF患者的心脏储备没有明显受损。对运动的异常血液动力学反应（峰值VO 2降低，Δ Q（c）/Δ VO 2斜率增加）与线粒体肌病患者中观察到的相似，表明骨骼肌氧化代谢受损。这种损伤可能通过两种机制限制功能能力：（i）骨骼肌过早疲劳和（ii）代谢信号增加对运动的心输出量反应，舒张功能受损的左心室可能耐受不良。
Aims Peak oxygen uptake (VO2) is diminished in patients with heart failure with preserved ejection fraction (HFpEF) suggesting impaired cardiac reserve. To test this hypothesis, we assessed the haemodynamic response to exercise in HFpEF patients.Methods and resultsEleven HFpEF patients (73 +/- 7 years, 7 females/4 males) and 13 healthy controls (70 +/- 4 years, 6 females/7 males) were studied during submaximal and maximal exercise. The cardiac output (Q(c), acetylene rebreathing) response to exercise was determined from linear regression of Q(c) and VO2 (Douglas bags) at rest, similar to 30% and similar to 60% of peak VO2, and maximal exercise. Peak VO2 was lower in HFpEF patients than in controls (13.7 +/- 3.4 vs. 21.6 +/- 3.6 mL/kg/min; P < 0.001), while indices of cardiac reserve were not statistically different: peak cardiac power output [CPO = Q(c) x mean arterial pressure (MAP); HFpEF 1790 +/- 509 vs. controls 2119 +/- 581 L/mmHg/min; P = 0.20]; peak stroke work [SW stroke volume (SV) x MAP; HFpEF 13 429 +/- 2269 vs. controls 13 200 +/- 3610 mL/mmHg; P = 0.80]. The Delta Q(c)/Delta VO2 slope was abnormally elevated in HFpEF patients vs. controls (11.2 +/- 3.6 vs. 8.3 +/- 1.5; P = 0.015).Conclusion Contrary to our hypothesis, cardiac reserve is not significantly impaired in well-compensated outpatients with HFpEF. The abnormal haemodynamic response to exercise (decreased peak VO2, increased Delta Q(c)/Delta VO2 slope) is similar to that observed in patients with mitochondrial myopathies, suggesting an element of impaired skeletal muscle oxidative metabolism. This impairment may limit functional capacity by two mechanisms: (i) premature skeletal muscle fatigue and (ii) metabolic signals to increase the cardiac output response to exercise which may be poorly tolerated by a left ventricle with impaired diastolic function.