The Institute for Exercise and Environmental Medicine, 7232 Greenville Avenue, Dallas, TX 75231, USA.
Eur J Heart Fail. 2011 Dec;13(12):1296-304. doi: 10.1093/eurjhf/hfr133. Epub 2011 Oct 5.
Peak oxygen uptake (VO(2)) 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.
Eleven 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 VO(2) (Douglas bags) at rest, ∼30% and ∼60% of peak VO(2), and maximal exercise. Peak VO(2) 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) × mean arterial pressure (MAP); HFpEF 1790 ± 509 vs. controls 2119 ± 581 L/mmHg/min; P = 0.20]; peak stroke work [SW = stroke volume (SV) × MAP; HFpEF 13 429 ± 2269 vs. controls 13 200 ± 3610 mL/mmHg; P = 0.80]. The ΔQ(c)/ΔVO(2) slope was abnormally elevated in HFpEF patients vs. controls (11.2 ±3.6 vs. 8.3 ± 1.5; P = 0.015).
Contrary to our hypothesis, cardiac reserve is not significantly impaired in well-compensated outpatients with HFpEF. The abnormal haemodynamic response to exercise (decreased peak VO(2), increased ΔQ(c)/ΔVO(2) 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.
射血分数保留的心力衰竭（HFpEF）患者的峰值摄氧量（VO2）降低，提示心脏储备受损。为了验证这一假说，我们评估了 HFpEF 患者在运动时的血液动力学反应。
研究了 11 例 HFpEF 患者（73 ± 7 岁，7 名女性/4 名男性）和 13 名健康对照者（70 ± 4 岁，6 名女性/7 名男性）在亚最大和最大运动时的情况。通过线性回归法，从休息时、约 30%和 60%的峰值 VO2 以及最大运动时的 VO2（Douglas 袋）中，确定了心输出量（Qc，乙炔再呼吸）对运动的反应。HFpEF 患者的峰值 VO2 低于对照组（13.7 ± 3.4 比 21.6 ± 3.6 mL/kg/min；P < 0.001），而心脏储备指数无统计学差异：峰值心输出量功率 [CPO = Qc × 平均动脉压（MAP）；HFpEF 为 1790 ± 509 比对照组 2119 ± 581 L/mmHg/min；P = 0.20]；峰值做功 [SW = 每搏量（SV）× MAP；HFpEF 为 13429 ± 2269 比对照组 13200 ± 3610 mL/mmHg；P = 0.80]。HFpEF 患者的ΔQc/ΔVO2 斜率异常升高，与对照组相比（11.2 ±3.6 比 8.3 ± 1.5；P = 0.015）。
与我们的假设相反，在病情良好的门诊 HFpEF 患者中，心脏储备并没有明显受损。异常的血液动力学反应（降低的峰值 VO2、增加的ΔQc/ΔVO2 斜率）与观察到的线粒体肌病患者相似，表明存在骨骼肌氧化代谢受损的因素。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，以及（ii）代谢信号增加心输出量对运动的反应，这可能对舒张功能受损的左心室耐受性较差。
