Central cardiac limit to aerobic capacity in patients with exertional pulmonary venous hypertension: implications for heart failure with preserved ejection fraction.
Central cardiac limit to aerobic capacity in patients with exertional pulmonary venous hypertension: implications for heart failure with preserved ejection fraction.
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DOI：
10.1161/circheartfailure.114.001551
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发表时间：
2015-03
期刊：
影响因子：
--
通讯作者：
Systrom DM
中科院分区：
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作者：
Santos M;Opotowsky AR;Shah AM;Tracy J;Waxman AB;Systrom DM
射血分数保留性心力衰竭（HFpEF）功能受限的机制仍存在争议。我们研究了中枢心脏和外周机制的作用，并假设肺血管对运动的反应是劳力性肺静脉高压（ePVH）患者有氧能力的重要决定因素。我们比较了31例ePVH患者（峰值VO 2 <80%预测值和峰值肺动脉楔压≥20 mmHg）和31例年龄和性别匹配的对照组（峰值VO 2>80%预测值），这些患者接受了有创心肺运动试验，以治疗原因不明的劳力不耐受。与对照组相比，ePVH患者的峰值心输出量较低（73±14 vs 103± 18%预测值; p<0.001），与变时性反应受损（峰值HR 111±25 vs 136±24 bpm; p<0.001）和峰值每搏输出量指数降低（47±10 vs 54±15 mL/min/m2; p=0.03）相关。两组之间的峰值全身O2提取率无差异（动脉-混合静脉氧含量差异：13.0±2.1 vs 13.4±2.4 mL/dL; p=0.46）。ePVH患者的静息（150±74 vs 106±50 dyne.s.cm−5; p=0.009）、峰值（124±74 vs 70±41 dyne.s.cm−5; p<0.001）和等流肺血管阻力（PVR; 124±74 vs 91±33 dyne.s.cm−5，CO~10.6L/min; p=0.04）更高。在所有对照受试者中，PVR随着运动而降低，但在36%（n=11）的ePVH患者中增加。肺血管反应异常与峰值VO 2无关。心输出量反应降低，而不是外周O2提取受损，限制了ePVH的氧输送和有氧能力。肺血管功能障碍在静息和运动时的ePVH患者中很常见。
The mechanism of functional limitation in heart failure with preserved ejection fraction (HFpEF) remains controversial. We examined the contributions of central cardiac and peripheral mechanisms and hypothesized that the pulmonary vascular response to exercise is an important determinant of aerobic capacity among patients with exertional pulmonary venous hypertension (ePVH). We compared 31 ePVH patients (peak VO2<80% predicted and peak pulmonary arterial wedge pressure≥20 mmHg) with 31 age and gender matched controls (peak VO2>80% predicted) who underwent invasive cardiopulmonary exercise testing for unexplained exertional intolerance. ePVH patients had lower peak cardiac output (73±14 vs 103±18 % predicted; p<0.001) compared to controls, related both to impaired chronotropic response (peak HR 111±25 vs 136±24 bpm; p<0.001) and to reduced peak stroke volume index (47±10 vs 54±15 mL/min/m2; p=0.03). Peak systemic O2 extraction was not different between groups (arterial-mixed venous oxygen content difference: 13.0±2.1 vs 13.4±2.4 mL/dL; p=0.46). ePVH patients had higher resting (150±74 vs 106±50 dyne.s.cm−5; p=0.009), peak (124±74 vs 70±41 dyne.s.cm−5; p<0.001) and isoflow pulmonary vascular resistance (PVR; 124±74 vs 91±33 dyne.s.cm−5 at CO~10.6L/min; p=0.04). PVR decreased with exercise in all control subjects but increased in 36% (n=11) of ePVH patients. Abnormal pulmonary vascular response was not associated with peak VO2. Reduced cardiac output response, rather than impaired peripheral O2 extraction, constrains oxygen delivery and aerobic capacity in ePVH. Pulmonary vascular dysfunction is common in patients with ePVH at rest and with exercise.