Coupling of hemodynamic measurements with oxygen consumption during exercise does not improve risk stratification in patients with heart failure
Coupling of hemodynamic measurements with oxygen consumption during exercise does not improve risk stratification in patients with heart failure
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DOI：
10.1161/01.cir.94.10.2492
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发表时间：
1996-11-15
期刊：
影响因子：
37.8
通讯作者：
Aaronson, K
中科院分区：
文献类型：
--
作者：
Mancini, D;Katz, S;Aaronson, K
背景 峰值摄氧量测量已成为选择心脏移植患者的公认方法。一些研究人员建议，增加运动血流动力学测量可以进一步增强风险分层，因为这些测量可能会识别出非心脏运动受限的患者。 方法和结果因此，我们对 65 名在哥伦比亚长老会医疗中心接受移植评估的患者（47 名男性，18 名女性）53+/-10 岁（平均值+/-SD）进行了最大程度的自行车运动，并进行了呼吸气体分析和血流动力学测量。使用近红外光谱评估运动期间股外侧肌的骨骼肌氧合。对所有患者进行运动血流动力学、通气和肌肉氧合测量。对于每个受试者，VO2 和肺动脉饱和度 (PA SaO(2)) 之间存在线性相关性。导出了该关系的斜率和 PA SaO(2) 为 0%（VO2 截距）时的理论 VO2maX。基线测量为左心室射血分数，22+/-9%；肺毛细血管楔压（PCWP），16+/-10 mm Hg；心脏指数（CI），2.1+/-0.5 L。分钟(-1) 。米（-2）； PA SaO(2)，53+/-8%。通过与 Higginbotham 描述的峰值摄氧量与峰值心输出量的线性方程进行比较，将运动对心输出量的反应分为正常或异常。运动测量值为峰值 VO2，12.1+/-3.0 mL。千克（-1）。分钟（-1）；摄氧量截距，19.1+/-5.5 mL。千克（-1）。分钟（-1）； PCWP，31+/-11 毫米汞柱：CI，3.8+/-1.3 L。分钟(-1) 。 m(-2) 和 PA SaO(2), 27+/-9%。只有 6% 的患者对运动表现出正常的心输出量反应。对峰值摄氧量、摄氧量截距、运动结束时骨骼肌氧合以及峰值运动血流动力学变量进行多变量分析。只有左心室每搏功和左心室每搏功指数被证明可以预测生存。结论 将运动血流动力学测量添加到无创代谢应激测试中可以最小程度地改善严重心力衰竭患者的风险预测。
Background Measurement of peak VO2 has become an accepted method to select patients for cardiac transplantation. Some investigators have suggested that the addition of exercise hemodynamic measurements can further enhance risk stratification because these measurements may identify patients with a noncardiac limitation to exercise.Methods and Results Accordingly, we performed maximal bicycle exercise with respiratory gas analysis and hemodynamic measurements in 65 patients (47 men, 18 women) 53+/-10 years old (mean+/-SD) who underwent a transplant evaluation at Columbia Presbyterian Medical Center. Skeletal muscle oxygenation of the vastus lateralis during exercise was assessed with near-infrared spectroscopy. Exercise hemodynamic, ventilatory, and muscle oxygenation measurements were obtained in all patients. For each subject, a linear correlation was derived between VO2 and pulmonary artery saturation (PA SaO(2)). The slope of this relationship and a theoretical VO2maX at a PA SaO(2) of 0% (VO2 intercept) was derived. Baseline measurements were left ventricular ejection fraction, 22+/-9%; pulmonary capillary wedge pressure (PCWP), 16+/-10 mm Hg; cardiac index (CI), 2.1+/-0.5 L . min(-1) . m(-2); and PA SaO(2), 53+/-8%. The cardiac output response to exercise was categorized as normal or abnormal by comparison to the linear equation of peak VO2 versus peak cardiac output as described by Higginbotham. Exercise measurements were peak VO2, 12.1+/-3.0 mL . kg(-1) . min(-1); VO2 intercept, 19.1+/-5.5 mL . kg(-1) . min(-1); PCWP, 31+/-11 mm Hg: CI, 3.8+/-1.3 L . min(-1) . m(-2), and PA SaO(2), 27+/-9%. Only 6% of patients exhibited a normal cardiac output response to exercise. Multivariate analysis was performed with peak VO2, VO2 intercept, skeletal muscle oxygenation at end exercise, and peak exercise hemodynamic variables. Only left ventricular stroke work and left ventricular stroke work index were shown to be predictive of survival.Conclusions Addition of exercise hemodynamic measurements to noninvasive metabolic stress testing minimally improves risk prognostication in patients with severe heart failure.