Impaired Pulmonary Diffusion in Heart Failure With Preserved Ejection Fraction.
Impaired Pulmonary Diffusion in Heart Failure With Preserved Ejection Fraction.
复制标题
DOI：
10.1016/j.jchf.2016.03.001
复制
发表时间：
2016-06
期刊：
影响因子：
--
通讯作者：
Borlaug BA
中科院分区：
文献类型：
--
作者：
Olson TP;Johnson BD;Borlaug BA
心力衰竭和保留射血分数（HFpEF）患者显示左心压力升高，但尚不清楚这如何影响肺气体传递或其在休息和运动时的决定因素。比较HFpEF受试者在休息和运动期间的气体交换测量与年龄和性别匹配的对照组。HFpEF患者（n=20）和对照组（n=26）完成平卧循环运动测试，同时测量通气和气体交换。在静息、低强度（20W）和峰值运动时测量肺一氧化碳弥散（DLCO）及其亚组分、肺毛细血管血容量（VC）和肺泡-毛细血管膜电导（DM）。经胸超声心动图测量脑卒中容量，计算心输出量。与对照组相比，HFpEF受试者表现出舒张功能受损和运动能力下降。HFpEF患者在休息时DLCO降低24%(11.0±2.3 vs 14.4±3.3 mL/mmHg/min, p<0.01)，与DM（18.1±4.9 vs 23.1±9.1 mL/mmHg/min, p=0.04）和VC（45.9±15.2）的降低相关。vs 58.9±16.2 mL, p=0.01)。与对照组相比，在运动的所有阶段，DLCO在HFpEF中的含量较低，但其决定因素表现出不同的反应。与对照组相比，低水平运动时，HFpEF受试者的VC相对增加更大，并伴有通气驱动增强和更严重的呼吸困难症状。在20W运动时，与对照组相比，HFpEF的DM明显减少。从20W到运动高峰，高强度pef组VC没有进一步升高，与DM降低同时，运动高峰DLCO降低30%（17.3±4.2 vs 24.7±7.1 mL/mmHg/min, p<0.01）。HFpEF患者在休息时，尤其是在运动时表现出肺功能和气体交换的改变，从而导致运动不耐受。改善气体扩散的新疗法可能有效改善HFpEF患者的运动耐受性。
Patients with heart failure and preserved ejection fraction (HFpEF) display elevation in left heart pressures, but it is unclear how this affects pulmonary gas transfer or its determinants at rest and during exercise. Compare measures of gas exchange at rest and during exercise in subjects with HFpEF to age and gender-matched controls. HFpEF patients (n=20) and controls (n=26) completed a recumbent cycle ergometry exercise test with simultaneous measurement of ventilation and gas exchange. Diffusion of the lungs for carbon monoxide (DLCO) and subcomponents, pulmonary capillary blood volume (VC) and alveolar-capillary membrane conductance (DM), were measured at rest, matched low-intensity (20W), and peak exercise. Stroke volume was measured by transthoracic echocardiography to calculate cardiac output. Compared to controls, HFpEF subjects displayed impaired diastolic function and reduced exercise capacity. HFpEF subjects demonstrated 24% lower DLCO at rest (11.0±2.3 vs 14.4±3.3 mL/mmHg/min, p<0.01), related to reductions in both DM (18.1±4.9 vs 23.1±9.1 mL/mmHg/min, p=0.04), and VC (45.9±15.2. vs 58.9±16.2 mL, p=0.01). DLCO was lower in HFpEF compared to controls in all stages of exercise, yet its determinants showed variable responses. With low-level exercise, HFpEF subjects demonstrated greater relative increases in VC, coupled with heightened ventilatory drive and more severe symptoms of dyspnea compared to controls. At 20W exercise, DM was markedly reduced in HFpEF compared to controls. From 20W to peak exercise, there was no further increase in VC in HFpEF subjects, which in tandem with reduced DM, led to 30% reduction in DLCO at peak exercise (17.3±4.2 vs 24.7±7.1 mL/mmHg/min, p<0.01). Patients with HFpEF display altered pulmonary function and gas exchange at rest and especially during exercise which contributes to exercise intolerance. Novel therapies that improve gas diffusion may be effective to improve exercise tolerance in patients with HFpEF.