Oliveira Rudolf K F, Faria-Urbina Mariana, Maron Bradley A, Santos Mario, Waxman Aaron B, Systrom David M
1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
2 Heart & Vascular Center, Brigham and Women's Hospital, Boston, MA, USA.
Pulm Circ. 2017 Jul-Sep;7(3):654-665. doi: 10.1177/2045893217709025. Epub 2017 Jun 8.
Borderline resting mean pulmonary arterial pressure (mPAP) is associated with adverse outcomes and affects the exercise pulmonary vascular response. However, the pathophysiological mechanisms underlying exertional intolerance in borderline mPAP remain incompletely characterized. In the current study, we sought to evaluate the prevalence and functional impact of exercise pulmonary hypertension (ePH) across a spectrum of resting mPAP's in consecutive patients with contemporary resting right heart catheterization (RHC) and invasive cardiopulmonary exercise testing. Patients with resting mPAP <25 mmHg and pulmonary arterial wedge pressure ≤15 mmHg (n = 312) were stratified by mPAP < 13, 13-16, 17-20, and 21-24 mmHg. Those with ePH (n = 35) were compared with resting precapillary pulmonary hypertension (rPH; n = 16) and to those with normal hemodynamics (non-PH; n = 224). ePH prevalence was 6%, 8%, and 27% for resting mPAP 13-16, 17-20, and 21-24 mmHg, respectively. Within each of these resting mPAP epochs, ePH negatively impacted exercise capacity compared with non-PH (peak oxygen uptake 70 ± 16% versus 92 ± 19% predicted, P < 0.01; 72 ± 13% versus 86 ± 17% predicted, P < 0.05; and 64 ± 15% versus 82 ± 19% predicted, P < 0.001, respectively). Overall, ePH and rPH had similar functional limitation (peak oxygen uptake 67 ± 15% versus 68 ± 17% predicted, P > 0.05) and similar underlying mechanisms of exercise intolerance compared with non-PH (peak oxygen delivery 1868 ± 599 mL/min versus 1756 ± 720 mL/min versus 2482 ± 875 mL/min, respectively; P < 0.05), associated with chronotropic incompetence, increased right ventricular afterload and signs of right ventricular/pulmonary vascular uncoupling. In conclusion, ePH is most frequently found in borderline mPAP, reducing exercise capacity in a manner similar to rPH. When borderline mPAP is identified at RHC, evaluation of the pulmonary circulation under the stress of exercise is warranted.
临界静息平均肺动脉压(mPAP)与不良预后相关,并影响运动时的肺血管反应。然而,临界mPAP患者运动不耐受的病理生理机制仍未完全明确。在本研究中,我们试图通过对连续接受当代静息右心导管检查(RHC)和有创心肺运动试验的患者,评估不同静息mPAP水平下运动性肺动脉高压(ePH)的患病率及其功能影响。静息mPAP<25 mmHg且肺动脉楔压≤15 mmHg的患者(n = 312),根据mPAP水平分为<13、13 - 16、17 - 20和21 - 24 mmHg四组。将发生ePH的患者(n = 35)与静息性毛细血管前肺动脉高压(rPH;n = 16)患者以及血流动力学正常的患者(非PH;n = 224)进行比较。静息mPAP为13 - 16、17 - 20和21 - 24 mmHg时,ePH的患病率分别为6%、8%和27%。在每个静息mPAP区间内,与非PH患者相比,ePH对运动能力有负面影响(预测的峰值摄氧量分别为70±16% vs 92±19%,P<0.01;72±13% vs 86±17%,P<0.05;64±15% vs 82±19%,P<0.001)。总体而言,与非PH患者相比,ePH和rPH具有相似的功能受限(预测的峰值摄氧量分别为67±15% vs 68±17%,P>0.05)以及相似的运动不耐受潜在机制(峰值氧输送分别为1868±599 mL/min vs 1756±720 mL/min vs 2482±875 mL/min;P<0.05),与变时性功能不全、右心室后负荷增加以及右心室/肺血管解耦的迹象有关。总之,ePH最常见于临界mPAP患者,其降低运动能力的方式与rPH相似。当在RHC检查中发现临界mPAP时,有必要评估运动应激状态下的肺循环情况。