Kim Chul-Ho, Jae Sae Young, Johnson Bruce D
Division of Cardiovascular Disease, Mayo Clinic, Rochester, Minn., USA.
The Health and Integrative Physiology Laboratory, University of Seoul, Seoul, Korea.
Pulse (Basel). 2014 May;1(3-4):143-51. doi: 10.1159/000360964.
In heart failure (HF), pulmonary hypertension (PH) is initially associated with a rise in the left ventricular filling pressure. PH is defined by pulmonary hemodynamic measurements including pulmonary capillary wedge pressure, mean pulmonary arterial pressure and pulmonary vascular resistance. Eventually, PH in HF may become more of a reactive process. Although the mechanism of the reactive PH development is not clearly understood, vascular dysfunction induced by remodeling, vasoactive substances and genetic variation appear to contribute significantly to this form of PH. Noninvasive cardiopulmonary exercise testing has been extensively utilized to assess disease severity in HF patients. It provides integrated information that is dependent on cardiopulmonary hemodynamics, lung mechanics, breathing pattern and strategy. In this review, we will discuss the mechanisms of PH development in HF and how noninvasive gas exchange measures obtained with submaximal exercise are influenced by PH in this population.
在心力衰竭(HF)中,肺动脉高压(PH)最初与左心室充盈压升高有关。PH通过包括肺毛细血管楔压、平均肺动脉压和肺血管阻力在内的肺血流动力学测量来定义。最终,HF中的PH可能更多地成为一个反应性过程。尽管反应性PH发展的机制尚不清楚,但由重塑、血管活性物质和基因变异引起的血管功能障碍似乎对这种形式的PH有显著贡献。无创心肺运动试验已被广泛用于评估HF患者的疾病严重程度。它提供了依赖于心肺血流动力学、肺力学、呼吸模式和策略的综合信息。在本综述中,我们将讨论HF中PH发展的机制,以及在这一人群中次极量运动时获得的无创气体交换测量如何受到PH的影响。