Physiological aspects of cardiopulmonary dysanapsis on exercise in adults born preterm.
Physiological aspects of cardiopulmonary dysanapsis on exercise in adults born preterm.
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DOI：
10.1113/jp281848
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发表时间：
2022-03
影响因子：
5.5
通讯作者：
Lovering, Andrew T.
中科院分区：
文献类型：
--
作者：
Duke, Joseph W.;Lewandowski, Adam J.;Abman, Steven H.;Lovering, Andrew T.
关键词：
在过去的几十年里，早产儿围产期护理和呼吸管理的逐步改善提高了极低胎龄新生儿的存活率。然而，早产后的慢性肺部疾病支气管肺发育不良（BPD）的发病率没有改变。对早产成年人的长期随访研究显示，呼吸、心血管和心肺功能持续异常，可能导致运动能力降低。这些异常的根本原因尚不完全清楚，但我们假设，呼吸系统和心血管系统的不协调生长和发育是导致早产年轻人与足月出生的年轻人相比运动能力较低的主要结构特征。我们讨论了如何假设系统dysanapsis强调观察到的呼吸，心血管和心肺限制。具体而言，早产的成年人具有1）正常的肺容量，但气道较小，导致呼气气流限制和异常的呼吸力学，但不影响肺气体交换效率; 2）正常的总心脏大小，但较小的心腔，以及3）在某些情况下，肺动脉高压的证据，特别是在运动期间，表明尽管心输出量减少，但肺血管容量减少。我们推测，这些潜在的发育异常可能会加速正常的年龄相关的运动能力下降，通过呼吸，心血管和心肺功能的加速下降。最后，我们建议未来的研究领域，特别是需要从婴儿期到成年期的纵向和干预性研究，以更好地了解早产如何改变整个生命周期的运动能力。非常早产，即，在妊娠32周之前分娩，对新生儿的生活造成了挑战。婴儿期和成年期的特征是发育异常，导致肺和心血管功能障碍。呼吸功能（例如，呼气气流减少、机械呼吸限制）、心肺功能（例如，肺血管容量减少、肺血管压力和阻力增加）和心血管功能（例如，心室容积和心肌功能储备减少）的各个方面受损。综合起来，这些方面导致早产儿的有氧运动能力显著降低。这篇专题综述概述了已知和未知的生理因素，解释观察到的有氧运动能力。
Progressive improvements in perinatal care and respiratory management of preterm infants has resulted in increased survival of extremely low gestational age newborns over the past few decades. However, the incidence of bronchopulmonary dysplasia (BPD), the chronic lung disease after preterm birth, has not changed. Studies of the long-term follow-up of adults born preterm have shown persistent abnormalities of respiratory, cardiovascular, and cardiopulmonary function possibly leading to a lesser exercise capacity. The underlying causes of these abnormalities are incompletely known, but we hypothesize that dysanapsis, i.e., discordant growth and development, in the respiratory and cardiovascular systems is a central structural feature that leads to the lesser exercise capacity in young adults born preterm compared to those born at term. We discuss how the hypothesized system dysanapsis underscores the observed respiratory, cardiovascular, and cardiopulmonary limitations. Specifically, adults born preterm have 1) normal lung volumes but smaller airways that causes expiratory airflow limitation and abnormal respiratory mechanics but without impacts on pulmonary gas exchange efficiency; 2) normal total cardiac size but smaller cardiac chambers, and 3) in some cases, evidence of pulmonary hypertension particularly during exercise, suggesting a reduced pulmonary vascular capacity despite reduced cardiac output. We speculate that these underlying developmental abnormalities may accelerate the normal age-associated decline in exercise capacity, via an accelerated decline in respiratory, cardiovascular, and cardiopulmonary function. Finally, we suggest areas of future research, especially the need for longitudinal and interventional studies from infancy into adulthood to better understand how preterm birth alters exercise capacity across the lifespan. Very preterm birth, i.e., birth occurring prior to completion of 32 weeks of gestation, creates challenges to neonatal life. The period of infancy and adolescences is characterized by abnormal development leading to pulmonary and cardiovascular dysanapsis. Various aspects of respiratory (e.g. lesser expiratory airflow, mechanical ventilatory constraints), cardiopulmonary (e.g. reduced pulmonary vascular capacity, greater pulmonary vascular pressures and resistance), and cardiovascular (e.g. reduced ventricular volumes and myocardial functional reserve) function are impaired. In combination, these aspects lead to a significantly reduced aerobic exercise capacity in adults born preterm. This topical review outlines the known and unknown physiologic factors that explain the observed aerobic exercise capacity.