慢性阻塞性肺病患者在病情稳定和恶化期间的心血管风险时间动态:机制与影响综述》。

IF 2.7 3区 医学 Q2 RESPIRATORY SYSTEM
Sami O Simons, Amy B Heptinstall, Zoe Marjenberg, Jonathan Marshall, Hana Mullerova, Paola Rogliani, Clementine Nordon, Nathaniel M Hawkins
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引用次数: 0

摘要

简介:慢性阻塞性肺疾病(COPD)的加重是导致严重心血管(CV)事件的风险因素,在加重的症状阶段过后的很长一段时间内,其风险仍会显著升高。人们对慢性阻塞性肺病急性发作与心血管疾病之间关系的病理生理学研究不足。我们的目标是回顾慢性阻塞性肺病恶化增加心血管事件风险的机制,并了解这种风险的时间性:方法:在包括肺病专家和心脏病专家在内的主题专家的指导下,我们进行了一次务实而有针对性的文献综述,重点是确定截至 2023 年 6 月的近期高影响力论文:大量相互关联的机制是慢性阻塞性肺病患者在稳定状态下肺部和心脏解剖和功能螺旋式恶化的基础。反过来,由于通气/灌注不匹配、氧供需失衡、氧化应激、全身炎症、高凝状态、动态过度充气、肺动脉高压和交感神经激活等原因,慢性阻塞性肺疾病恶化可能会在症状期及症状期之后引发心血管事件。然而,我们没有发现任何一项研究探讨了病情恶化导致心血管事件持续风险的机制:我们的综述发现,慢性阻塞性肺病加重期间和之后的多种动态和相互作用的病理生理机制会增加各种心脏事件的风险,但对于急性加重后的确切长期机制却知之甚少,无法解释无症状阶段之后持续增加的心血管事件风险。需要进一步确定静态和动态基质的时间变化特征,以便更好地了解病情加重后发生心血管事件的不同风险因素和风险期。此外,应不失时机地实施指南指导下的心肺疗法;预防病情恶化和强化治疗传统的心血管疾病风险因素应成为慢性阻塞性肺疾病管理的重点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Temporal Dynamics of Cardiovascular Risk in Patients with Chronic Obstructive Pulmonary Disease During Stable Disease and Exacerbations: Review of the Mechanisms and Implications.

Introduction: Exacerbations of chronic obstructive pulmonary disease (COPD) are risk factors for severe cardiovascular (CV) events, with the risk remaining significantly elevated long after the symptomatic phase of the exacerbation. The pathophysiology underpinning the relationship between acute events of both COPD and CV diseases has been understudied. Our objectives were to review the mechanisms by which COPD exacerbations increase the risk of CV events and understand the temporality of this risk.

Methods: A pragmatic and targeted literature review was conducted with a focus on identifying recent, high-impact papers up to June 2023, guided by insights from subject matter experts including pulmonologists and cardiologists.

Results: A substantial number of inter-related mechanisms underpin the spiral of anatomical and functional deterioration of lung and heart affecting COPD patients during stable state. In turn, an exacerbation of COPD may trigger a CV event, during and beyond the symptomatic phase, due to ventilation/perfusion mismatch, oxygen supply-demand imbalance, oxidative stress, systemic inflammation, hypercoagulable state, dynamic hyperinflation, pulmonary hypertension, and sympathetic activation. However, no study was identified that explored the mechanisms by which an exacerbation confers a sustained risk of CV event.

Conclusion: While our review identified multiple dynamic and interacting pathophysiological mechanisms during and after an exacerbation of COPD that contribute to increasing the risk of a wide range of cardiac events, little is known regarding the precise long-term mechanisms after acute exacerbation to explain the persistent increased CV event risk beyond the symptomatic phase. The temporal changes in static and dynamic substrates need further characterization to better understand the different risk factors and risk periods for a CV event following the onset of an exacerbation. Moreover, guideline-directed cardiopulmonary therapies should be implemented at every opportunity; preventing exacerbations and intensively treating traditional CV risk factors should be a focus in COPD management.

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来源期刊
CiteScore
4.80
自引率
10.70%
发文量
372
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed journal of therapeutics and pharmacology focusing on concise rapid reporting of clinical studies and reviews in COPD. Special focus will be given to the pathophysiological processes underlying the disease, intervention programs, patient focused education, and self management protocols. This journal is directed at specialists and healthcare professionals
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