Comparative effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on the risk of pneumonia and severe exacerbations in patients with COPD

Lai, Chih‐Cheng; Wang, Yahui; Chen, Ming-Fong; Wang, Hao-Chien; Yu, Chong‐Jen; Chen, Likwang

doi:10.2147/copd.s158634

Cited by 36 publications

(35 citation statements)

References 20 publications

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“…Although uncommon, worsening airflow obstruction has been associated with ACEI treatment, leading to suggestions that these agents be used with caution or as a second-line in patients with COPD [158]. No such safety concerns have been reported with ARBs [158]; indeed, data from an observational cohort study among patients with COPD who used ACEIs or ARBs found that ARBs were associated with fewer COPD complications, including severe exacerbations, pneumonia and mortality, than ACEIs [122]. Although these findings require further confirmation, this may suggest that ARBs are a better choice for patients with COPD requiring treatment with a RAAS inhibitor compared with ACEIs [122].…”

Section: Renin-angiotensin-aldosterone System Inhibitors Aceis and Arbsmentioning

confidence: 99%

Cardiovascular disease and COPD: dangerous liaisons?

2018

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Chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) frequently occur together and their coexistence is associated with worse outcomes than either condition alone. Pathophysiological links between COPD and CVD include lung hyperinflation, systemic inflammation and COPD exacerbations. COPD treatments may produce beneficial cardiovascular (CV) effects, such as long-acting bronchodilators, which are associated with improvements in arterial stiffness, pulmonary vasoconstriction, and cardiac function. However, data are limited regarding whether these translate into benefits in CV outcomes. Some studies have suggested that treatment with long-acting β2-agonists and long-acting muscarinic antagonists leads to an increase in the risk of CV events, particularly at treatment initiation, although the safety profile of these agents with prolonged use appears reassuring. Some CV medications may have a beneficial impact on COPD outcomes, but there have been concerns about β-blocker use leading to bronchospasm in COPD, which may result in patients not receiving guideline-recommended treatment. However, there are few data suggesting harm with these agents and patients should not be denied β-blockers if required. Clearer recommendations are necessary regarding the identification and management of comorbid CVD in patients with COPD in order to facilitate early intervention and appropriate treatment.

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Section: Renin-angiotensin-aldosterone System Inhibitors Aceis and Arbsmentioning

confidence: 99%

Cardiovascular disease and COPD: dangerous liaisons?

2018

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“…In chronic obstructive lung disease (COPD), patients treated with ARBs (compared to those on ACEi) had less severe exacerbations, fewer exacerbations overall, lower mortality, lower mechanical ventilation requirements, and fewer hospitalizations. [72] Moreover, veterans over 65 years old that were on ARBs before and during their hospitalization for pneumonia had decreased mortality when compared to patients without such treatment. [73] Acute Lung Injury…”

Section: Chronic Lung Diseasementioning

confidence: 99%

Understanding the renin–angiotensin–aldosterone–SARS-CoV axis: a comprehensive review

et al. 2020

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ImportanceCoronavirus disease 2019 (COVID-19), the disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been declared a global pandemic with significant morbidity and mortality since first appearing in Wuhan, China, in late 2019. As many countries are grappling with the onset of their epidemics, pharmacotherapeutics remain lacking. The window of opportunity to mitigate downstream morbidity and mortality is narrow but remains open. The renin–angiotensin–aldosterone system (RAAS) is crucial to the homeostasis of both the cardiovascular and respiratory systems. Importantly, SARS-CoV-2 utilises and interrupts this pathway directly, which could be described as the renin–angiotensin–aldosterone–SARS-CoV (RAAS–SCoV) axis. There exists significant controversy and confusion surrounding how anti-hypertensive agents might function along this pathway. This review explores the current state of knowledge regarding the RAAS–SCoV axis (informed by prior studies of SARS-CoV), how this relates to our currently evolving pandemic, and how these insights might guide our next steps in an evidence-based manner.ObservationsThis review discusses the role of the RAAS–SCoV axis in acute lung injury and the effects, risks and benefits of pharmacological modification of this axis. There may be an opportunity to leverage the different aspects of RAAS inhibitors to mitigate indirect viral-induced lung injury. Concerns have been raised that such modulation might exacerbate the disease. While relevant preclinical, experimental models to date favour a protective effect of RAAS–SCoV axis inhibition on both lung injury and survival, clinical data related to the role of RAAS modulation in the setting of SARS-CoV-2 remain limited.ConclusionProposed interventions for SARS-CoV-2 predominantly focus on viral microbiology and aim to inhibit viral cellular injury. While these therapies are promising, immediate use may not be feasible, and the time window of their efficacy remains a major unanswered question. An alternative approach is the modulation of the specific downstream pathophysiological effects caused by the virus that lead to morbidity and mortality. We propose a preponderance of evidence that supports clinical equipoise regarding the efficacy of RAAS-based interventions, and the imminent need for a multisite randomised controlled clinical trial to evaluate the inhibition of the RAAS–SCoV axis on acute lung injury in COVID-19.

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“…A smaller Korean study showed reduced pneumonia risk in elderly patients (aged <70 years) with chronic obstructive pulmonary disease (COPD) treated with ACEIs or ARBs [75]. A retrospective analysis of 215,225 American patients revealed that treatment with ACEIs or ARBs slowed the progression of pulmonary complications in COPD patients [76]. The analysis of the medical records of 182 ARDS patients showed an increased survival rate in patients treated with ACEIs or ARBs [77].…”

Section: Pharmacological Inhibition Of Ace and At1r In Pulmonary Disementioning

confidence: 99%

Renin–Angiotensin System: An Important Player in the Pathogenesis of Acute Respiratory Distress Syndrome

Hrenak

Šimko

2020

IJMS

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Acute respiratory distress syndrome (ARDS) is characterized by massive inflammation, increased vascular permeability and pulmonary edema. Mortality due to ARDS remains very high and even in the case of survival, acute lung injury can lead to pulmonary fibrosis. The renin–angiotensin system (RAS) plays a significant role in these processes. The activities of RAS molecules are subject to dynamic changes in response to an injury. Initially, increased levels of angiotensin (Ang) II and des-Arg9-bradykinin (DABK), are necessary for an effective defense. Later, augmented angiotensin converting enzyme (ACE) 2 activity supposedly helps to attenuate inflammation. Appropriate ACE2 activity might be decisive in preventing immune-induced damage and ensuring tissue repair. ACE2 has been identified as a common target for different pathogens. Some Coronaviruses, including SARS-CoV-2, also use ACE2 to infiltrate the cells. A number of questions remain unresolved. The importance of ACE2 shedding, associated with the release of soluble ACE2 and ADAM17-mediated activation of tumor necrosis factor-α (TNF-α)-signaling is unclear. The roles of other non-classical RAS-associated molecules, e.g., alamandine, Ang A or Ang 1–9, also deserve attention. In addition, the impact of established RAS-inhibiting drugs on the pulmonary RAS is to be elucidated. The unfavorable prognosis of ARDS and the lack of effective treatment urge the search for novel therapeutic strategies. In the context of the ongoing SARS-CoV-2 pandemic and considering the involvement of humoral disbalance in the pathogenesis of ARDS, targeting the renin–angiotensin system and reducing the pathogen’s cell entry could be a promising therapeutic strategy in the struggle against COVID-19.

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Comparative effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on the risk of pneumonia and severe exacerbations in patients with COPD

Cited by 36 publications

References 20 publications

Cardiovascular disease and COPD: dangerous liaisons?

Cardiovascular disease and COPD: dangerous liaisons?

Understanding the renin–angiotensin–aldosterone–SARS-CoV axis: a comprehensive review

Renin–Angiotensin System: An Important Player in the Pathogenesis of Acute Respiratory Distress Syndrome

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