Risk of Stroke and Post-Stroke Adverse Events in Patients with Exacerbations of Chronic Obstructive Pulmonary Disease

Lin, Chao-Shun; Shih, Chun Chuan; Yeh, Chun Chieh; Hu, Chaur‐Jong; Chung, Chi-Li; Chen, Ta-Liang; Liao, Chien-Chang

doi:10.1371/journal.pone.0169429

Cited by 14 publications

(17 citation statements)

References 49 publications

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“…However, in a study using Taiwan's National Health Insurance Research Database, a comparison cohort of 1918 adults with COPD exacerbations, 3836 adults with COPD no exacerbations, and 7672 adults without COPD who were frequency matched by age and sex, were selected. 84 Patients with exacerbations had increased stroke incidence (adjusted HR 1.28, 95% CI 1.03-1.59) and post-stroke mortality (OR 1.34, 95% CI 1.20-1.52) and complications, including, epilepsy and pneumonia. In a study that assessed the prevalence of COPD among hospitalized stroke patients in the National Inpatient Sample, a nationally representative dataset of US hospital admissions between January 2004 and December 2009, 12% of the hospitalized stroke patients have COPD.…”

Section: Primary Studiesmentioning

confidence: 95%

<p>Insights into Chronic Obstructive Pulmonary Disease as Critical Risk Factor for Cardiovascular Disease</p>

Almagro¹,

Boixeda²,

Díez-Manglano³

et al. 2020

COPD

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In patients with chronic obstructive pulmonary disease (COPD), cardiovascular comorbidities are highly prevalent and associated with considerable morbidity and mortality. This coincidence is increasingly seen in the context of a "cardiopulmonary continuum" rather than being simply attributed to shared risk factors, in particular, cigarette smoking. Both disease entities are centrally linked to systemic inflammation as well as aging, arterial stiffness, and several common biomarkers that led to the development of pulmonary hypertension, left ventricular diastolic dysfunction, atherosclerosis, and reduced physical activity and exercise capacity. For these reasons, COPD should be considered an independent factor of high cardiovascular risk, and efforts should be directed to early identification of cardiovascular disease (CVD) in COPD patients. Assessment of the overall cardiovascular risk is especially important in patients with severe exacerbation episodes, and the same therapeutic target levels for glycosylated hemoglobin, low-density lipoprotein cholesterol (LDL-C), or blood pressure than those recommended by clinical practice guidelines for patients at high cardiovascular risk, should be achieved. In this review, we will discuss the most recent evidence of the role of COPD as a critical cardiovascular risk factor and try to find new insights and potential prevention strategies for this disease.

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Section: Primary Studiesmentioning

confidence: 95%

<p>Insights into Chronic Obstructive Pulmonary Disease as Critical Risk Factor for Cardiovascular Disease</p>

Almagro¹,

Boixeda²,

Díez-Manglano³

et al. 2020

COPD

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“…Cigarette smoking is also a major cause of chronic obstructive pulmonary disease (COPD), accounting for more than 95% of cases in industrialized countries 5 . Recent studies have shown that strokes are more prevalent in COPD patients compared with the general population 6–8 , and clinical studies have revealed that COPD is linked to worse stroke outcomes including mortality 9,10 . Given smoking is an established risk factor for stroke and is linked to worse stroke outcomes the association between COPD and stroke may be largely dependent on exposure to cigarette smoke 6 .…”

Section: Introductionmentioning

confidence: 99%

Cigarette smoke extract exacerbates hyperpermeability of cerebral endothelial cells after oxygen glucose deprivation and reoxygenation

Bernard

Vlahos

et al. 2019

Sci Rep

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Cigarette smoking is a risk factor for stroke and is linked to stroke severity. Previous studies have shown that cigarette smoke extract (CSE) triggers endothelial dysfunction in vitro by initiating oxidative stress and/or an inflammatory response. In addition, cerebral endothelial dysfunction (particularly at the level of the blood-brain barrier [BBB]) contributes to stroke pathogenesis. Therefore, we hypothesized that cigarette smoking may influence stroke, at least in part, by exacerbating ischaemia-induced BBB disruption. To test this, we examined the effect of CSE on the permeability of cerebral endothelial cells exposed to oxygen glucose deprivation and reoxygenation (OGD + RO). We found that the loss of BBB integrity following ischaemic/reperfusion-like conditions was significantly worsened by CSE. Despite this being associated with increased mRNA expression of Nox catalytic subunits, reactive oxygen species (ROS) levels were however markedly lower. Furthermore, this occurred in association with elevated expression of antioxidant enzymes (SOD1, SOD2, and Gpx-1), suggesting an antioxidant defence response. Lastly, we found that CSE significantly upregulated mRNA expression of cytokines (IL-6 and TGF-β). Collectively, these results show that acute exposure to CSE worsens BBB disruption caused by OGD + RO, however, this is not linked to elevated ROS levels but may involve inflammatory mechanisms.

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“…Recent studies show that the risk of stroke is 20% greater in COPD patients compared to the general population, and this risk is estimated to be 7-fold higher following an exacerbation of COPD [ 21 , 22 ]. There is also some evidence to suggest that there is a relationship between COPD and worse stroke outcomes such as mortality, pneumonia, epilepsy, length of hospital stay and also intensive care unit care [ 23 ]. COPD is an independent risk factor for mortality among patients with stroke [ 24 ], and stroke patients with COPD are at an increased risk of aspiration [ 25 ], which is a leading cause of death following a stroke.…”

Section: Introductionmentioning

confidence: 99%

“…However, no causal mechanism has been established between COPD and worse outcomes following a stroke. Heightened levels of systemic inflammation and oxidative stress may contribute to increased stroke severity and the occurrence of post-stroke adverse events [ 20 , 23 ]. It is difficult to determine the causal mechanisms that may explain worse outcomes following a stroke in human COPD.…”

Section: Introductionmentioning

confidence: 99%

Prior cigarette smoke exposure does not affect acute post-stroke outcomes in mice

2019

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Chronic obstructive pulmonary disease (COPD) is currently the third leading cause of death globally and is characterized by airflow limitation that is progressive and not fully reversible. Cigarette smoking is the major cause of COPD. Fifty percent of deaths in the COPD population are due to a cardiovascular event and it is now recognised that COPD is a risk factor for stroke. Whether COPD increases stroke severity has not been explored. The aim of this study was to investigate whether functional and histological endpoints of stroke outcomes in mice after transient middle cerebral artery occlusion (tMCAo) were more severe in mice exposed to cigarette smoke (CS). 7-week-old male C57BL/6 mice were exposed to room air or CS generated from 9 cigarettes/day, 5 days/week for 2, 8 and 12 weeks. Following air or CS exposure, mice underwent tMCAO surgery with an ischaemic period of 30–40 min or sham surgery. Mice were euthanised 24 h following the induction of ischaemia and bronchoalveolar lavage fluid (BALF), lungs and brains collected. Mice exposed to CS for 2 weeks and subjected to a stroke had similar BALF macrophages to air-exposed and stroke mice. However, CS plus stroke mice had significantly more BALF total cells, neutrophils and lymphocytes than air plus stroke mice. Mice exposed to CS for 8 and 12 weeks had significantly greater BALF total cells, macrophages, neutrophils and lymphocytes than air-exposed mice, but stroke did not affect CS-induced BALF cellularity. Prior CS exposure did not worsen stroke-induced neurological deficit scores, reduced foregrip strength, infarct and oedema volumes. Collectively, we found that although CS exposure caused significant BALF inflammation, it did not worsen acute post-stroke outcomes in mice. This data suggests that while patients with COPD are at increased risk of stroke, it may not translate to COPD patients having more severe stroke outcomes.

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Risk of Stroke and Post-Stroke Adverse Events in Patients with Exacerbations of Chronic Obstructive Pulmonary Disease

Cited by 14 publications

References 49 publications

<p>Insights into Chronic Obstructive Pulmonary Disease as Critical Risk Factor for Cardiovascular Disease</p>

<p>Insights into Chronic Obstructive Pulmonary Disease as Critical Risk Factor for Cardiovascular Disease</p>

Cigarette smoke extract exacerbates hyperpermeability of cerebral endothelial cells after oxygen glucose deprivation and reoxygenation

Prior cigarette smoke exposure does not affect acute post-stroke outcomes in mice

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