A Case-Crossover Analysis of Out-of-Hospital Cardiac Arrest and Air Pollution

Ensor, Katherine B.; Raun, Loren; Persse, David

doi:10.1161/circulationaha.113.000027

Cited by 104 publications

(119 citation statements)

References 34 publications

(36 reference statements)

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“…Earthquakes have been reported to trigger sudden cardiac death (1007). Increased risks were seen within hours after elevations in air particulates and ozone (481). Even watching a stressful soccer match (1961) or rooting for the losing Super Bowl team seems to have its risks (920).…”

Section: Overview Of Atherogenesismentioning

confidence: 99%

Molecular Biology of Atherosclerosis

Hopkins

2013

Physiological Reviews

382

344

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At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-␣ and related family members leading to activation of NF-B; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.

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Section: Overview Of Atherogenesismentioning

confidence: 99%

Molecular Biology of Atherosclerosis

Hopkins

2013

Physiological Reviews

382

344

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“…39,40 An association between air pollution (fine particulate matter with an aerodynamic diameter <2.5 µm and ozone) and out-of-hospital cardiac arrest has recently been demonstrated. 41 SCDs account for most cardiac and many non-AIDS-related natural deaths in HIV-infected patients. 42 Lower socioeconomic status, depression, anxiety, social isolation and acute emotional stress have all been linked to increased SCD risk.…”

Section: Department Of Defense Cardiovascular Death Registry In the Umentioning

confidence: 99%

A Clinical Perspective on Sudden Cardiac Death

2016

Arrhythmia &Amp; Electrophysiology Review

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This article presents the epidemiology, aetiology and pathophysiology of sudden cardiac death. The modern management of survivors as well as of family members of victims is discussed, as are the relevant recommendations of guidelines prepared by learned societies. KeywordsOut-of-hospital cardiac arrest, sports-related sudden death, sudden cardiac death, sudden unexplained death syndrome Disclosure: The authors have no conflicts of interest to declare.

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“…There is suggestive evidence that short-term O 3 is associated with adverse cardiovascular effects (2)(3)(4). Epidemiological studies of long-term O 3 exposure are scarce, and the causal nature of associations uncertain (4,5).…”

mentioning

confidence: 99%

Long-Term Ozone Exposure and Mortality in a Large Prospective Study

Turner

Jerrett

Pope

et al. 2016

Am J Respir Crit Care Med

685

590

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Rationale: Tropospheric ozone (O 3 ) is potentially associated with cardiovascular disease risk and premature death. Results from longterm epidemiological studies on O 3 are scarce and inconclusive.Objectives: In this study, we examined associations between chronic ambient O 3 exposure and all-cause and cause-specific mortality in a large cohort of U.S. adults.Methods: Cancer Prevention Study II participants were enrolled in 1982. A total of 669,046 participants were analyzed, among whom 237,201 deaths occurred through 2004. We obtained estimates of O 3 concentrations at the participant's residence from a hierarchical Bayesian space-time model. Estimates of fine particulate matter (particulate matter with an aerodynamic diameter of up to 2.5 mm [PM 2.5 ]) and NO 2 concentrations were obtained from land use regression. Cox proportional hazards regression models were used to examine mortality associations adjusted for individual-and ecological-level covariates. Measurements and Main Results:In single-pollutant models, we observed significant positive associations between O 3 , PM 2.5 , and NO 2 concentrations and all-cause and cause-specific mortality. In two-pollutant models adjusted for PM 2.5 , significant positive associations remained between O 3 and all-cause (hazard ratio [HR] per 10 ppb, 1.02; 95% confidence interval [CI], 1.01-1.04), circulatory (HR, 1.03; 95% CI, 1.01-1.05), and respiratory mortality (HR, 1.12; 95% CI, 1.08-1.16) that were unchanged with further adjustment for NO 2 . We also observed positive mortality associations with both PM 2.5 (both near source and regional) and NO 2 in multipollutant models.Conclusions: Findings derived from this large-scale prospective study suggest that long-term ambient O 3 contributes to risk of respiratory and circulatory mortality. Substantial health and environmental benefits may be achieved by implementing further measures aimed at controlling O 3 concentrations.

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A Case-Crossover Analysis of Out-of-Hospital Cardiac Arrest and Air Pollution

Cited by 104 publications

References 34 publications

Molecular Biology of Atherosclerosis

Molecular Biology of Atherosclerosis

A Clinical Perspective on Sudden Cardiac Death

Long-Term Ozone Exposure and Mortality in a Large Prospective Study

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