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      Fine Particulate air Pollution is Associated with Higher Vulnerability to Atrial Fibrillation—The APACR Study

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          Abstract

          The acute effects and the time course of fine particulate pollution (PM 2.5) on atrial fibrillation/flutter (AF) predictors, including P-wave duration, PR interval duration, and P-wave complexity, were investigated in a community-dwelling sample of 106 nonsmokers. Individual-level 24-h beat-to-beat electrocardiogram (ECG) data were visually examined. After identifying and removing artifacts and arrhythmic beats, the 30-min averages of the AF predictors were calculated. A personal PM 2.5 monitor was used to measure individual-level, real-time PM 2.5 exposures during the same 24-h period, and corresponding 30-min average PM 2.5 concentration were calculated. Under a linear mixed-effects modeling framework, distributed lag models were used to estimate regression coefficients (βs) associating PM 2.5 with AF predictors. Most of the adverse effects on AF predictors occurred within 1.5–2 h after PM 2.5 exposure. The multivariable adjusted βs per 10-µg/m 3 rise in PM 2.5 at lag 1 and lag 2 were significantly associated with P-wave complexity. PM 2.5 exposure was also significantly associated with prolonged PR duration at lag 3 and lag 4. Higher PM 2.5 was found to be associated with increases in P-wave complexity and PR duration. Maximal effects were observed within 2 h. These findings suggest that PM 2.5 adversely affects AF predictors; thus, PM 2.5 may be indicative of greater susceptibility to AF.

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          Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

          C. Pope, Richard Burnett, George Thurston … (2004)
          Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.
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            Risk factors for stroke and efficacy of antithrombotic therapy in atrial fibrillation. Analysis of pooled data from five randomized controlled trials.

            S Connolly, MD Ezekowitz, RG Hart … (1994)
            Atrial fibrillation is associated with an increased risk of ischemic stroke. Data on individual patients were pooled from five recently completed randomized trials comparing warfarin (all studies) or aspirin (the Atrial Fibrillation, Aspirin, Anticoagulation Study and the Stroke Prevention in Atrial Fibrillation Study) with control in patients with atrial fibrillation. The purpose of the analysis was to (1) identify patient features predictive of a high or low risk of stroke, (2) assess the efficacy of antithrombotic therapy in major patient subgroups (eg, women), and (3) obtain the most precise estimate of the efficacy and risks of antithrombotic therapy in atrial fibrillation. For the warfarin-control comparison there were 1889 patient-years receiving warfarin and 1802 in the control group. For the aspirin-placebo comparison there were 1132 patient-years receiving aspirin and 1133 receiving placebo. The daily dose of aspirin was 75 mg in the Atrial Fibrillation, Aspirin, Anticoagulation Study and 325 mg in the Stroke Prevention in Atrial Fibrillation Study. To monitor warfarin dosage, three studies used prothrombin time ratios and two used international normalized ratios. The lowest target intensity was a prothrombin time ratio of 1.2 to 1.5 and the highest target intensity was an international normalized ratio of 2.8 to 4.2. The primary end points were ischemic stroke and major hemorrhage, as assessed by each study. At the time of randomization the mean age was 69 years and the mean blood pressure was 142/82 mm Hg. Forty-six percent of the patients had a history of hypertension, 6% had a previous transient ischemic attack or stroke, and 14% had diabetes. Risk factors that predicted stroke on multivariate analyses in control patients were increasing age, history of hypertension, previous transient ischemic attack or stroke, and diabetes. Patients younger than 65 years who had none of the other predictive factors (15% of all patients) had an annual rate of stroke of 1.0%, 95% confidence interval (CI) 0.3% to 3.0%. The annual rate of stroke was 4.5% for the control group and 1.4% for the warfarin group (risk reduction, 68%; 95% CI, 50% to 79%). The efficacy of warfarin was consistent across all studies and subgroups of patients. In women, warfarin decreased the risk of stroke by 84% (95% CI, 55% to 95%) compared with 60% (95% CI, 35% to 76%) in men. The efficacy of aspirin was not as consistent. The risk reduction with 75 mg of aspirin in the Atrial Fibrillation, Aspirin, Anticoagulation Study was 18% (95% CI, 60% to 58%), and with 325 mg of aspirin in the Stroke Prevention in Atrial Fibrillation Study the risk reduction was 44% (95% CI, 7% to 66%). When both studies were combined the risk reduction was 36% (95% CI, 4% to 57%). The annual rate of major hemorrhage (intracranial bleeding or a bleed requiring hospitalization or 2 units of blood) was 1.0% for the control group, 1.0% for the aspirin group, and 1.3% for the warfarin group. In these five randomized trials warfarin consistently decreased the risk of stroke in patients with atrial fibrillation (a 68% reduction in risk) with virtually no increase in the frequency of major bleeding. Patients with atrial fibrillation younger than 65 years without a history of hypertension, previous stroke or transient ischemic attack, or diabetes were at very low risk of stroke even when not treated. The efficacy of aspirin was less consistent. Further studies are needed to clarify the role of aspirin in atrial fibrillation.
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              Inhalation of fine particulate air pollution and ozone causes acute arterial vasoconstriction in healthy adults.

              Robert D Brook, Jeffrey Brook, Bruce Urch … (2002)
              Fine particulate air pollution and ozone are associated with increased cardiovascular events. To help explain the mechanism behind these observations, we investigated the effect of air pollution exposure on vascular function. Twenty-five healthy adults underwent a randomized, double-blind, crossover study comparing the vascular response to the 2-hour inhalation of approximately 150 microg/m(3) of concentrated ambient fine particles (CAP) plus ozone (120 ppb) versus the response to the inhalation of filtered air. High-resolution vascular ultrasonography was used to measure alterations in brachial artery diameter, endothelial-dependent flow-mediated dilatation (FMD) and endothelial-independent nitroglycerin-mediated dilatation (NMD). Exposure to CAP plus ozone caused a significant brachial artery vasoconstriction compared with filtered air inhalation (-0.09+/-0.15 mm versus +0.01+/-0.18 mm, P=0.03). There were no significant differences in FMD (+0.29+/-4.11% versus -0.03+/-6.63%, P=0.88), NMD (+3.87+/-5.43% versus +3.46+/-7.92%, P=0.83), or blood pressure responses between exposures. Short-term inhalation of fine particulate air pollution and ozone at concentrations that occur in the urban environment causes acute conduit artery vasoconstriction.
              Article 0 comments Cited 198 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Toxicol Environ Health A
                Journal ID (publisher-id): uteh
                Title: Journal of Toxicology and Environmental Health. Part a
                Publisher: Taylor & Francis
                ISSN (Print): 1528-7394
                ISSN (Electronic): 1087-2620
                Publication date (Electronic): 8 April 2011
                Publication date (Print): June 2011
                Volume: 74
                Issue: 11
                Pages: 693-705
                Affiliations
                1Department of Public Health Sciences, Penn State University College of Medicine, Hershey, Pennsylvania
                2Departments of Epidemiology and Medicine, Gillings School of Global Public Health and School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina
                3Sleep Research & Treatment Center, Department of Psychiatry, Penn State University College of Medicine, Hershey, Pennsylvania
                4Department of Cardiovascular Sciences, Brody School of Medicine, and the East Carolina Heart Institute at East Carolina University, Greenville, North Carolina, USA
                Author notes
                Address correspondence to Duanping Liao, MD, PhD, Department of Public Health Sciences, Penn State University College of Medicine, 600 Centerview Dr. Suite 2200, A210, Hershey, PA 17033, USA. E-mail: dliao@ 123456psu.edu
                Article
                DOI: 10.1080/15287394.2011.556056
                PMC ID: 3082849
                PubMed ID: 21480044
                SO-VID: 475b9e85-824f-484a-9627-19f6ff572130
                Copyright © © 2011 Taylor & Francis
                License:

                This is an open access article distributed under the Supplemental Terms and Conditions for iOpenAccess articles published in Taylor & Francis journals , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 8 September 2010
                Date accepted : 14 November 2010
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Toxicology
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                ScienceOpen disciplines: Toxicology

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