Air Pollution, Heart Rate Variability, and Arrhythmia
Air Pollution, Heart Rate Variability, and Arrhythmia
Background: Decreased heart rate variability (HRV) has been associated with future cardiac morbidity and mortality and is often used as a marker of altered cardiac autonomic balance in studies of health effects of airborne particulate matter. Fewer studies have evaluated associations between air pollutants and cardiac arrhythmia.
Objectives: We examined relationships between cardiac arrhythmias, HRV, and exposures to airborne particulate matter.
Methods: We measured HRV and arrhythmia with ambulatory electrocardiograms in a cohort panel study for up to 235 hr per participant among 50 nonsmokers with coronary artery disease who were ≥ 71 years of age and living in four retirement communities in the Los Angeles, California, Air Basin. Exposures included hourly outdoor gases, hourly traffic-related and secondary organic aerosol markers, and daily size-fractionated particle mass. We used repeated measures analyses, adjusting for actigraph-derived physical activity and heart rate, temperature, day of week, season, and community location.
Results: Ventricular tachycardia was significantly increased in association with increases in markers of traffic-related particles, secondary organic carbon, and ozone. Few consistent associations were observed for supraventricular tachycardia. Particulates were significantly associated with decreased ambulatory HRV only in the 20 participants using ACE (angiotensin I–converting enzyme) inhibitors.
Conclusions: Although these data support the hypothesis that particulate exposures may increase the risk of ventricular tachycardia for elderly people with coronary artery disease, HRV was not associated with exposure in most of our participants. These results are consistent with previous findings in this cohort for systemic inflammation, blood pressure, and ST segment depression.
Decreased heart rate variability (HRV) has been associated with cardiac morbidity and mortality and is often used as a marker of autonomic dysfunction in the assessment of the impact of air pollution on cardiac autonomic control (Link and Dockery 2010). Associations also have been found between HRV and ischemia in coronary artery disease (CAD) patients who are monitored by ambulatory electrocardiograms (ECGs), including findings of asymptomatic ST segment depression indicative of cardiac ischemia (Vardas et al. 1996). Given that many patients with CAD already have decreased HRV, pollutant exposures that lead to further HRV decreases might be expected to precipitate adverse clinical events such as ventricular tachycardia and myocardial ischemia and infarction. Indeed, a number of recent air pollution studies have focused on CAD patients, although with mixed findings regarding associations between air pollutants and HRV (Barclay et al. 2009; Folino et al. 2009; Hampel et al. 2010; Schneider et al. 2010; Zanobetti et al. 2010). Nevertheless, in a recent review of the literature on particulate air pollution and cardiovascular outcomes, Brook et al. (2010) concluded that there was strong epidemiological evidence for an association between decreased HRV and short-term exposures to particulate matter (PM) air pollution in various populations, with the most consistent findings in older or clinically susceptible populations.
In contrast, Brook et al. (2010) also concluded that there was limited or weak epidemiological evidence for associations of cardiac arrhythmia with short-term exposures to PM. In another review, Link and Dockery (2010) suggested that there was evidence of an association of PM with cardiac arrhythmias, particularly ventricular arrhythmias, in patients with underlying cardiac disease. Studies published since those reviews had mixed results: He et al. (2011) reported a significant association between personal PM2.5 (PM with an aerodynamic diameter of ≤ 2.5 μm) exposure and premature ventricular contractions among 105 middle-aged participants using ambulatory ECGs, but only among participants without cardiovascular disease, and Mills et al. (2011) reported no "serious arrhythmias" or HRV effects in a randomized trial of dilute diesel exhaust exposure with 52 middle-aged participants. Little is known about possible mechanisms for PM effects on arrhythmia, although altered HRV, repolarization abnormalities, oxidative stress, and myocardial ischemia have been proposed as contributing factors (Link and Dockery 2010).
Between 2005 and 2007 we conducted a cohort panel study of acute cardiovascular outcomes with home-based ambient air pollution monitoring in the Los Angeles, California, Air Basin, where ambient air pollution is dominated by mobile sources. Our focus was on traffic-related ultrafine particles, which are particularly high in redox-active chemical components (Ayres et al. 2008; Verma et al. 2009) that are hypothesized to induce arrhythmias via lipid peroxidation, endothelial dysfunction, and other mechanisms involving oxidative stress (Griendling and FitzGerald 2003). In the present study, we used data from the same Los Angeles cohort to study the hypothesis that increased cardiac arrhythmia and decreased HRV are associated with exposure to PM.
Abstract and Introduction
Abstract
Background: Decreased heart rate variability (HRV) has been associated with future cardiac morbidity and mortality and is often used as a marker of altered cardiac autonomic balance in studies of health effects of airborne particulate matter. Fewer studies have evaluated associations between air pollutants and cardiac arrhythmia.
Objectives: We examined relationships between cardiac arrhythmias, HRV, and exposures to airborne particulate matter.
Methods: We measured HRV and arrhythmia with ambulatory electrocardiograms in a cohort panel study for up to 235 hr per participant among 50 nonsmokers with coronary artery disease who were ≥ 71 years of age and living in four retirement communities in the Los Angeles, California, Air Basin. Exposures included hourly outdoor gases, hourly traffic-related and secondary organic aerosol markers, and daily size-fractionated particle mass. We used repeated measures analyses, adjusting for actigraph-derived physical activity and heart rate, temperature, day of week, season, and community location.
Results: Ventricular tachycardia was significantly increased in association with increases in markers of traffic-related particles, secondary organic carbon, and ozone. Few consistent associations were observed for supraventricular tachycardia. Particulates were significantly associated with decreased ambulatory HRV only in the 20 participants using ACE (angiotensin I–converting enzyme) inhibitors.
Conclusions: Although these data support the hypothesis that particulate exposures may increase the risk of ventricular tachycardia for elderly people with coronary artery disease, HRV was not associated with exposure in most of our participants. These results are consistent with previous findings in this cohort for systemic inflammation, blood pressure, and ST segment depression.
Introduction
Decreased heart rate variability (HRV) has been associated with cardiac morbidity and mortality and is often used as a marker of autonomic dysfunction in the assessment of the impact of air pollution on cardiac autonomic control (Link and Dockery 2010). Associations also have been found between HRV and ischemia in coronary artery disease (CAD) patients who are monitored by ambulatory electrocardiograms (ECGs), including findings of asymptomatic ST segment depression indicative of cardiac ischemia (Vardas et al. 1996). Given that many patients with CAD already have decreased HRV, pollutant exposures that lead to further HRV decreases might be expected to precipitate adverse clinical events such as ventricular tachycardia and myocardial ischemia and infarction. Indeed, a number of recent air pollution studies have focused on CAD patients, although with mixed findings regarding associations between air pollutants and HRV (Barclay et al. 2009; Folino et al. 2009; Hampel et al. 2010; Schneider et al. 2010; Zanobetti et al. 2010). Nevertheless, in a recent review of the literature on particulate air pollution and cardiovascular outcomes, Brook et al. (2010) concluded that there was strong epidemiological evidence for an association between decreased HRV and short-term exposures to particulate matter (PM) air pollution in various populations, with the most consistent findings in older or clinically susceptible populations.
In contrast, Brook et al. (2010) also concluded that there was limited or weak epidemiological evidence for associations of cardiac arrhythmia with short-term exposures to PM. In another review, Link and Dockery (2010) suggested that there was evidence of an association of PM with cardiac arrhythmias, particularly ventricular arrhythmias, in patients with underlying cardiac disease. Studies published since those reviews had mixed results: He et al. (2011) reported a significant association between personal PM2.5 (PM with an aerodynamic diameter of ≤ 2.5 μm) exposure and premature ventricular contractions among 105 middle-aged participants using ambulatory ECGs, but only among participants without cardiovascular disease, and Mills et al. (2011) reported no "serious arrhythmias" or HRV effects in a randomized trial of dilute diesel exhaust exposure with 52 middle-aged participants. Little is known about possible mechanisms for PM effects on arrhythmia, although altered HRV, repolarization abnormalities, oxidative stress, and myocardial ischemia have been proposed as contributing factors (Link and Dockery 2010).
Between 2005 and 2007 we conducted a cohort panel study of acute cardiovascular outcomes with home-based ambient air pollution monitoring in the Los Angeles, California, Air Basin, where ambient air pollution is dominated by mobile sources. Our focus was on traffic-related ultrafine particles, which are particularly high in redox-active chemical components (Ayres et al. 2008; Verma et al. 2009) that are hypothesized to induce arrhythmias via lipid peroxidation, endothelial dysfunction, and other mechanisms involving oxidative stress (Griendling and FitzGerald 2003). In the present study, we used data from the same Los Angeles cohort to study the hypothesis that increased cardiac arrhythmia and decreased HRV are associated with exposure to PM.
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