38 research outputs found

    Acute Effects of Fine Particulate Air Pollution on Cardiac Arrhythmia: The APACR Study

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    Background: The mechanisms underlying the relationship between particulate matter (PM) air pollution and cardiac disease are not fully understood

    Acute Adverse Effects of Fine Particulate Air Pollution on Ventricular Repolarization

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    Background The mechanisms for the relationship between particulate pollution and cardiac disease are not fully understood. Objective We examined the effects and time course of exposure to fine particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) on ventricular repolarization of 106 nonsmoking adults who were living in communities in central Pennsylvania. Methods The 24-hr beat-to-beat electrocardiogram (ECG) data were obtained using a high-resolution 12-lead Holter system. After visually identifying and removing artifacts and arrhythmic beats, we summarized normal beat-to-beat QTs from each 30-min segment as heart rate (HR)-corrected QT measures: QT prolongation index (QTI), Bazett’s HR-corrected QT (QTcB), and Fridericia’s HR-corrected QT (QTcF). A personal PM2.5 monitor was used to measure individual-level real-time PM2.5 exposures for 24 hr. We averaged these data and used 30-min time-specific average PM2.5 exposures. Results The mean age of the participants was 56 ± 8 years, with 41% male and 74% white. The means ± SDs for QTI, QTcB, and QTcF were 111 ± 6.6, 438 ± 23 msec, and 422 ± 22 msec, respectively; and for PM2.5, the mean ± SD was 14 ± 22 μg/m3. We used distributed lag models under a framework of linear mixed-effects models to assess the autocorrelation-corrected regression coefficients (β) between 30-min PM2.5 and the HR-corrected QT measures. Most of the adverse ventricular repolarization effects from PM2.5 exposure occurred within 3–4 hr. The multivariable adjusted β (SE, p-value) due to a 10-μg/m3 increase in lag 7 PM2.5 on QTI, QTcB, and QTcF were 0.08 (0.04, p < 0.05), 0.22 (0.08, p < 0.01), and 0.09 (0.05, p < 0.05), respectively. Conclusions Our results suggest a significant adverse effect of PM2.5 on ventricular repolarization. The time course of the effect is within 3–4 hr of elevated PM2.5

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

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    The acute effects and the time course of fine particulate pollution (PM2.5) 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 PM2.5 monitor was used to measure individual-level, real-time PM2.5 exposures during the same 24-h period, and corresponding 30-min average PM2.5 concentration were calculated. Under a linear mixed-effects modeling framework, distributed lag models were used to estimate regression coefficients (βs) associating PM2.5 with AF predictors. Most of the adverse effects on AF predictors occurred within 1.5–2 h after PM2.5 exposure. The multivariable adjusted βs per 10-µg/m3 rise in PM2.5 at lag 1 and lag 2 were significantly associated with P-wave complexity. PM2.5 exposure was also significantly associated with prolonged PR duration at lag 3 and lag 4. Higher PM2.5 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 PM2.5 adversely affects AF predictors; thus, PM2.5 may be indicative of greater susceptibility to AF

    Acute effects of fine particulate air pollution on ST segment height: A longitudinal study

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    Background The mechanisms for the relationship between particulate air pollution and cardiac disease are not fully understood. Air pollution-induced myocardial ischemia is one of the potentially important mechanisms. Methods We investigate the acute effects and the time course of fine particulate pollution (PM2.5) on myocardium ischemic injury as assessed by ST-segment height in a community-based sample of 106 healthy non-smokers. Twenty-four hour beat-to-beat electrocardiogram (ECG) data were obtained using a high resolution 12-lead Holter ECG system. After visually identifying and removing all the artifacts and arrhythmic beats, we calculated beat-to-beat ST-height from ten leads (inferior leads II, III, and aVF; anterior leads V3 and V4; septal leads V1 and V2; lateral leads I, V5, and V6,). Individual-level 24-hour real-time PM2.5 concentration was obtained by a continuous personal PM2.5 monitor. We then calculated, on a 30-minute basis, the corresponding time-of-the-day specific average exposure to PM2.5 for each participant. Distributed lag models under a linear mixed-effects models framework were used to assess the regression coefficients between 30-minute PM2.5 and ST-height measures from each lead; i.e., one lag indicates a 30-minute separation between the exposure and outcome. Results The mean (SD) age was 56 (7.6) years, with 41% male and 74% white. The mean (SD) PM2.5 exposure was 14 (22) μg/m3. All inferior leads (II, III, and aVF) and two out of three lateral leads (I and V6), showed a significant association between higher PM2.5 levels and higher ST-height. Most of the adverse effects occurred within two hours after PM2.5 exposure. The multivariable adjusted regression coefficients β (95% CI) of the cumulative effect due to a 10 μg/m3 increase in Lag 0-4 PM2.5 on ST-I, II, III, aVF and ST-V6 were 0.29 (0.01-0.56) μV, 0.79 (0.20-1.39) μV, 0.52 (0.01-1.05) μV, 0.65 (0.11-1.19) μV, and 0.58 (0.07-1.09) μV, respectively, with all p < 0.05. Conclusions Increased PM2.5 concentration is associated with immediate increase in ST-segment height in inferior and lateral leads, generally within two hours. Such an acute effect of PM2.5 may contribute to increased potential for regional myocardial ischemic injury among healthy individuals

    Abstract P242: Abdominal Adipose Tissue Distribution and Metabolic Syndrome Burden in Adolescents - Penn State Child Cohort (PSCC) Study

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    Objectives: To investigate the association between abdominal adipose tissue distribution and metabolic syndrome burden in a population-based sample of adolescents. Methods: We used available data from 400 adolescents who completed the follow up examinations in the PSCC study. We used whole body low-dose dual energy absorptiometry (DXA) to assess and calculate the following abdominal and body fat distribution measures: Android/Gynoid Fat ratio, Android/whole body fat ratio, Gynoid/whole body fat ratio, visceral fat area, and subcutaneous fat area in the abdominal region. . Metabolic syndrome burden was assessed by using continuous metabolic syndrome score (cMetS) - the sum of the age and sex adjusted standardized residual (Z-score) of five established metabolic syndrome components: waist circumference, mean arterial pressure, homeostatic model assessment of insulin resistance (HOMA-IR), triglycerides, and HDL cholesterol. Linear regression models were used to data analysis. Results: The mean age was 16.9 yrs (SD=2.19), with 54% male and 77% white. The average cMets score was 0.04 SD (3.01). The regression coefficients on cMets score per one SD increase in abdominal adipose tissue measures are shown in Table 1. In summary, higher abdominal adipose tissue, especially in the android (visceral) area, of the abdomen is associated with higher cMetS score. Conclusion: Obesity, especially visceral obesity, is associated with higher metabolic syndrome burden in adolescent population, which may result in increased metabolic syndrome risk in adulthood. </jats:p

    Abstract P200: The Circadian Pattern of Cardiac Autonomic Modulation and its Correlates in Adolescents- Penn State Child Cohort (PSCC) Study

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    Objective: To examine the circadian pattern of cardiac autonomic modulation (CAM) and its correlates in a population-based sample of adolescents. Methods: We used the data from 400 adolescents who completed the follow up exam in the PSCC study. CAM was assessed by heart rate variability (HRV) analysis of beat-to-beat normal R-R intervals from a 24-hour (7:00 PM to 7:00 PM) ECG, on a 30-minute basis (48 segments/person). The HRV indices included frequency domain: [high and low frequency powers (HF, LF), and LF/HF ratio] and time domain: [standard deviation of normal RRs (SDNN), and the square root of the mean squared difference of successive normal RRs (RMSSD), and heart rate (HR)]. We used a cosine periodic model to estimate each participant’s circadian parameters: mean (M), amplitude (Â), and crescent time (θ). We then used mixed-effects models to calculate group level circadian pattern as the overall M, Â of the oscillation, and θ of the highest oscillation. Results: The mean age was 16.9 yrs (SD=2.2), with 54% male and 77% white. The mean BMI percentile is 61, with 16% were obese (BMI percentile ≥ 95). Overall, the parasympathetic modulation gradually increases from late afternoon throughout the evening, and reaches the peak amplitude around 3:00 AM, at which it gradually decrease throughout most of the daytime until late afternoon. The age, sex and race showed varying differences on the CAM circadian parameters. In contrast, obesity in adolescents had adverse effects on all three circadian parameters. Using HF (a reliable index of parasympathetic modulation) as an example, the circadian pattern of the entire sample, and stratified by obesity are shown in Figure 1. Conclusion: Circadian pattern of CAM can be quantified by three cosine parameters (M, Â, and θ). Obesity in adolescents is already associated with a CAM profile indicative of sympathetic overflow and reduced parasympathetic modulation, at all levels of the CAM circadian rhythm. </jats:p

    Abstract P105: Sleep Disordered Breathing and Cardiac Autonomic Modulation in Adolescents - Penn State Child Cohort (PSCC) Study

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    Objectives: To investigate the relationship between sleep disordered breathing (SDB) and cardiac autonomic modulation (CAM) in a population-based sample of adolescents. Methods: We used available data from 400 adolescents who completed the follow up examinations in the population-based PSCC study. 1-night polysomnography was used to assess apnea hypopnea index (AHI). AHI was used to define no-SDB (AHI&lt;1), mild SDB (1≤AHI&lt;5), and moderate SDB (AHI≥5). CAM was assessed by heart rate variability (HRV) analysis of beat-to-beat normal R-R intervals from a 39-hour high resolution Holter ECG. The HRV indices in frequency domain [high frequency power (HF), low frequency power (LF), and LF/HF ratio] and time domain [standard deviation of normal RR intervals (SDNN), and the square root of the mean squared difference of successive normal RR intervals (RMSSD), and heart rate (HR)] were calculated on a 30-minute basis (78 repeated measures). Mixed-effects models were used to assess the SDB and HRV relationship. Results: The mean age was 16.9 yrs (SD=2.19), with 54% male and 77% white. The mean (SD) AHI were 0.52 (0.26), 2.38 (1.03), and 12.27 (14.54) for no-, mild-, and moderate-SDB participants. The age, race, sex, and BMI percentile adjusted mean (SE) HRV indices across three SDB groups are presented in Table 1. In summary, sleep disordered breathing was associated with lower HRV and higher HR in this population-based adolescent sample, with a significant dose-response relationship. Conclusion: moderate SDB in adolescents is already associated with lower HRV, indicative of sympathetic activation and lower parasympathetic modulation, which has been associated with cardiac events in adults. </jats:p
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