gms | German Medical Science

49. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds)
19. Jahrestagung der Schweizerischen Gesellschaft für Medizinische Informatik (SGMI)
Jahrestagung 2004 des Arbeitskreises Medizinische Informatik (ÖAKMI)

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie
Schweizerische Gesellschaft für Medizinische Informatik (SGMI)

26. bis 30.09.2004, Innsbruck/Tirol

Repolarization Changes Induced by Air Pollution in Ischemic Heart Disease Patients

Meeting Abstract (gmds2004)

  • corresponding author presenting/speaker Alexandra Henneberger - Ludwig-Maximilians-University of Munich, Munich, Deutschland
  • W. Zareba - Cardiology Unit, Department of Medicine, University of Rochester, New York, USA
  • A. Ibald-Mulli - Ludwig-Maximilians-University of Munich, Munich, Deutschland
  • R. Rückerl - Institute of Epidemiology, GSF-National Research Center for Environment and Health, Neuherberg, Deutschland
  • J. Cyrys - Ludwig-Maximilians-University of Munich, Munich, Deutschland
  • J.P. Couderc - Cardiology Unit, Department of Medicine, University of Rochester, New York, USA
  • B. Mykins - Cardiology Unit, Department of Medicine, University of Rochester, New York, USA
  • G. Woelke - Institute of Epidemiology, GSF-National Research Center for Environment and Health, Neuherberg, Deutschland
  • H.E. Wichmann - Ludwig-Maximilians-University of Munich, Munich, Deutschland
  • A. Peters - nstitute of Epidemiology, GSF-National Research Center for Environment and Health, Neuherberg, Deutschland

Kooperative Versorgung - Vernetzte Forschung - Ubiquitäre Information. 49. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 19. Jahrestagung der Schweizerischen Gesellschaft für Medizinische Informatik (SGMI) und Jahrestagung 2004 des Arbeitskreises Medizinische Informatik (ÖAKMI) der Österreichischen Computer Gesellschaft (OCG) und der Österreichischen Gesellschaft für Biomedizinische Technik (ÖGBMT). Innsbruck, 26.-30.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04gmds007

The electronic version of this article is the complete one and can be found online at:

Published: September 14, 2004

© 2004 Henneberger et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Epidemiologic studies report associations between particulate air pollution and cardiovascular morbidity and mortality [1], but the underlying pathophysiologic mechanisms still are unclear. Cardiac rhythm disorders are the leading cause of the hospital admissions for cardiovascular diseases. More than half of the deaths due to ischemia, myocardial infarction and cardiomyopathies are directly related to cardiac arrhythmias, and these deaths are usually sudden [2]. Myocardial substrate (myocardial damage due to coronary disease, infarction, or cardiomyopathy), the autonomic nervous system (sympathetic activation or/and parasympathetic withdrawal), and myocardial vulnerability (ventricular arrhythmias, repolarization dynamics) are believed to be key factors that contribute to the mechanism of arrhythmogenic conditions and arrhythmic death [3] and represent the so called "cardiac death triangle".


We tested the hypothesis that patients with pre-existing coronary heart disease experience changes in the repolarization parameters in association with high concentrations of particulate and gaseous air pollution. Novel measures of repolarization (e.g. T wave complexity) were used to investigate the underlying pathophysiological mechanisms leading to adverse reactions of the heart in response to air pollution.


A prospective panel study was conducted in Erfurt, East Germany, with 12 repeated ECG recordings in 56 males with ischemic heart disease.Hourly particulate (ultrafine particle counts (UFP, 0.01-0.1 µm), accumulation mode particle counts (ACP, 0.1-1.0 µm) and PM2.5 (mass of particles < 2.5 µm diameter), elemental (EC) and organic (OC) carbon) and gaseous (SO2, NO2, NO, CO) air pollution and meteorological data (air temperature, barometric pressure and relative humidity) were acquired. The following electrocardiogram (ECG)-parameters reflecting myocardial substrate and vulnerability were measured: QT duration (corrected for heart rate with Bazett formula), T wave amplitude, T wave complexity, and variability of T wave complexity. Generalized additive models (GAM) including pollutant and confounder variables were used for fixed effect regression analysis adjusting for subject, trend, weekday and meteorology with non-parametric smooth functions based on locally weighted least squares.Model building was done for each ECG variable separately. Model fit was based on the Akaike Information Criterion (AIC).Air pollution was measured in different time intervals before the ECG measurements because current knowledge on the underlying biological mechanisms supports an immediate as well as a cumulative response over 5 days.For every patient his individual 0-5, 6-11, 12-17, 18-23, 0-23 hours and 2-5 days of air pollution exposure before the ECG recording were used for analysis to look for immediate and delayed responses of the patients.


The study group consisted of 56 male patients at a mean age of 66±6 years (range, 52 to 76 years).The majority of patients had prior myocardial infarction and all patients had stable coronary artery disease.The patients were current non-smokers, but almost three-fourth were ex-smokers.

This longitudinal study showed that increased levels of particulate air pollution are associated with significant changes in ECG repolarization parameters reflecting myocardial substrate and vulnerability. The analyzed repolarization parameters showed different pollutant-specific responses although some of the measured particulate pollutants were highly correlated.In association with ACP, PM2.5 and OC concentrations for the whole 0-23 hours period before the recording, an increase in QTc could be seen, being significant especially for OC. T wave amplitude showed a significant decrease with UFP, ACP, PM2.5 and EC concentrations measured during 0-5 hours (only borderline for EC) and during 0-23 hours before the recording (significant only for UFP and ACP). Consistently with this finding, T wave complexity, a computerized measure of repolarization morphology, increased significantly in association with PM2.5 concentrations in the same time interval. The variability of T wave complexity also showed an immediate borderline increase with PM2.5 concentrations measured during the 0-5 and the 0-23 hours time interval before the ECG and a significant increase in association with OC and EC concentrations during the whole 24 hours prior to recording the ECG.


This study demonstrates that air pollution affects two components of the "cardiac death triangle", the myocardial substrate and myocardial vulnerability, assessed by repolarization parameters. Previous studies on the daily variation of particulate air pollution and heart rate variability in elderly subjects showed an increase in heart rate and a decrease in heart rate variability [4], [5] associated with particulate air pollution. Animal data support the concept that the autonomic nervous system may be a target for the adverse effects of air pollution [6], [7]. All these findings suggest that inhaled particles may affect the balance between the sympathetic and parasympathetic control of the heart, and promote a stress response that potentially leads to arrhythmias. The observed inhomogeneous reaction to the individual particle measuers for the analyzed repolarization parameters might point towards different action of air pollution components on the complex repolarization process [8]. It is very well conceivable that the combined effect of transient increases in blood coagulability [9], an acute-phase response [10], [11], an increase in blood viscosity [12] and a an immediate effect of air pollution on repolarization duration and morphology representing myocardial substrate and vulnerability, as suggested in this study, could precipitate adverse cardiac events especially in susceptible individuals.


The authors wish to thank Patricia Severski and Mark Andrews for their assistance with ECG data management and analysis.

The study is funded through the US Environmental Protection Agency STAR center grant R-827354 and the Focus-Network of Aerosols and Health, GSF. The Focus-Network of Aerosols and Health coordinates and focuses all GSF research on health effects and the characterization of aerosols. It comprises research projects of the GSF Institutes of Ecological Chemistry, Epidemiology, Inhalation Biology, Radiation Protection, and Toxicology at GSF.


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