Cardiovascular effects of air pollution: what to measure in ECG?
Epidemiologic evidence indicates that air pollution adversely affects the cardiovascular system, leading to increased cardiovascular morbidity and mortality. However, the mechanisms of such an association are unknown. Although potential mechanisms of deleterious effects of air pollution may involve response of the respiratory system, immunologic response, or coagulation abnormalities, the cardiovascular system seems to be the common end point of these pathways. Cardiovascular response to any stress (which may include air pollution) is a consequence of a complex interplay between the autonomic nervous system governing centrally mediated control of the cardiovascular system, a myocardial substrate (current state of the myocardium) altered in the course of disease processes, and myocardial vulnerability leading to arrhythmogenic or ischemic response. Through the use of standard electrocardiograms (ECGs), exercise ECG testing, and long-term ambulatory ECG monitoring, modern electrocardiology makes a valuable contribution to understanding the different mechanistic factors involved in the increase in adverse cardiovascular events due to air pollution. Heart rate variability analysis can provide quantitative insight into the autonomic response of the cardiovascular system to air pollution. Analysis of ventricular repolarization in an ECG (both duration and morphology) gives valuable information about the status and dynamic behavior of myocardium, reflecting myocardial substrate and vulnerability. ST-segment analysis of ECGs is used routinely to monitor the magnitude of ischemia and could be used to monitor subtle changes in the myocardium in subjects exposed to air pollution. Comprehensive analysis of ECG parameters describing the influence of the autonomic nervous system, the role of myocardial substrate, and the contribution of myocardial vulnerability could and should be employed in air pollution studies, especially as those mechanistic components have been proven to contribute to increased cardiovascular morbidity and mortality in general.
Zareba
W
W
Heart Research, Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA. heartwz@heart.rochester.edu
Nomura
A
A
Couderc
J P
JP
D000393:Air Pollutants / Q000009:adverse effects*; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000503:physiopathology; D004562:Electrocardiography; D006801:Humans
D000393:Air Pollutants