Cardiovascular effects of air pollution: What to measure in ECG?

Epidemiologic evidence indicates that air pollution adversely affects the c ardiovascular system, leading to increased cardiovascular morbidity and mor tality. However, the mechanisms of such an association are unknown. Althoug h potential mechanisms of deleterious effects of air pollution may involve response of the respiratory system, immunologic response, or coagulation ab normalities, the cardiovascular system seems to be the common end point of these pathways. Cardiovascular response to any stress (which may include ai r pollution) is a consequence of a complex interplay between the autonomic nervous system governing centrally mediated control of the cardiovascular s ystem, a myocardial substrate (current state of the myocardium) altered in the course of disease processes, and myocardial vulnerability leading to ar rhythmogenic or ischemic response. Through the use of standard electrocardi ograms (ECGs), exercise ECG testing, and long-term ambulatory ECG monitorin g, modern electrocardiology makes a valuable contribution to understanding the different mechanistic factors involved in the increase in adverse cardi ovascular events due to air pollution. Heart rate variability analysis can provide quantitative insight into the autonomic response of the cardiovascu lar system to air pollution. Analysis of ventricular repolarization in an E CG (both duration and morphology) gives valuable information about the stat us 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 m yocardium in subjects exposed to air pollution. Comprehensive analysis of E CG parameters describing the influence of the autonomic nervous system, the role of myocardial substrate, and the contribution of myocardial vulnerabi lity could and should be employed in air pollution studies, especially as t hose mechanistic components have been proven to contribute to increased car diovascular morbidity and mortality in general.