Mechanisms mediating adverse effects of air pollution on cardiovascular hemodynamic function and vulnerability to cardiac arrhythmias

Epidemiologic studies indicate an association between airborne particulate matter and cardiovascular morbidity and mortality. However, the underlying pathophysiologic mechanisms require further investigation. This review examines insights derived from large animal inhalation studies on systemic and coronary hemodynamic function and susceptibility to cardiac arrhythmias. We present evidence of acute cardiovascular alterations in chronically instrumented or anesthetized large animals exposed to concentrated ambient particles. Significant changes were observed in a number of clinically relevant variables. These included elevations in arterial blood pressure and reductions in myocardial perfusion during coronary occlusion that resulted in the exacerbation of ischemic parameters, such as ST-segment elevation and vasoconstriction. The involvement of sympathetic nerve activity was implicated by the fact that alpha-adrenergic blockade with prazosin significantly blunted the vasoconstrictor effects. Alterations in baroreceptor function during air particulate exposure were also substantial. Enhanced susceptibility to both atrial and ventricular arrhythmias was demonstrated. These studies with clinically relevant large animal models underscore the importance of the role of air particulate pollution in inducing adverse effects on cardiovascular function and warrant further exploration of specific components of air pollution as well as the physiologic triggers that lead to cardiovascular events. New clinically applicable research tools have evolved, particularly heart rate turbulence, a noninvasive measure of baroreceptor function, and T-wave alternans, an index of susceptibility to life-threatening arrhythmias, which can be employed clinically to evaluate the impact of air pollution on cardiovascular risk.