Hourly Ambient Air Pollution and Icd Detected Ventricular Arrhythmias in St. Louis, Mo, Usa

Rich, D. Q.; Schwartz, Jules I.; Kim, M H; Osborn, Jeffrey S.; Dockery, Douglas W.

doi:10.1097/00001648-200309001-00089

Cited by 1 publication

(2 citation statements)

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“…Several implantable cardioverter defibrillator (ICD) studies have shown associations between ambient air pollution and ICD discharge, which is automatically activated to terminate major ventricular arrhythmias (Peters et al 2000;Rich et al 2005Rich et al , 2006Dockery et al 2005). In patients with stable ischemic heart disease, air pollution affects cardiac repolarization properties, as evidenced by a significant increase in QT duration, in the variability of Twave complexity in response to increases in organic carbon (Henneberger et al, 2005;Yue et al, 2007), and in T-wave alternans (TWA) magnitude (Zanobetti et al 2009).…”

Section: Caps and Ventricular Arrhythmiasmentioning

confidence: 99%

“…Both short-term (Pope et al 2006) and long-term (Pope et al 2004) exposures to daily concentrations of ambient particles result in an increased incidence of acute cardiovascular events, namely, unstable angina pectoris (Pope et al 2006), myocardial infarction (Peters et al 2001;D'Ippoliti et al 2003;Zanobetti and Schwartz 2005), life-threatening ventricular arrhythmias (Peters et al 2000;Dockery et al 2005;Rich et al 2005), myocardial ischemia (Pekkanen et al 2002;Gold et al 2005;Mills et al 2007), and stroke (Lokken et al 2009).…”

Section: Introductionmentioning

confidence: 99%

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

Bartoli

Godleski

Verrier

2010

Air Qual Atmos Health

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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 Twave alternans, an index of susceptibility to lifethreatening arrhythmias, which can be employed clinically to evaluate the impact of air pollution on cardiovascular risk.

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