Increased Risk of Paroxysmal Atrial Fibrillation Episodes Associated with Acute Increases in Ambient Air Pollution

Rich, David Q.; Mittleman, Murray A.; Link, Mark S.; Schwartz, Joel; Luttmann‐Gibson, Heike; Catalano, Paul J.; Speizer, Frank E.; Gold, Diane R.; Dockery, Douglas W.

doi:10.1289/ehp.8371

Cited by 140 publications

(96 citation statements)

References 24 publications

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“…It has been reported that acute increases in ambient air pollution were associated with increased risk of paroxysmal AF episodes (30). Sarı et al (1) also showed that chronic CO exposure increased P max and Pwd durations.…”

Section: Discussionmentioning

confidence: 96%

Effects of acute carbon monoxide poisoning on the P-wave and QT interval dispersions

Hancı¹,

Ayoğlu²,

Yurtlu³

et al. 2011

Anadolu Kardiyol Derg

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ÖZETAmaç: Çalışmamızın amacı, akut karbonmonoksit (CO) zehirlenmesi olan hastalarda atriyal ileti ve ventriküler repolarizasyon homojenlik bozukluklarını P dalga dispersiyonu (PDD), ve QT dispersiyonu (QTd) aracılığı ile araştırılmasıdır. Yöntemler: Retrospektif ve vaka-kontrollü olarak planlanan çalışmamıza, 30 akut CO zehirlenmesi olgusu ile (Grup ACOP), 30 sağlıklı olgu (Grup C) dâhil edildi. Grup ACOP' da acil servise başvuru anında çekilmiş standart 12 derivasyonlu elektrokardiyografi (EKG) kayıtları değerlendirildi. EKG kayıtlarından PDD, QT aralığı, QTd süreleri belirlendi. Düzeltilmiş QT aralığı (QTc) ve QTc dispersiyonu (QTcd) süreleri Bazett formülü kullanılarak belirlendi. Grup ACOP' da ve Grup C' de EKG kaydı ile eş zamanlı olarak alınmış kan örneklerinden serum elektrolit değeri ile Grup ACOP' da COHb değerleri belirlendi. İstatistik analiz için bağımsız örneklerde t ve Ki-kare testleri kullanıldı. Bulgular: Gruplar arasında yaş, cinsiyet dağılımları, antropometrik ölçümleri, serum elektrolit düzeyleri PR ve QT süreleri açısından anlamlı farklılık yoktu. Grup ACOP'da PDD (56.33±17.11 msn'ye karşın 28.33±11.16 msn, p<0.001), ve QTd (63.33±26.69 msn'ye karşın 42.16±7.84 msn, p<0.001) süreleri Grup C'den anlamlı olarak daha uzundu. Ek olarak, QTc ve QTcd süreleri de Grup ACOP'da Grup C' den anlamlı olarak daha uzun saptandı (p<0.001). Sonuç: Akut CO zehirlenmesi olgularında uzamış PDD, QTc ve QTcd süreleri nedeniyle atriyal ve ventriküler aritmi riski yüksektir. Bu olguların yoğun bakım ünitelerindeki takibi sırasında, oluşabilecek atriyal ve ventriküler aritmilere karşı dikkatli olunmalıdır.(Anadolu Kardiyol Derg 2011 1: 48-52) Anahtar kelimeler: Akut karbonmonoksit zehirlenmesi, P dalga dispersiyonu, düzeltilmiş QT süresi, düzeltilmiş QT dispersiyonu ABSTRACT Objective: The aim of our study was to investigate atrial conduction and ventricular repolarization inhomogeneities using P-wave dispersion (Pwd) and QT dispersion (QTd) analyses in acute carbon monoxide (CO) poisoning. Methods: Sixty patients were retrospectively included in this case-controlled study. Thirty acute CO poisoning patients were assigned to the Group with acute CO poisoning (ACOP). Patients who did not have acute CO poisoning were assigned to the control group (Group C, n=30). Anthropometric measurement, body mass index, electrocardiogram (ECG) and serum electrolyte levels were recorded in all patients. Also, carboxyhemoglobin (COHb) levels were recorded in Group ACOP. Pwd, QT interval and QTd durations were measured. Corrected QT (QTc) and QTc dispersion (QTcd) intervals were determined with the Bazett formula. Independent samples t and Chi-square tests were used for statistical analysis. Results: No statistically significant difference was found between the age, gender distribution, anthropometric measurement, serum electrolytes, PR and QT durations between the groups. The Pwd (56.33±17.11 msec vs 28.33±11.16 msec, p<0.001) and QTd (63.33±26.69 msec vs 42.16±7.84 msec, p<0.001) were significantly longer in Group ACOP than in Grou...

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Section: Discussionmentioning

confidence: 96%

Effects of acute carbon monoxide poisoning on the P-wave and QT interval dispersions

Hancı¹,

Ayoğlu²,

Yurtlu³

et al. 2011

Anadolu Kardiyol Derg

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“…HRV has been used frequently in air pollution research as a signal of cardiovascular effect, and to explore for potential pathophysiological mechanisms by which air pollution may lead to cardiovascular mortality and morbidity. Epidemiological studies in susceptible populationsespecially panel study designs-have shown a relationship between air pollution and decreased HRV (Adar, et al 2007;Chan, et al 2004;Liao, et al 1999;Liao, et al 2004;Park, et al 2005) as well as increased cardiac arrhythmia with exposure to components of ambient particulate air pollution (Dockery, et al 2005;Peters, et al 2000;Rich, et al 2006;Sarnat, et al 2006). The previously observed effects of air pollutants on HRV and arrhythmia are not entirely consistent across studies.…”

Section: Discussionmentioning

confidence: 97%

Effects of diesel exhaust inhalation on heart rate variability in human volunteers

Peretz

Kaufman

Trenga

et al. 2008

Environmental Research

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Objectives-Particulate matter (PM) air pollution is associated with alterations in cardiac conductance and sudden cardiac death in epidemiological studies. Traffic-related air pollutants, including diesel exhaust (DE) may be at least partly responsible for these effects. In this experimental study we assessed whether short-term exposure to DE would result in alterations in heart rate variability (HRV), a non-invasive measure of autonomic control of the heart.Methods-In a double-blind, crossover, controlled-exposure study, 16 adult volunteers were exposed (at rest) in randomized order to filtered air (FA) and two levels of diluted DE (100 or 200 μg/m 3 of fine particulate matter) in two-hour sessions. Before, and at four time-points after each exposure we assessed HRV. HRV parameters assessed included both time domain statistics (standard deviation of N-N intervals (SDNN), and the square root of the mean of the sum of squared differences between successive N-N intervals (RMSSD)) and frequency domain statistics (high frequency power (HF), low frequency power (LF), and the LF/HF ratio).Results-We observed an effect at 3-hours after initiation of DE inhalation on the frequency domain statistics of HRV. DE at 200 μg/m 3 elicited an increase in HF power compared to FA (Δ=0.33; 95% CI: 0.01 to 0.7) and a decrease in LF/HF ratio (Δ=-0.74; 95% CI: -1.2 to -0.2). The effect of DE on HF power was not consistent among study participants. There was no DE-effect on time domain statistics and no significant DE effect on HRV in later time-points.Conclusions-We did not observe a consistent DE effect on the autonomic control of the heart in a controlled exposure experiment in young participants. Efforts are warranted to understand discrepancies between epidemiological and experimental studies of air pollution's impact on HRV.

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“…Rich et al (2006) recently provided evidence of a linkage between particulates and AF in human subjects. To examine this problem, we developed an experimental model with intratracheal insufflation using a Penn Century nebulizer and induced AF by stimulating the right vagus nerve in a closed-chest porcine model.…”

Section: Atrial Arrhythmiasmentioning

confidence: 99%

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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Increased Risk of Paroxysmal Atrial Fibrillation Episodes Associated with Acute Increases in Ambient Air Pollution

Cited by 140 publications

References 24 publications

Effects of acute carbon monoxide poisoning on the P-wave and QT interval dispersions

Effects of acute carbon monoxide poisoning on the P-wave and QT interval dispersions

Effects of diesel exhaust inhalation on heart rate variability in human volunteers

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

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