Preventive cardiologyT-Wave Alternans, Air Pollution and Traffic in High-Risk Subjects
Section snippets
Methods
The study design has been previously described.3 Briefly, before discharge, we recruited a panel of patients with documented coronary artery disease from the greater Boston area (within Interstate 495, a 40-km radius of our central monitoring site) who had undergone percutaneous coronary intervention for acute coronary syndromes (acute myocardial infarctions or unstable angina pectoris) or for worsening stable coronary artery disease. We excluded those with atrial fibrillation and left bundle
Results
Table 1 lists the median and range for TWA-MAX and 0.5-hour averaged heart rate for the 48 subjects, who had a total of 5,830 0.5-hour observations. The range of values for TWA-MAX ≥75th percentile was 26 to 61 μV. At the first home visit, 13 of 48 subjects described ≥1 episode of pain or discomfort in their chest since hospital discharge; 11 of the 13 with any chest pain described chest pain at rest. Over the subsequent visits 2 to 4, as activity levels increased, when asked “Since we last saw
Discussion
In the first 1 to 2 weeks after a myocardial infarction, the American College of Cardiology and American Heart Association guidelines recommend avoiding driving, particularly under stressful circumstances such as heavy traffic.9 These recommendations are based on studies suggesting that stress,9 including the stress of driving in traffic, may increase the risk for post–myocardial infarction complications. Our findings suggest that the particulate pollution from traffic sources itself, not only
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Cited by (45)
Fine particle environmental pollution and cardiovascular diseases
2019, Metabolism: Clinical and ExperimentalCitation Excerpt :An observational study conducted in London suggested an association between air pollutant and activation of implantable cardioverter defibrillator [39]. T-wave alternans, which is a marker of cardiac electrical instability, was also increased after short-term exposure to traffic exhausts in patients with preexisting ischemic cardiopathy [40]. In a meta-analysis of 35 studies, rates of heart failure hospitalization or death increased by 2% per 10 μg/m3 in PM2.5 concentration, with strongest associations seen on the day of exposure.
A systematic review of cardiovascular responses associated with ambient black carbon and fine particulate matter
2019, Environment InternationalCitation Excerpt :These authors did not find consistent changes in T wave complexity across the Augsburg or Rochester panel studies. Zanobetti et al. (2009) reported a stronger association of T wave alternans ≥26 μV with BC than with PM2.5. Overall, the limited number of studies evaluated point to an effect of both BC and PM2.5 on ST segment depression while there was no consistent trend for the relationship of these pollutants with repolarizations abnormalities.
High level of source-specific particulate matter air pollution associated with cardiac arrhythmias
2019, Science of the Total EnvironmentCitation Excerpt :Similarly, Folino et al. (2017) reported that exposure to PM2.5 from air pollution mixtures with large contribution from non-industrial combustion was associated with higher risk of ventricular tachycardia. Studies also showed significant associations between ambient fossil fuel combustion-related pollutant exposures and reduced HRV (Dong et al., 2018; Weichenthal et al., 2014), prolonged QT interval (Baja et al., 2010), depressed ST-segment (Delfino et al., 2011), and increased T-wave alternans (Zanobetti et al., 2009). However, research on the potential impact of PM2.5 from coal burning on arrhythmic risks has been scarce, and our results are largely in line with existing evidence of anthropogenic activity related sources (coal burning, vehicle exhaust and secondary particles) on adverse cardiovascular events (Berger et al., 2018; Ostro et al., 2016; Thurston et al., 2005).
Proposed pathophysiologic framework to explain some excess cardiovascular death associated with ambient air particle pollution: Insights for public health translation
2016, Biochimica et Biophysica Acta - General SubjectsCitation Excerpt :Such changes in QT intervals and dynamics have been measured in man in response to ambient air pollutant exposures as well as during controlled human exposure studies [81–84]. In four cohorts of people with prevalent coronary heart disease short-term exposure to ambient air particle pollution increased heart rate [85], repolarization duration [85,86], T-wave morphology and variability [86], Tp-Te interval [87] and T-wave alternans [88]. In the Veterans Affairs Normative Aging Study, QTc interval prolongation has been observed among an aging adult population in relation to the black carbon content of the PM.
A structured review of panel studies used to investigate associations between ambient air pollution and heart rate variability
2016, Environmental ResearchCitation Excerpt :An additional 74 publications were found in reference lists of the selected papers and through inspection of relevant reviews of the literature. A total of 130 articles underwent full-text review, from which 97 were excluded for the following reasons: in 63 papers the selected heart rate variability indices of interest were not investigated (Baccarelli et al., 2011; Berger et al., 2006; Bind et al., 2012; Brook et al., 2011a, 2011b; Bruske et al., 2011; Chuang et al., 2008; de Hartog et al., 2003; Delfino et al., 2011, 2009, 2008, 2010; DeMeo et al., 2004; Dubowsky et al., 2006; Frampton et al., 2012; Gold et al., 2005; Goldberg et al., 2008, 2009; Hampel et al., 2011, 2010; He et al., 2010; Henneberger et al., 2005; Hertel et al., 2010; Hildebrandt et al., 2009; Hoffmann et al., 2012; Hou et al., 2012; Huttunen et al., 2012; Ibald-Mulli et al., 2004; Jacobs et al., 2012; Jansen et al., 2005; Lanki et al., 2008; Liao et al., 2011; Liu et al., 2009, 2007; Louwies et al., 2013; Luttmann-Gibson et al., 2010; Lux and Pope, 2009; Mar et al., 2005; Pekkanen et al., 2002; Peters et al., 2001, 2007; Ren et al., 2011; Rich et al., 2012b; Ruckerl et al., 2007a, 2006, 2009, 2007b; Sarnat et al., 2006; Schneider et al., 2008; Seaton et al., 1999; Sorensen et al., 2003; Stebbings and Hayes, 1976; Wellenius et al., 2013, 2007; Wu et al., 2013a, 2013b, 2012; Yue et al., 2007; Zanobetti et al., 2004, 2009; Zhao et al., 2013; Williams et al., 2012; Smargiassi et al., 2014); in six papers (Chan et al., 2005; Pope et al., 1999b, 1999a; Wu S. et al., 2011b; Wu C.F. et al., 2012; Davoodi et al., 2010; Sarnat et al., 2014) association were not investigated for the selected air pollutants whereas in five papers the exposure occurred indoor (Huang et al., 2014) or in occupational (Magari et al., 2001; Meier et al., 2014) or controlled (Devlin et al., 2003; Pope et al., 2011) exposure settings; in 11 papers the observation period was on only one day (Chahine et al., 2007; Chan et al., 2005; Chang et al., 2007; Chuang et al., 2005; 2007b Hampel et al., 2013; Jia et al., 2012; Magari et al., 2002; O’Neill et al., 2005; Park et al., 2005; Vallejo et al., 2006); in three papers more than one year elapsed between measurements of the outcome (Liao et al., 2004; Whitsel et al., 2009; Baja et al., 2013); in four studies a crossover design was used (Weichenthal et al., 2011; 2014; Laumbach et al., 2010; Huang et al., 2013). In addition, there were two papers published for each of four studies (Wheeler et al., 2006; de Hartog et al., 2009; Wu S. et al., 2010; McBride et al., 2011).
Black carbon exposure, oxidative stress markers and major adverse cardiovascular events in patients with acute coronary syndromes
2015, International Journal of Cardiology
This work was supported in part by Grant P01 ES009825, NIEHS-00002, from the National Institute of Environment Health Sciences, Research Triangle Park, North Carolina; Grant R832416-01-0 from the Environmental Protection Agency, Washington, District of Columbia.