Environmental Triggers of Acute Coronary Syndromes

HomeCirculationVol. 145, No. 24Environmental Triggers of Acute Coronary Syndromes Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBEnvironmental Triggers of Acute Coronary Syndromes Nicholas L. Mills, MD, PhD and C. Arden Pope, PhD Nicholas L. MillsNicholas L. Mills Correspondence to: Nicholas L Mills, MD, PhD, BHF/University Centre for Cardiovascular Science, The University of Edinburgh, Edinburgh EH16 4SA, United Kingdom. Email E-mail Address: [email protected] https://orcid.org/0000-0003-0533-7991 BHF Centre for Cardiovascular Science, University of Edinburgh, United Kingdom (N.L.M.). Usher Institute, University of Edinburgh, United Kingdom (N.L.M.). Search for more papers by this author and C. Arden PopeC. Arden Pope https://orcid.org/0000-0002-4239-6686 Brigham Young University, Provo, UT (C.A.P.). Search for more papers by this author Originally published13 Jun 2022https://doi.org/10.1161/CIRCULATIONAHA.122.059861Circulation. 2022;145:1761–1763This article is a commentary on the followingHourly Air Pollutants and Acute Coronary Syndrome Onset in 1.29 Million PatientsArticle, see p 1749The term “acute coronary syndrome” comprises a range of presentations from unstable angina to myocardial infarction and sudden cardiac death, one that emerged as a direct consequence of improved understanding of the pathogenesis of atherothrombosis.1 We now appreciate that coronary artery disease is a dynamic process involving plaque vulnerability, fibrinolytic function, and platelet activation responsible for the sudden transition from an apparently stable state to a potentially life-threatening acute event.2 This understanding has culminated in effective and clinically meaningful personal and public health measures to prevent acute coronary syndromes.Physical, Psychological, and Environmental Triggers of Acute Coronary SyndromeIn clinical practice, the trigger that initiates this transition to an acute coronary syndrome is not often apparent. Multiple physical and psychological stressors have been described, from the strenuous exertion of shoveling snow or firefighting to severe emotional distress during natural disasters.3,4 However, in most acute coronary syndromes, the period before onset is unremarkable, and the event is apparently unprovoked. Although physical or emotional stressors may be more apparent, the role of environmental triggers is likely to be underappreciated, because not all sources of environmental stress are overt or recognized by the patient or their physician.It is in this context that the findings from Chen and colleagues5 linking transient exposure to environmental air pollutants with the onset of acute coronary syndrome represents an important advance in our understanding. They conducted a time-stratified case-crossover study linking the Chinese Cardiovascular Association database, which includes information regarding the timing of symptom onset in >1.2 million consecutive patients with acute coronary syndrome from 2239 hospitals to hourly air pollution measurements from the National Urban Air Quality Platform. This study design compares air pollution levels for each person in the hours before symptom onset with levels of pollution in 4 control periods at the same hour and day of the week at which the event did not occur. Because each patient acts as their own control, the potential for confounding from demographic, socioeconomic, and some behavioral risk factors is minimized.The investigators observed consistent associations between an increase in fine particulate matter (PM2.5), NO2, SO2, and CO in the preceding 24-hour period and the onset of symptoms of acute coronary syndrome. These associations were strongest for increases in air pollution levels in the hours immediately before symptom onset and were consistent in patients with unstable angina and myocardial infarction with or without ST-segment elevation. These findings add meaningfully to a body of evidence suggesting that exposure to daily environmental stressors, such as air pollution and road traffic, may trigger acute coronary events.The first observation of an association between PM2.5 and myocardial infarction was reported >20 years ago.6 In 772 patients from the greater Boston area, an increase in PM2.5 levels of 25 μg/m3 in the preceding 2 hours was associated with the onset of symptoms of myocardial infarction (odds ratio, 1.48 [95% CI, 1.09–2.02]). Likewise, in a small cohort from Augsburg, Germany, an association was found between exposure to road traffic and the onset of myocardial infarction (odds ratio, 2.92 [95% CI, 2.22–3.83]).7 Not all studies have been able to validate these early reports. For example, a study of 79 889 patients in the United Kingdom observed small increases in the risk of myocardial infarction 1 to 6 hours after exposure but lower risk at longer lags and no net excess risk over a 72-hour period.8Novel Insights From Linking Health and Environmental Data at ScaleThe scale, scope, and rigor of the study by Chen et al5 provides new insights. First, as the largest study to date, including 3 times more hospitals than there were patients in the first report from Boston,6 the estimates of risk are more precise, which is helpful to provide context for patients. Second, the large sample size enabled subgroup analyses to explore susceptibility and effect modification. Associations were similar in men and women and in those with and without known coronary artery disease, but were modified by season, with stronger associations for all pollutants in the cold season. Third, rather than relying on aggregated hospital rates or admission times, access to patient-level data enabled an evaluation of the association between hourly changes in pollutant levels and the more relevant measure of time of symptom onset. Fourth, unlike previous reports that have evaluated associations with a single air pollutant, here, the authors evaluated associations with all monitored pollutants, reporting no association for ozone and course particular matter. Sensitivity analyses demonstrated that associations were not confounded by collinearity between pollutants or other environmental exposures, such as air temperature or humidity. Last, this evaluation was performed in China, home to 6 of the world’s megacities, where residents are exposed to some of the highest levels of air pollution in the world. If exposure to air pollution triggers acute coronary syndromes, it is more likely to be apparent here. Despite the average hourly pollutant levels being substantially higher than the standards outlined in the new World Health Organization Global Air Quality Guidelines 2021,9 the associations were linear without apparent threshold, providing additional support for more stringent air-quality targets worldwide.Pathogenic Mechanisms Linking Air Pollution and Acute Coronary SyndromeObservational studies examining associations between exposure to air pollution and acute coronary syndromes are not without limitations, including imprecision in the measurement of exposure and potential confounding from other environmental and social factors. However, the breadth and consistency of the evidence from observational, experimental, and clinical studies make a compelling case that air pollution, in particular, from combustion sources and road traffic, contributes to the pathogenesis of acute coronary syndromes.10,11 PM2.5 and reactive gaseous pollutants promote acute adverse cardiovascular effects after translocation or diffusion into the circulation or through secondary mediators derived from proinflammatory pathways initiated in the lungs.10 Long-term exposure contributes to the progression of atherosclerosis, whereas short-term exposures may trigger acute events as a consequence of changes in blood pressure or autonomic function, vascular dysfunction, impaired fibrinolysis, or through systemic oxidative, inflammatory, and prothrombotic pathways.10 Evidence of the adverse vascular and atherogenic effects of exposure to air pollutants is at least as compelling as that from exposure to environmental tobacco smoke,12 but public health action on air pollution has not received the same attention. Interventions demonstrated that reducing exposure to environmental tobacco smoke through the banning of smoking in public places were associated with reductions in the incidence of acute coronary syndrome,13 and similar studies are needed to evaluate the impact of transitioning from petrochemical to electric engines and from fossil fuels to green energy sources.Implications for Patients and PolicyAir pollution is an important contributing factor to acute coronary syndromes, not only because of the risk associated with exposure to the individual but also because exposures are involuntary, affecting the entire population, and are modifiable through societal change. In the present analysis, an interquartile range increase in PM2.5, NO2, SO2, and CO over a 24-hour period, which occurs infrequently, was associated with small increases in the risk of acute coronary syndrome of between 1% and 4% across the population.5 In practice, risk to the individual may be higher or lower, but is likely to be concentrated in the subset of the population with coronary artery disease and vulnerable plaque.14 Whilst it is not possible to identify those who are truly susceptible in clinical practice, interventions to reduce risk of exposure to air pollution should focus on policies to reduce emissions and population exposure. Physicians should be aware that there is evidence that long-term exposure to air pollution contributes to the initiation and progression of coronary artery disease.10 For those with existing disease, short-term exposures are further associated with small increased risks of triggering an acute event. Whereas personal interventions to reduce exposure through facemasks or air filtration systems alter surrogate measures of cardiovascular health,15 they are only partially effective at reducing exposure to fine particulates or have no impact on gaseous pollutants. Given that there is limited evidence that interventions to reduce personal exposure to air pollution prevent adverse cardiovascular events, sensible advice for potentially susceptible individuals would be to avoid strenuous physical exertion when the levels of air pollution are high. With increasing availability of environmental and air-quality monitoring data through personal devices, common sense approaches to reducing risk are feasible.ConclusionsOur appreciation that the quality of the air we breathe influences our health is growing. The environment is an increasingly important issue for patients and the wider public. It is incumbent that we understand the strengths and limitations of evidence linking environmental exposures to coronary risk so that our patients receive appropriate advice and we promote health and economic policies to address these inherently modifiable risk factors.Article InformationSources of FundingDr Mills is supported by a Chair Award (CH/F/21/90010), Programme Grant (RG/20/10/34966), and a Research Excellent Award (RE/18/5/34216) from the British Heart Foundation.Disclosures Dr Mills reports research grants awarded to the University of Edinburgh from Abbott Diagnostics and Siemens Healthineers, and honoraria from Abbott Diagnostics, Siemens Healthineers, Roche Diagnostics, and LumiraDx. Dr Pope reports no conflicts.FootnotesCirculation is available at www.ahajournals.org/journal/circThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.For Sources of Funding and Disclosures, see page 1763.Correspondence to: Nicholas L Mills, MD, PhD, BHF/University Centre for Cardiovascular Science, The University of Edinburgh, Edinburgh EH16 4SA, United Kingdom. Email nick.[email protected]ac.ukReferences1. Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes (1).N Engl J Med. 1992; 326:242–250. doi: 10.1056/NEJM199201233260406CrossrefMedlineGoogle Scholar2. Falk E, Nakano M, Bentzon JF, Finn AV, Virmani R. Update on acute coronary syndromes: the pathologists’ view.Eur Heart J. 2013; 34:719–728. doi: 10.1093/eurheartj/ehs411CrossrefMedlineGoogle Scholar3. Mittleman MA, Mostofsky E. 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Ischemic heart disease events triggered by short-term exposure to fine particulate air pollution.Circulation. 2006; 114:2443–2448. doi: 10.1161/CIRCULATIONAHA.106.636977LinkGoogle Scholar15. Langrish JP, Li X, Wang S, Lee MM, Barnes GD, Miller MR, Cassee FR, Boon NA, Donaldson K, Li J, et al. Reducing personal exposure to particulate air pollution improves cardiovascular health in patients with coronary heart disease.Environ Health Perspect. 2012; 120:367–372. doi: 10.1289/ehp.1103898CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesHourly Air Pollutants and Acute Coronary Syndrome Onset in 1.29 Million PatientsRenjie Chen, et al. Circulation. 2022;145:1749-1760 June 14, 2022Vol 145, Issue 24 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.122.059861PMID: 35696455 Originally publishedJune 13, 2022 KeywordsEditorialsacute coronary syndromemyocardial infarctionstress, physiologicalair pollutionPDF download Advertisement SubjectsEpidemiologyRisk Factors