Air pollution and ST-elevation myocardial infarction treated with primary percutaneous coronary angioplasty: A direct correlation
Introduction
Over the last years, different studies have suggested that death and hospitalization for cardiovascular (CV) causes are associated with both short- and long-term air pollution exposure [1], [2]. However, the relationships between air pollutant concentration levels and admission for primary percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI) have never been assessed. Air pollution could be defined as a heterogeneous complex mixture of particulate matter (PM), gasses and liquids. In the past, some of these pollutants have been investigated as triggering factors for CV disease (CVD), such as nitrogen dioxide (NO2), carbon monoxide (CO), particulate matter (PM) (both PM10 and PM2.5) and sulfur dioxide (SO2) [3]. In particular, previous studies have demonstrated an association between air pollution and AMI, heart failure exacerbation, stroke and ventricular arrhythmias [4], [5], [6]. However, the impact of air pollution on CVD is more complex to assess. Indeed, air pollution is a dynamic event since the different concentration levels of these substances change throughout days, months and seasons. Moreover, some meteorological variables, as air temperature and atmospheric pressure (AP), could significantly influence their air concentration levels. As well known, STEMI typically involves plaque rupture, thrombus formation and coronary artery occlusion. In this regard, it has already been demonstrated that exposure to PM2.5 is associated to inflammation, enhanced thrombosis, autonomic imbalance and vascular dysfunction [1], [7]. Furthermore, PM size seems to be related with both CV morbidity and mortality [8], [9].
In the present study, using four consecutive years of data on STEMI patients, admitted in our institution, and same day ambient air pollutant concentrations, we want to verify the hypothesis that the increased concentrations of these substances, are associated with an increased incidence of STEMI and related primary PCI.
Section snippets
Study population
We retrospectively reviewed the medical and instrumental data of 4 consecutive years (1st January 2012 to 1st January 2016) to identify patients admitted in our third referral center for primary percutaneous coronary intervention (PCI) due to STEMI. Diagnosis and treatment of STEMI was made according to the current European guidelines on the management of AMI [10]. We defined STEMI as a new ST-segment elevation at 12-lead electrocardiogram ≥ 2 mm in contiguous chest leads and/or ST elevation ≥ 1 mm
Results
During the study period, 678 patients met our inclusion criteria (518 males and 178 females, mean age 67.35 ± 11.80 years). Conversely, a total of 48 patients were excluded from the study because they did not live in our province during the 7 days before the acute CV event or they came to our institution from the nearest province which did not have a 24-hour cath lab service. The general characteristics of the population are shown in Table 1. At baseline, previous CAD and dyslipidaemia were present
Discussion
To the best of our knowledge, this is the first study that assesses the relationship between the incidence of STEMI treated with primary PCI and air pollutant concentration levels. Our results showed that there exists a direct and significant correlation between the number of daily STEMI patients and the NO2, PM10 and O3 air concentration levels of the same day. Despite that the aim of our study is slightly different, our findings partially confirm those showed in the study by Wang et al.,
Disclosures
The authors report no relationships that could be construed as a conflict of interest.
References (19)
- et al.
Circadian rhythms of angina: similarity to circadian rhythms of myocardial infarction, ischemic ST segment depression, and sudden cardiac death: the Amlodipine Angina Study Group
Am. Heart J.
(1989) - et al.
Ambient fine particulate air pollution triggers ST-elevation myocardial infarction, but not non-ST elevation myocardial infarction: a case-crossover study
Part. Fibre Toxicol.
(2014) - et al.
Long-term exposure to air pollution is associated with survival following acute coronary syndrome
Eur. Heart J.
(2013) - et al.
Short-term exposure to fine particulate matter air pollution is preferentially associated with the risk of ST-segment elevation acute coronary events
J. Am. Heart Assoc.
(2015) - et al.
Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association
Circulation
(2004) - et al.
Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases
JAMA
(2006) - et al.
The effect of particulate air pollution on emergency admissions for myocardial infarction: a multicity case-crossover analysis
Environ. Health Perspect.
(2005) - et al.
Air pollution and hospital admissions for ischemic and hemorrhagic stroke among medicare beneficiaries
Stroke
(2005) - et al.
Increased particulate air pollution and the triggering of myocardial infarction
Circulation
(2001)
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Dr. Roncon takes responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.