Ambient fine particulate air pollution triggers ST-elevation myocardial infarction, but not non-ST elevation myocardial infarction: a case-crossover study.

Ambient fine particulate air pollution triggers ST-elevation myocardial infarction, but not non-ST elevation myocardial infarction: a case-crossover study.
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DOI:
10.1186/1743-8977-11-1
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发表时间:
2014-01-02
影响因子:
10
通讯作者:
Rich DQ
Rich DQ
中科院分区:
医学1区
文献类型:
--
作者:
Gardner B;Ling F;Hopke PK;Frampton MW;Utell MJ;Zareba W;Cameron SJ;Chalupa D;Kane C;Kulandhaisamy S;Topf MC;Rich DQ

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我们和其他人已经表明,在前几小时和几天内颗粒物空气污染物(PM)浓度的增加与心肌梗死的风险增加有关,但对空气污染与特定心肌梗死亚群(如st段抬高型心肌梗死(STEMI)和非st段抬高型心肌梗死(NSTEMI)之间的关系知之甚少。使用急性冠状动脉综合征STEMI (n = 338)和NSTEMI (n = 339)患者的数据和病例交叉方法,我们估计STEMI和NSTEMI的风险与前几小时和几天内环境细颗粒(<2.5 um)浓度、超细颗粒(10-100 nm)数量浓度和积聚模式颗粒(100-500 nm)数量浓度的增加有关。我们发现,急性冠状动脉综合征发病前1小时PM2.5浓度每增加7.1 μg/m3, STEMI风险显著增加18%,而细颗粒物浓度在发病前3、12和24小时增加的风险则较小,无显著增加。我们没有发现NSTEMI的模式。前1 ~ 96小时内超细颗粒和积聚模式颗粒数浓度四分位数范围增加与STEMI风险的估计均大于1.0,但无统计学意义。先前存在高血压的患者发生STEMI的风险与前一小时细颗粒浓度升高相关,明显高于无高血压的患者。急性冠脉综合征发病前1小时细颗粒物浓度升高与STEMI风险增加相关,但与NSTEMI无关。已有高血压和其他心血管疾病的患者尤其容易受到影响。需要进一步研究PM在如此快速的时间尺度内优先触发STEMI而非NSTEMI的机制。
We and others have shown that increases in particulate air pollutant (PM) concentrations in the previous hours and days have been associated with increased risks of myocardial infarction, but little is known about the relationships between air pollution and specific subsets of myocardial infarction, such as ST-elevation myocardial infarction (STEMI) and non ST-elevation myocardial infarction (NSTEMI). Using data from acute coronary syndrome patients with STEMI (n = 338) and NSTEMI (n = 339) and case-crossover methods, we estimated the risk of STEMI and NSTEMI associated with increased ambient fine particle (<2.5 um) concentrations, ultrafine particle (10-100 nm) number concentrations, and accumulation mode particle (100-500 nm) number concentrations in the previous few hours and days. We found a significant 18% increase in the risk of STEMI associated with each 7.1 μg/m3 increase in PM2.5 concentration in the previous hour prior to acute coronary syndrome onset, with smaller, non-significantly increased risks associated with increased fine particle concentrations in the previous 3, 12, and 24 hours. We found no pattern with NSTEMI. Estimates of the risk of STEMI associated with interquartile range increases in ultrafine particle and accumulation mode particle number concentrations in the previous 1 to 96 hours were all greater than 1.0, but not statistically significant. Patients with pre-existing hypertension had a significantly greater risk of STEMI associated with increased fine particle concentration in the previous hour than patients without hypertension. Increased fine particle concentrations in the hour prior to acute coronary syndrome onset were associated with an increased risk of STEMI, but not NSTEMI. Patients with pre-existing hypertension and other cardiovascular disease appeared particularly susceptible. Further investigation into mechanisms by which PM can preferentially trigger STEMI over NSTEMI within this rapid time scale is needed.
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