In today’s NEJM is an article from Augsburg, Germany looking at exposure to automobile traffic as a trigger for myocardial infarction. The statistical methods employed were almost completely incomprehensible to me ï¿½ I would ask anyone who understands the “statistical analysis” paragraph to email me an explanation. But the bottom line is that, during the hour before onset of an MI, patients were more likely to have been in traffic than would have been expected based on their previous days’ patterns. This association held for automobile, public transportation and bicycle traffic. It also held after a number of adjustments (including adjustment for “the stress of getting up in the morning”!)
The authors speculate that stress, noise and particulate air-pollution may all explain the association, but they concentrate almost exclusively on air-pollution as the triggering factor. In an accompanying perspective piece, Stone reviews the substrate-trigger theory of acute coronary events. The substrate is the atheromatous plaque. Triggers are those events that cause plaque to become unstable and thrombose, including inflammation, increased sympathetic stimulation, vasoconstriction and hypercoagulability. In discussing the current study, he, too, emphasizes the role of particulate air pollution, via inflammation, vasoconstriction and hypercoagulability.
I would be more inclined to view the stress of traffic as the principle trigger, rather than air pollution, but thatï¿½s just my gut feeling. I think itï¿½s important to note that substrates are causal, whereas triggers are sometimes causal but sometimes affect timing more than anything else. Thus, if an event is likely to happen, the trigger may influence the “when” more than the “whether”. Treating a substrate is often more effective than suppressing all possible triggers. Reducing risk factors for atherogenesis is a better approach than attempting to avoid traffic, although who could argue against reducing air-pollution?