LETTERS TO THE EDITOR
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To the Editor:
It has been well documented that exposure to extreme environments and physical exertion during fire suppression tasks could promote myocardial ischemia, thereby potentially triggering sudden cardiac deaths, which is the leading cause of death in firefighters in the United States.1 Smith et al2 rightly draw attention to the need for a simple field countermeasure to mitigate the firefighting-induced cardiovascular inflammation. An important contribution from their study is that an 18-minute simulated fire suppression task elevated cardiovascular inflammatory biomarkers, highlighting the needs of preventive countermeasures for this cohort.
The current paper of Smith et al2 examined the ability of acute and chronic low-dose aspirin (81 mg) on inflammatory biomarkers. This concept is based on the fact that, aspirin is a cornerstone in the treatment of myocardial infarction, and it could be a simple solution to be adopted by firefighters in the field, albeit its effectiveness yet to be verified. Smith et al2 suggested that “neither chronic nor acute aspirin supplementation attenuated this inflammatory response”. The authors reached this conclusion based on an experimental protocol of participants ingested aspirin 60 minutes before simulated firefighting, and then undertook 18-minute simulated fire suppression task under hot conditions (venue temperature 35°C to 41°C and 70°C to 82°C). Blood samples were taken before aspirin supplementation and 2 to 3 minutes after simulated firefighting.
Unfortunately, this study design did not and could not disprove the effectiveness of aspirin on mitigating acute inflammation, as its inhibitory effect on platelet aggregation is subject to the timing of ingestion. For example, pharmacokinetics of aspirin shows that the time to peak plasma concentration of dispersible aspirin is 28.3 minutes and the half-life is 36.6 minutes.3 Therefore, the maximal inhibitory effect is typically achieved within 30 minutes after drug ingestion, reflecting a rapid onset of inhibition. However, the acute inflammatory biomarkers were not measured until nearly 80 minutes after aspirin supplementation,2 which should not be viewed as “acute” supplementation in this case, hence it would become entirely possible that the true drug effect in the study by Smith et al2 could not be detected due to the critical timing issue.
I would encourage the authors to pursue a true exploration of the acute effect of aspirin (eg, 15 minutes and immediately before fire suppression tasks) in the future. I would also recommend relevant researchers to further explore the acute administration of higher dose aspirin (eg, 243 mg) as suggested by the American Heart Association4 in the prevention of myocardial infarction for this high-risk occupation.
1. Yang J, Teehan D, Farioli A, Baur DM, Smith D, Kales SN. Sudden cardiac death among firefighters ≤45 years of age in the United States. Am J Cardiol
2. Smith DL, Friedman NMG, Bloom SI, et al. Firefighting induces acute inflammatory responses that are not relieved by aspirin in older firefighters. J Occup Environ Med
3. Muir N, Nichols JD, Clifford JM, Stillings MR, Hoare RC. The influence of dosage form on aspirin kinetics: implications for acute cardiovascular use. Curr Med Res Opin
4. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol