University of Illinois at Chicago
Effect of Aspirin.pdf (693.22 kB)

Effect of Aspirin Supplementation on Hemostatic Responses in Firefighters Aged 40 to 60 Years.

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journal contribution
posted on 2017-07-16, 00:00 authored by Smith DL, Horn GP, Woods J, Ploutz-Snyder R, Fernhall B
Sudden cardiovascular events account for approximately 45% to 50% of all duty-related deaths among firefighters and a disproportionate number of these fatalities occur after strenuous fire suppression activities. The purpose of this study was to evaluate the effect of acute and chronic aspirin supplementation on hemostatic function before and after live firefighting activities in older firefighters. A double-blind, crossover design included 4 treatments: a 2-week aspirin/placebo treatment ("chronic") and a single prefirefighting aspirin/placebo treatment ("acute"). Hemostatic function was assessed in 24 male firefighters (mean age = 48.2 ± 5.9 years) immediately before and after 18 minutes of live-fire firefighting activity. An acute bout of firefighting activity significantly decreased platelet aggregation time and decreased activated partial thromboplastin time. Compared with placebo, acute aspirin supplementation resulted in a significant increase in epinephrine closure time, which was further augmented by chronic supplementation. Aspirin supplementation had no effect on coagulatory or fibrinolytic factors. Our findings suggest that an acute bout of firefighting leads to increased coagulatory potential in older firefighters. In conclusion, aspirin supplementation had an antiplatelet effect that decreased platelet aggregability at rest and after an acute bout of firefighting compared with placebo.


This study was funded by the Department of Homeland Security (EMW-2009-FP-00544).


Publisher Statement

This is the author’s version of a work that was accepted for publication in American Journal of Cardiology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in American Journal of Cardiology. 2016. 118(2): 275-280. doi: 10.1016/j.amjcard.2016.04.032.


Elsevier Inc.



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