Fire Simulation and Cardiovascular Health in Firefighters

Amanda L Hunter, Anoop S V Shah, Jeremy P Langrish, Jennifer B Raftis, Andrew J Lucking, Mairi Brittan, Sowmya Venkatasubramanian, Catherine L Stables, Dominik Stelzle, James Marshall, Richard Graveling, Andrew D Flapan, David E Newby, Nicholas L Mills, Amanda L Hunter, Anoop S V Shah, Jeremy P Langrish, Jennifer B Raftis, Andrew J Lucking, Mairi Brittan, Sowmya Venkatasubramanian, Catherine L Stables, Dominik Stelzle, James Marshall, Richard Graveling, Andrew D Flapan, David E Newby, Nicholas L Mills

Abstract

Background: Rates of myocardial infarction in firefighters are increased during fire suppression duties, and are likely to reflect a combination of factors including extreme physical exertion and heat exposure. We assessed the effects of simulated fire suppression on measures of cardiovascular health in healthy firefighters.

Methods: In an open-label randomized crossover study, 19 healthy firefighters (age, 41±7 years; 16 males) performed a standardized training exercise in a fire simulation facility or light duties for 20 minutes. After each exposure, ex vivo thrombus formation, fibrinolysis, platelet activation, and forearm blood flow in response to intra-arterial infusions of endothelial-dependent and -independent vasodilators were measured.

Results: After fire simulation training, core temperature increased (1.0±0.1°C) and weight reduced (0.46±0.14 kg, P<0.001 for both). In comparison with control, exposure to fire simulation increased thrombus formation under low-shear (73±14%) and high-shear (66±14%) conditions (P<0.001 for both) and increased platelet-monocyte binding (7±10%, P=0.03). There was a dose-dependent increase in forearm blood flow with all vasodilators (P<0.001), which was attenuated by fire simulation in response to acetylcholine (P=0.01) and sodium nitroprusside (P=0.004). This was associated with a rise in fibrinolytic capacity, asymptomatic myocardial ischemia, and an increase in plasma cardiac troponin I concentrations (1.4 [0.8-2.5] versus 3.0 [1.7-6.4] ng/L, P=0.010).

Conclusions: Exposure to extreme heat and physical exertion during fire suppression activates platelets, increases thrombus formation, impairs vascular function, and promotes myocardial ischemia and injury in healthy firefighters. Our findings provide pathogenic mechanisms to explain the association between fire suppression activity and acute myocardial infarction in firefighters.

Clinical trial registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01812317.

Keywords: endothelium-dependent relaxation; firefighters; thrombosis; vascular.

© 2017 The Authors.

Figures

Figure 1.
Figure 1.
Core temperature and hemodynamic changes during fire simulation exposure. Core temperature and heart rate rapidly increased during the fire simulation accompanied by asymptomatic ST-segment depression. Core temperature remained increased for 120 minutes, and ST segments returned to baseline gradually during the same time period. Mean arterial pressure was unchanged throughout. Values are mean±95% confidence interval.
Figure 2.
Figure 2.
Thrombus formation and platelet activation after fire simulation exposure. Thrombus formation ex vivo was increased in response to fire simulation in under both low-shear and high-shear conditions in comparison with control (Student t test, P<0.001 for both, A and B, respectively). Platelet-monocyte aggregates were increased after fire simulation exposure in comparison with control (Student t test, P=0.004, n=12, C). Where venipuncture and sample processing resulted in significant ex vivo platelet activation, data were excluded from further analysis by a researcher blinded to the exposure. There was a dose-dependent increase in t-PA (tissue-type plasminogen activator) in response to bradykinin in both exposures (2-way ANOVA with repeated measures, P<0.001), that was augmented after fire simulation in comparison with control (ANOVA, P=0.006, D). ANOVA indicates analysis of variance.
Figure 3.
Figure 3.
Vascular vasomotor function after fire simulation exposure. There was a dose-dependent increase in forearm blood flow with each vasodilator (2-way ANOVA with repeated measures, P<0.001 for all). Vasodilatation expressed as a ratio of the forearm blood flow between the infused and noninfused arm, was attenuated in response to acetylcholine and sodium nitroprusside (P=0.01 and P=0.004, A and B, respectively) after fire simulation in comparison with control. There was no difference in forearm blood flow in response to bradykinin or verapamil (P>0.05 for both, C and D, respectively) between the 2 exposures. **P<0.01. ANOVA indicates analysis of variance.

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