579935
editorial2015
VMJ0010.1177/1358863X15579935Vascular MedicineEditorial
Editorial
Firefighting: Can our arteries take the heat?
Vascular Medicine 2015, Vol. 20(3) 219–221 © The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1358863X15579935 vmj.sagepub.com
Mobin Malik1 and Michael E Widlansky1,2,3
Currently, there are approximately 1.1 million volunteer and career firefighters in the United States.1 Firefighting remains one of the most hazardous and challenging lines of work with multiple occupational hazards including smoke inhalation, exposure to high-intensity heat, dehydration, potential falls and vehicular collisions. Since 1977, sudden cardiac death has accounted for the largest share of on-duty cardiac deaths among firefighters – surpassing burns, trauma, asphyxiation and smoke inhalation. Despite the steady decline in the average number of deaths among firefighters over the past decade, sudden cardiac death still accounts for 42% of the on-duty deaths in the last five years.2 Adverse cardiovascular (CV) events in firefighters, including sudden cardiac death, most commonly coincide with active strenuous duties rather than non-emergency situations. Thus, while traditional CV risk factors are prevalent in firefighters and are associated with greater CV risk in this population,3–6 the unique physical and environmental hazards faced by firefighters likely acutely magnify their CV risk in the peri-emergency setting. Research to determine the most important factors with an adverse impact remains speculative. Firefighters are subjected to high levels of dynamic and static physical exertion during performance of duties while wearing heavy, insulating protective equipment (PPE) often weighing in excess of 25 kg. Emergency situations are highly stressful and often chaotic, leading to profound sympathetic activation that manifests in part with elevated blood pressure and maximal or near maximal heart rates in firefighters during emergencies. Working under these conditions can rapidly lead to dehydration, reduced plasma volume and potentially stroke volume. Firefighting is also associated with increased number and aggregability of circulating platelets, attributable at least in part to hemoconcentration and increased sympathetic activity.7 Together with exposure to smoke containing toxic chemicals and carbon monoxide, the cardiovascular system is placed under significant strain during firefighting. Firefighters also experience significant heat stress. Firefighting produces large amounts of metabolic heat while insulating PPE limits its dissipation. In addition, fire-related heat also adds further thermal strain. The core temperature can increase as much as 0.05 degrees Celsius/min or 1°C over 20 minutes of acute firefighting activity.8,9 The increase in core temperature experienced by firefighters is significantly greater than that seen during routine aerobic exercise. Prior work by Fahs and colleagues demonstrates that three hours of firefighting activity results in impairment of microvascular
endothelial function, faster wave reflection and increased vascular stiffness when assessed within 30 minutes of cessation of these activities.10 These effects were not mitigated by oral supplementation with ascorbic acid (2 grams) prior to activity.10 These data suggest firefighting activities adversely impact vascular physiology, leading to elevated blood pressure, reduced coronary perfusion and increased plaque vulnerability in a manner that is not mitigated by oral antioxidants. The specific contribution of heat stress to the acute adverse vascular effects of firefighting and whether these effects can be mitigated pharmacologically are unclear. These open questions are the subject of two articles published in the current issue of Vascular Medicine.11,12 Lefferts and colleagues explore the impact of moderate exercise induced heat stress (EIHS) compared to normothermic exercise on aortic stiffness, pressure from wave reflections and non-invasive estimates of myocardial work and coronary perfusion.11 Twelve young, healthy, and physically active men were randomized in a crossover design to two distinct alternative exercise/rest protocols: no heat stress (NHS) and heat stress (HS). Peripheral artery tonometry was performed prior to and within 15–30 minutes following each activity session. Compared to NHS, HS protocol resulted in significant increases in both rate pressure product (RPP) and systolic pressure time integral (SPTI) with concomitant decreases in both diastolic pressure time integral (DPTI) and reflected wave velocity. These data suggest heat stress results in an increase in myocardial workload with concomitant reductions in coronary perfusion. However, in contrast to prior work, no appreciable effect on aortic stiffness was noted as measured by carotid-femoral pulse wave velocity. The lack of impact of heat stress on large elastic artery stiffness reported by Lefferts and colleagues suggests that the effect on elastic arteries may require the presence of 1Department
of Medicine, Division of Cardiovascular Medicine, Medical College of Wisconsin, Milwaukee, WI, USA 2Department of Pharmacology, Medical College of Wisconsin, Milwaukee, WI, USA 3Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI, USA Corresponding author: Michael E Widlansky, Division of Cardiovascular Medicine, Medical College of Wisconsin, 9200 W Wisconsin Ave, FEC E5100, Milwaukee, WI 53226, USA. Email: [email protected]
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additional stressors that occur with firefighting. While these findings may be related in part to the elevation in heart rate, they still suggest heat stress may alter vascular wave reflection properties that may increase CV risk by reducing coronary perfusion. The magnitude of cardiovascular effects of heat stress observed in the study by Lefferts and colleagues may also have been mitigated by the young, healthy, risk-factor-free study population. Adverse vascular effects may be more pronounced and magnified in a population of individuals with a cardiovascular risk profile more closely mirroring that of firefighters. In light of previously reported associations of heat stress with both inflammation and platelet activation, Olafiranye and colleagues report a study designed to test the hypothesis that anti-platelet therapy with aspirin (ASA) could prevent and/or reverse the adverse effects of heat stress in a simulated firefighting environment.12 In the setting of a 2 x 2 factorial design study, 52 primarily male firefighters were randomized to either two weeks of low-dose (81 mg) aspirin prior to exposure to heat stress or placebo control and to either a single dose of 325 mg aspirin immediately post heat stress exposure or placebo control. Compared to the study by Lefferts and colleagues, subjects enrolled were older, with higher blood pressure (still within normal range) and body mass index. The heat stress protocol was shorter (50 min). Treatment with aspirin, particularly pre-treatment with low dose aspirin, resulted in more favorable waveform deflection properties at baseline as reflected by lower AI75 (Augmentation Index indexed to a heart rate of 75 beats/min). Aspirin therapy was also associated with overall lower AI75 throughout the recovery period. Aspirin therapy did not impact reactive hyperemic index (RHI) significantly, although the data suggest there may be some favorable effects that cannot be clearly discerned due to small study size. High dose aspirin did not show any beneficial effect. Interpretation of the data is somewhat complicated by differences in baseline measurements. Between-group differences do not appear to have a clear explanation and likely relate in part to small sample size. Similar to the study by Lefferts and colleagues, the magnitude of the results seen could potentially be more striking in a higher-risk population than tested, and the results cannot be generalized to women in light of the overwhelmingly male study populations in both papers. These two papers add important information to our body of understanding of how heat stress may contribute to adverse CV events in firefighters by implicating heat stress alterations in the microvasculature as a potential mediator of the effect. Microvascular endothelial function, but not muscular artery conduit vessel function, predicts future CV risk in firefighters.13 In both studies in this issue, the adverse effect of heat stress appears to be mediated by an acute impairment of the magnitude and timing of pulse wave reflection that likely relates to the overall state of the microvasculature. The acuity of the changes and the rapid recovery reported by Olafiranye and colleagues suggest these changes are secondary to dynamic rather than fixed vascular attributes that fit well with a paradigm of dynamic microvascular changes governing the systemic effects
seen. The exact mechanisms for the development of microvascular dysfunction during heat stress remain unclear. Interestingly, prior work suggests that alterations in acute exertional stress such as heavy resistance exercise, particularly in sedentary individuals, may alter the mediators of flow-induced vasodilation.14 Heat stress is also associated with platelet activation and animal studies of heat stroke suggest severe microvascular dysfunction with increased platelet-leukocyte-endothelial interaction and increased tissue factor and von Willebrand factor expression.15 Together with these data and the favorable impact of aspirin therapy reported by Olafiranye and colleagues, further studies of platelet and microvascular interactions under heat stress are warranted to further delineate this potential mechanism. Both studies reported in this issue suggest that heat stress has unique adverse effects on the microvasculature of firefighters independent of the other potential stressors that occur during firefighting.11,12 The favorable effects of aspirin reported by Olafiranye and colleagues suggest the potential for pharmacotherapy to mitigate the adverse effects of heat stress and could favorably impact CV risk in firefighters. Future studies designed to determine optimal timing and dosing of aspirin as well as its overall efficacy are still needed prior to making a definitive recommendation for aspirin therapy as a preventive medication for all firefighters. These two investigative groups should be commended for their efforts in further advancing our understanding of the impact of heat stress on vasculature and pointing us in the direction of potential mechanisms and therapies. Declaration of conflicting interest The authors declare that there is no conflict of interest.
Funding This editorial received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Haynes H, Stein G. US fire department profile 2013. Quincy, MA: National Fire Protection Association (NFPA), 2014. 2. Fahy R, Leblanc P, Molis J. Fire fighter fatalities in the United States – 2013. Quincy, MA: NFPA Fire analysis and reserach, 2014. 3. Kales SN, Soteriades ES, Christophi CA, et al. Emergency duties and deaths from heart disease among firefighters in the United States. N Engl J Med 2007; 356: 1207–1215. 4. Kales SN, Soteriades ES, Christoudias SG, et al. Firefighters and on-duty deaths from coronary heart disease: a case control study. Environ Health 2003; 2: 14. 5. Smith D, Fehling P, Frisch A, et al. The prevalence of cardiovascular disease risk factors and obesity in firefighters. Journal of Obesity 2012; 2012: 1–9. 6. Holder JD, Stallings LA, Peeples L, et al. Firefighter heart presumption retirements in Massachusetts 1997–2004. J Occup Environ Med 2006; 48: 1047–1053. 7. Smith DL, Petruzzello SJ, Goldstein E, et al. Effect of livefire training drills on firefighters’ platelet number and function. Prehosp Emerg Care 2011; 15: 233–239.
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Editorial 8. Smith DL, Petruzzello SJ. Selected physiological and psychological responses to live-fire drills in different configurations of firefighting gear. Ergonomics 1998; 41: 1141–1154. 9. Soteriades ES, Smith DL, Tsismenakis AJ, et al. Cardiovascular disease in US firefighters: a systematic review. Cardiol Rev 2011; 19: 202–215. 10. Fahs CA, Yan H, Ranadive S, et al. Acute effects of firefighting on arterial stiffness and blood flow. Vasc Med 2011; 16: 113–118. 11. Lefferts W, Hultquist E, Heffernan K, et al. Vascular and central hemodynamic changes following exercise induced heat stress. Vasc Med 2015; 20: 222–229. 12. Olafiranye O, Hostler D, Winger D, et al. Effect of aspirin on acute changes in peripheral arterial stiffness and endothelial function following exertional heat stress in firefighters: the
factorial group results of Enhanced Firefighter Rehab Trial. Vasc Med 2015; 20: 230–236. 13. Anderson TJ, Charbonneau F, Title LM, et al. Microvascular function predicts cardiovascular events in primary prevention: long-term results from the Firefighters and Their Endothelium (FATE) study. Circulation 2011; 123: 163–169. 14. Durand MJ, Dharmashankar K, Bian JT, et al. Acute exertion elicits a H2O2-dependent vasodilator mechanism in the microvasculature of exercise-trained but not sedentary adults. Hypertension 2015; 65: 140–145. 15. Roberts GT, Ghebeh H, Chishti MA, et al. Microvascular injury, thrombosis, inflammation, and apoptosis in the pathogenesis of heatstroke: a study in baboon model. Arterioscler Thromb Vasc Biol 2008; 28: 1130–1136.
Downloaded from vmj.sagepub.com by guest on November 15, 2015
editorial2015
VMJ0010.1177/1358863X15579935Vascular MedicineEditorial
Editorial
Firefighting: Can our arteries take the heat?
Vascular Medicine 2015, Vol. 20(3) 219–221 © The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1358863X15579935 vmj.sagepub.com
Mobin Malik1 and Michael E Widlansky1,2,3
Currently, there are approximately 1.1 million volunteer and career firefighters in the United States.1 Firefighting remains one of the most hazardous and challenging lines of work with multiple occupational hazards including smoke inhalation, exposure to high-intensity heat, dehydration, potential falls and vehicular collisions. Since 1977, sudden cardiac death has accounted for the largest share of on-duty cardiac deaths among firefighters – surpassing burns, trauma, asphyxiation and smoke inhalation. Despite the steady decline in the average number of deaths among firefighters over the past decade, sudden cardiac death still accounts for 42% of the on-duty deaths in the last five years.2 Adverse cardiovascular (CV) events in firefighters, including sudden cardiac death, most commonly coincide with active strenuous duties rather than non-emergency situations. Thus, while traditional CV risk factors are prevalent in firefighters and are associated with greater CV risk in this population,3–6 the unique physical and environmental hazards faced by firefighters likely acutely magnify their CV risk in the peri-emergency setting. Research to determine the most important factors with an adverse impact remains speculative. Firefighters are subjected to high levels of dynamic and static physical exertion during performance of duties while wearing heavy, insulating protective equipment (PPE) often weighing in excess of 25 kg. Emergency situations are highly stressful and often chaotic, leading to profound sympathetic activation that manifests in part with elevated blood pressure and maximal or near maximal heart rates in firefighters during emergencies. Working under these conditions can rapidly lead to dehydration, reduced plasma volume and potentially stroke volume. Firefighting is also associated with increased number and aggregability of circulating platelets, attributable at least in part to hemoconcentration and increased sympathetic activity.7 Together with exposure to smoke containing toxic chemicals and carbon monoxide, the cardiovascular system is placed under significant strain during firefighting. Firefighters also experience significant heat stress. Firefighting produces large amounts of metabolic heat while insulating PPE limits its dissipation. In addition, fire-related heat also adds further thermal strain. The core temperature can increase as much as 0.05 degrees Celsius/min or 1°C over 20 minutes of acute firefighting activity.8,9 The increase in core temperature experienced by firefighters is significantly greater than that seen during routine aerobic exercise. Prior work by Fahs and colleagues demonstrates that three hours of firefighting activity results in impairment of microvascular
endothelial function, faster wave reflection and increased vascular stiffness when assessed within 30 minutes of cessation of these activities.10 These effects were not mitigated by oral supplementation with ascorbic acid (2 grams) prior to activity.10 These data suggest firefighting activities adversely impact vascular physiology, leading to elevated blood pressure, reduced coronary perfusion and increased plaque vulnerability in a manner that is not mitigated by oral antioxidants. The specific contribution of heat stress to the acute adverse vascular effects of firefighting and whether these effects can be mitigated pharmacologically are unclear. These open questions are the subject of two articles published in the current issue of Vascular Medicine.11,12 Lefferts and colleagues explore the impact of moderate exercise induced heat stress (EIHS) compared to normothermic exercise on aortic stiffness, pressure from wave reflections and non-invasive estimates of myocardial work and coronary perfusion.11 Twelve young, healthy, and physically active men were randomized in a crossover design to two distinct alternative exercise/rest protocols: no heat stress (NHS) and heat stress (HS). Peripheral artery tonometry was performed prior to and within 15–30 minutes following each activity session. Compared to NHS, HS protocol resulted in significant increases in both rate pressure product (RPP) and systolic pressure time integral (SPTI) with concomitant decreases in both diastolic pressure time integral (DPTI) and reflected wave velocity. These data suggest heat stress results in an increase in myocardial workload with concomitant reductions in coronary perfusion. However, in contrast to prior work, no appreciable effect on aortic stiffness was noted as measured by carotid-femoral pulse wave velocity. The lack of impact of heat stress on large elastic artery stiffness reported by Lefferts and colleagues suggests that the effect on elastic arteries may require the presence of 1Department
of Medicine, Division of Cardiovascular Medicine, Medical College of Wisconsin, Milwaukee, WI, USA 2Department of Pharmacology, Medical College of Wisconsin, Milwaukee, WI, USA 3Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI, USA Corresponding author: Michael E Widlansky, Division of Cardiovascular Medicine, Medical College of Wisconsin, 9200 W Wisconsin Ave, FEC E5100, Milwaukee, WI 53226, USA. Email: [email protected]
Downloaded from vmj.sagepub.com by guest on November 15, 2015
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Vascular Medicine 20(3)
additional stressors that occur with firefighting. While these findings may be related in part to the elevation in heart rate, they still suggest heat stress may alter vascular wave reflection properties that may increase CV risk by reducing coronary perfusion. The magnitude of cardiovascular effects of heat stress observed in the study by Lefferts and colleagues may also have been mitigated by the young, healthy, risk-factor-free study population. Adverse vascular effects may be more pronounced and magnified in a population of individuals with a cardiovascular risk profile more closely mirroring that of firefighters. In light of previously reported associations of heat stress with both inflammation and platelet activation, Olafiranye and colleagues report a study designed to test the hypothesis that anti-platelet therapy with aspirin (ASA) could prevent and/or reverse the adverse effects of heat stress in a simulated firefighting environment.12 In the setting of a 2 x 2 factorial design study, 52 primarily male firefighters were randomized to either two weeks of low-dose (81 mg) aspirin prior to exposure to heat stress or placebo control and to either a single dose of 325 mg aspirin immediately post heat stress exposure or placebo control. Compared to the study by Lefferts and colleagues, subjects enrolled were older, with higher blood pressure (still within normal range) and body mass index. The heat stress protocol was shorter (50 min). Treatment with aspirin, particularly pre-treatment with low dose aspirin, resulted in more favorable waveform deflection properties at baseline as reflected by lower AI75 (Augmentation Index indexed to a heart rate of 75 beats/min). Aspirin therapy was also associated with overall lower AI75 throughout the recovery period. Aspirin therapy did not impact reactive hyperemic index (RHI) significantly, although the data suggest there may be some favorable effects that cannot be clearly discerned due to small study size. High dose aspirin did not show any beneficial effect. Interpretation of the data is somewhat complicated by differences in baseline measurements. Between-group differences do not appear to have a clear explanation and likely relate in part to small sample size. Similar to the study by Lefferts and colleagues, the magnitude of the results seen could potentially be more striking in a higher-risk population than tested, and the results cannot be generalized to women in light of the overwhelmingly male study populations in both papers. These two papers add important information to our body of understanding of how heat stress may contribute to adverse CV events in firefighters by implicating heat stress alterations in the microvasculature as a potential mediator of the effect. Microvascular endothelial function, but not muscular artery conduit vessel function, predicts future CV risk in firefighters.13 In both studies in this issue, the adverse effect of heat stress appears to be mediated by an acute impairment of the magnitude and timing of pulse wave reflection that likely relates to the overall state of the microvasculature. The acuity of the changes and the rapid recovery reported by Olafiranye and colleagues suggest these changes are secondary to dynamic rather than fixed vascular attributes that fit well with a paradigm of dynamic microvascular changes governing the systemic effects
seen. The exact mechanisms for the development of microvascular dysfunction during heat stress remain unclear. Interestingly, prior work suggests that alterations in acute exertional stress such as heavy resistance exercise, particularly in sedentary individuals, may alter the mediators of flow-induced vasodilation.14 Heat stress is also associated with platelet activation and animal studies of heat stroke suggest severe microvascular dysfunction with increased platelet-leukocyte-endothelial interaction and increased tissue factor and von Willebrand factor expression.15 Together with these data and the favorable impact of aspirin therapy reported by Olafiranye and colleagues, further studies of platelet and microvascular interactions under heat stress are warranted to further delineate this potential mechanism. Both studies reported in this issue suggest that heat stress has unique adverse effects on the microvasculature of firefighters independent of the other potential stressors that occur during firefighting.11,12 The favorable effects of aspirin reported by Olafiranye and colleagues suggest the potential for pharmacotherapy to mitigate the adverse effects of heat stress and could favorably impact CV risk in firefighters. Future studies designed to determine optimal timing and dosing of aspirin as well as its overall efficacy are still needed prior to making a definitive recommendation for aspirin therapy as a preventive medication for all firefighters. These two investigative groups should be commended for their efforts in further advancing our understanding of the impact of heat stress on vasculature and pointing us in the direction of potential mechanisms and therapies. Declaration of conflicting interest The authors declare that there is no conflict of interest.
Funding This editorial received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Haynes H, Stein G. US fire department profile 2013. Quincy, MA: National Fire Protection Association (NFPA), 2014. 2. Fahy R, Leblanc P, Molis J. Fire fighter fatalities in the United States – 2013. Quincy, MA: NFPA Fire analysis and reserach, 2014. 3. Kales SN, Soteriades ES, Christophi CA, et al. Emergency duties and deaths from heart disease among firefighters in the United States. N Engl J Med 2007; 356: 1207–1215. 4. Kales SN, Soteriades ES, Christoudias SG, et al. Firefighters and on-duty deaths from coronary heart disease: a case control study. Environ Health 2003; 2: 14. 5. Smith D, Fehling P, Frisch A, et al. The prevalence of cardiovascular disease risk factors and obesity in firefighters. Journal of Obesity 2012; 2012: 1–9. 6. Holder JD, Stallings LA, Peeples L, et al. Firefighter heart presumption retirements in Massachusetts 1997–2004. J Occup Environ Med 2006; 48: 1047–1053. 7. Smith DL, Petruzzello SJ, Goldstein E, et al. Effect of livefire training drills on firefighters’ platelet number and function. Prehosp Emerg Care 2011; 15: 233–239.
Downloaded from vmj.sagepub.com by guest on November 15, 2015
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Editorial 8. Smith DL, Petruzzello SJ. Selected physiological and psychological responses to live-fire drills in different configurations of firefighting gear. Ergonomics 1998; 41: 1141–1154. 9. Soteriades ES, Smith DL, Tsismenakis AJ, et al. Cardiovascular disease in US firefighters: a systematic review. Cardiol Rev 2011; 19: 202–215. 10. Fahs CA, Yan H, Ranadive S, et al. Acute effects of firefighting on arterial stiffness and blood flow. Vasc Med 2011; 16: 113–118. 11. Lefferts W, Hultquist E, Heffernan K, et al. Vascular and central hemodynamic changes following exercise induced heat stress. Vasc Med 2015; 20: 222–229. 12. Olafiranye O, Hostler D, Winger D, et al. Effect of aspirin on acute changes in peripheral arterial stiffness and endothelial function following exertional heat stress in firefighters: the
factorial group results of Enhanced Firefighter Rehab Trial. Vasc Med 2015; 20: 230–236. 13. Anderson TJ, Charbonneau F, Title LM, et al. Microvascular function predicts cardiovascular events in primary prevention: long-term results from the Firefighters and Their Endothelium (FATE) study. Circulation 2011; 123: 163–169. 14. Durand MJ, Dharmashankar K, Bian JT, et al. Acute exertion elicits a H2O2-dependent vasodilator mechanism in the microvasculature of exercise-trained but not sedentary adults. Hypertension 2015; 65: 140–145. 15. Roberts GT, Ghebeh H, Chishti MA, et al. Microvascular injury, thrombosis, inflammation, and apoptosis in the pathogenesis of heatstroke: a study in baboon model. Arterioscler Thromb Vasc Biol 2008; 28: 1130–1136.
Downloaded from vmj.sagepub.com by guest on November 15, 2015
