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Harsh conditions faced by firefighters may increase risk for MI
The extreme environments that firefighters are exposed to contributed to an increased risk for acute MI, according to data published in Circulation.
The leading cause of death in firefighters is CV events, which cause an estimated 45% of on-duty fatalities in the United States annually. The risk for CV events increases during fire suppression, as heat, physical exertion and exposure to pollution reflect risk factors.
“These harsh conditions can cause injury to the heart muscle in healthy firefighters and may explain the link between fire suppression and risk [for MI],” Nicholas Mills, MD, PhD, chair of cardiology and consultant cardiologist at the University of Edinburgh, Scotland, said in a press release.
Researchers reviewed data from 19 healthy, nonsmoking firefighters (mean age, 41 years; 16 men) from Scotland. Participants were excluded if they had CVD, current smoking, diabetes, arrhythmias, hypertension, regularly used medication, kidney or liver failure, intercurrent infective illness or asthma.
Most participants (n = 17) took part in two 20-minute fire simulation training exercises at least 1 week apart, in which the same tasks were completed in the same order. Researchers performed CV assessments after each exposure.
Brachial artery cannulation was performed in which an infusion of treatments was administered after a 30-minute saline infusion: bradykinin at 100 pmol per minute, 300 pmol per minute and 1,000 pmol per minute; acetylcholine at 5 µg per minute, 10 µg per minute and 20 µg per minute; verapamil at 10 µg per minute, 30 µg per minute and 100 µg per minute; and sodium nitroprusside at 2 µg per minute, 4 µg per minute and 8 µg per minute.
The primary endpoints were forearm blood flow, ex vivo thrombus formation and net tissue plasminogen activator release. Secondary endpoints composed a variety of factors such as ambulatory heart rate, ischemic burden, cardiac troponin I concentration, BP monitoring and platelet activation.
Study results
The mean baseline core temperature was 37.4°C, which then peaked at 38.4°C (P < .001). Participants’ body weight decreased by 0.46 kg (P < .001). Temperature and heart rate increased during each exposure, which researchers associated with asymptomatic ST segment depression (analysis of variance, P < .01 for all). The Borg scale rated perceived exertion as 14 ± 0.2.
After fire simulation exposure, researchers noted that thrombus formation increased by 66% in the high-shear chamber (6,563 µm2; 95% CI, 3,481-9,645) and 73% in the low-shear chamber (5,781 µm2; 95% CI, 3,340-8,221; P < .001 for both). Platelet-monocyte binding, although it differed at baseline between the fire simulation and control groups, increased after exposure by 7% (95% CI, 0-13; P = .03). This was not affected throughout the control group (–6%; 95% CI, –15 to 1; P = .09).
Participants experienced a decrease in systolic (125 mm Hg) and diastolic BP (75 mm Hg) after fire simulation exposure compared with the control group (134 mm Hg and 82 mm Hg, respectively; P < .01 for both), according to the findings.
Forearm blood flow increased after vasodilators were administered (P < .001). Acetylcholine (P = .01) and sodium nitroprusside (P = .004) decreased vasodilatation vs. the control group, but was not affected by verapamil (P > .05) or bradykinin (P > .05), the researchers wrote.
One hour after fire simulation, participants experienced an increase in cardiac troponin I concentration (3 ng/L) compared with the control group (1.5 ng/L; P = .01). Maximum ST segment depression, cumulative ischemic burden and episodes of ST segment depression increased during the fire simulation (P < .05 for all), but these did not fluctuate after the exposure, according to the researchers.
Effects of fire exposure
“It is intriguing that fire simulation was associated with evidence of minor myocardial injury and asymptomatic myocardial ischemia,” Amanda L. Hunter, MB ChB, a postgraduate student at the University of Edinburgh Centre for Cardiovascular Science in Scotland, and colleagues wrote. “Taken together, this comprehensive [CV] assessment has detected plausible mechanistic links between participation in fire suppression duties and acute [MI].”
In a related editorial, Stefanos N. Kales, MD, MPH, from Harvard T.H. Chan School of Public Health, and Denise L. Smith, PhD, from the department of health and exercise sciences at Skidmore College in Saratoga Springs, New York, wrote: “While Hunter et al emphasize that this state promotes [MI], it is crucial to recognize that the same constellation of [CV] stressors is also arrhythmogenic. In fact, the autopsies of firefighters succumbing to on-duty sudden cardiac arrest strongly suggest that most of these fatalities result from arrhythmias.” – by Darlene Dobkowski
Disclosure: One researcher reports receiving support from the Fire Brigade Union. Kales reports financial compensation in workers’ compensation and disability cases involving firefighters. Smith reports consulting in cases involving medical evaluations and firefighter fatalities.