Key result
High-intensity firefighting drills are linked to impaired ventricular-arterial coupling and reduced coronary perfusion.
Why the study?
Firefighting-induced afterload and ventricular-arterial coupling mismatch increase cardiac risk, and because this risk rises with age, the responses in middle-aged firefighters needed examination.
Does acute high-intensity firefighting alter ventricular-arterial coupling and pulsatile afterload in middle-aged male firefighters?
Observational (n=22)
Does acute high-intensity firefighting alter ventricular-arterial coupling and pulsatile afterload in middle-aged male firefighters?
Acute firefighting in middle-aged men induces cardiovascular strain and reduces coronary perfusion, though the exact role of ventricular-arterial interactions remains confounded by heart rate changes.
Answers are grounded in this paper and cite their sources.
May signal heightened cardiovascular strain in middle-aged firefighters; leaves open whether elastance shifts are independent of heart rate.
Firefighting increases afterload, leading to ventricular‐arterial coupling mismatch in young firefighters that may contribute to coronary hypoperfusion and the elevated risk of on‐duty cardiac events. Since this risk is higher with aging in firefighters, we examined their ventricular‐vascular coupling and afterload responses to acute firefighting. Twenty‐two male firefighters (40–59 years) performed 18‐min high‐intensity firefighting drills while wearing protective gear and breathing apparatus. Echocardiography was conducted before and within 10 min after firefighting to estimate cardiac volumes, while tonometry‐derived pulse wave analysis estimated wasted pressure effort (Ew) and aortic reservoir function. Ventricular‐arterial coupling was quantified using the arterial (Ea) to ventricular (Ees) elastance ratio, and coronary perfusion was estimated via the Buckberg index. Firefighting reduced stroke volume (difference (∆) = −17 mL, p < 0.001), Ew (∆ = −800 dyne cm −2 s, p = 0.005), aortic reservoir function (∆ = −6.9%, p < 0.001), and Buckberg index (∆ = −0.28, p < 0.001). Firefighting augmented Ea/Ees (∆ = 0.10, p = 0.035) stemming from increases in Ea (∆ = 0.16 mmHg.mL −1 , p = 0.046) not counteracted by Ees. Heart rate changes were associated with Ew ( r = −0.60, p = 0.017) and aortic reservoir function ( r = −0.80, p < 0.001). Although middle‐aged firefighters exhibited typical post‐firefighting cardiovascular strain, including reduced coronary perfusion, the role of ventricular‐arterial interactions and pulsatile afterload remains unclear due to heart rate confounding.
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Marôco et al. (2025) conducted an observational in Healthy firefighters (n=22). High-intensity firefighting drills vs. Baseline (pre-firefighting) was evaluated on Ventricular-arterial coupling (Ea/Ees ratio) (∆ = 0.10, p=0.035). Acute high-intensity firefighting drills augmented the arterial to ventricular elastance ratio (∆ = 0.10, p = 0.035) and reduced coronary perfusion (Buckberg index ∆ = -0.28, p < 0.001).
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