Key result
Dogs with BOAS exhibited significantly higher heart rate variability compared to non-brachycephalic controls (median cSDNN 0.365 vs 0.246 ms, P=0.0058), indicating heightened baseline vagal tone.
Why the study?
Brachycephalic obstructive airway syndrome affects upper airways in brachycephalic dogs and might alter heart rate variability during wakefulness and sleep.
Does the presence of brachycephalic obstructive airway syndrome (BOAS) alter heart rate variability during wakefulness and sleep in dogs?
Cross-Sectional (n=46)
No
Does the presence of brachycephalic obstructive airway syndrome (BOAS) alter heart rate variability during wakefulness and sleep in dogs?
The presence of brachycephalic obstructive airway syndrome in dogs increases autonomic modulation and vagal tone compared to craniofacial conformation alone, with more pronounced differences observed during wakefulness.
Background Brachycephalic obstructive airway syndrome (BOAS) affects the upper airways of brachycephalic dogs and might alter heart rate variability (HRV). Hypothesis/Objectives This study aimed to evaluate HRV in dogs with BOAS during wakefulness and sleep. Animals Forty-six client-owned dogs: 34 brachycephalic (with and without BOAS) and 12 non-brachycephalic controls. Methods A prospective cross-sectional study utilizing 24-h Holter monitoring and segments recorded during wakefulness and sleep. The evaluated variables included heart rate, mean RR interval, the longest sinus pause, and HRV indices calculated over 24 h, as well as during segments of wakefulness and sleep: corrected standard deviation of NN intervals (cSDNN), corrected root mean square of successive differences (cRMSSD), the vagal tone index (VVTI), and Poincaré plot analysis. Results In the 24-h Holter analysis, BOAS dogs showed significantly higher values than controls, particularly in cSDNN (0.365 [IQR: 0.306-0.465] vs 0.246 [IQR: 0.208-0.359] ms, P = .0058) and cRMSSD (0.476 [IQR: 0.409-0.599] vs 0.312 [IQR: 0.259-0.462] ms, P = .0119). Sleep was associated with higher cSDNN, cRMSSD, and VVTI in all groups (StateSleep estimates: 0.105 [95% CI, 0.062-0.149], 0.426 [95% CI, 0.264-0.588], and 1.758 [95% CI, 1.378-2.139], respectively; all P < .001), with no significant group-by-state interaction for these variables. Presence of BOAS was moderately correlated with the longest sinus pause (r = 0.4197, P = .0023), cSDNN (r = 0.4600, P = .0006), and cRMSSD (r = 0.4214, P = .0018). Conclusions and clinical importance The presence of BOAS influences autonomic modulation more than the dogs’ craniofacial conformation. Differences in HRV were more pronounced in awake dogs, likely due to chronic respiratory alterations and intermittent hypoxia.
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Buriticá-Gaviria et al. (2026) conducted a cross-sectional in Brachycephalic obstructive airway syndrome (BOAS) (n=46). Brachycephalic obstructive airway syndrome (BOAS) vs. Non-brachycephalic conformation (Controls) was evaluated on Corrected standard deviation of NN intervals (cSDNN) over 24-hour Holter monitoring (p=0.0058). Dogs with BOAS exhibited significantly higher heart rate variability compared to non-brachycephalic controls (median cSDNN 0.365 vs 0.246 ms, P=0.0058), indicating heightened baseline vagal tone.
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