Circadian misalignment, due to shiftwork and/or individual chronotype and/or social jetlag (SJL), quantified as the difference between internal and social timing, may contribute to cardiovascular disease. Markers of endothelial dysfunction and activation of the coagulation system may predict cardiovascular pathology. The present study aim was to investigate the effects of shift work, SJL, and chronotype on endothelial function and coagulation parameters. One hundred female nurses underwent endothelial function testing using the EndoPAT and blood sampling for coagulation markers, repeated at 06:00–9:00 and 18:00–21:00. We found that compared with day workers, endothelial function and fibrinogen levels were lower (p = 0.001, p = 0.005, respectively) and the procoagulant parameters of plasminogen activator inhibitor-1 (PAI-1) and heparanase level and activity were higher amongst shift workers (p = 0.009, p = 0.03, p = 0.029, respectively). High SJL was associated with lower endothelial function (p = 0.002) and higher PAI-1, heparanase procoagulant activity, heparanase level, and D-Dimer level (p = 0.004, p = 0.003, p = 0.021, p = 0.006, respectively). In the late chronotype, PAI-1 and heparanase procoagulant activity were higher than in the early chronotype (p = 0.009, p = 0.007, respectively). Diurnal variation was found for PAI-1, von-Willebrand factor (vWF), heparanase, and heparan-sulfate with higher levels in the mornings. The correlation between shift/day workers and SJL or chronotype was moderately strong, indicating that SJL and chronotype are independent factors. In conclusion, findings suggest endothelial impairment and increased thrombotic risk in nurses working in shifts or with high SJL or late chronotype. The thrombotic risk is increased in the morning independent of circadian misalignment cause. These findings strengthen the importance of the alliance to the biological daily rhythm in daily life. Further research is needed to evaluate inhibitors of heparanase to attenuate the thrombotic risk in individuals with circadian misalignment.

BACKGROUND: Sleep disturbances and shift work are associated with increased cardiovascular risk, possibly through disruptions in endothelial and hemostatic function. While prior studies link acute sleep deprivation to vascular dysfunction, the impact of chronic sleep quality and circadian misalignment on endothelial health in healthy individuals, particularly shift workers, remains underexplored. AIM: To examine the association between objectively measured sleep quality and endothelial/hemostatic function in healthy female hospital nurses, comparing shift and day workers, and considering time-of-dayvariation. METHODS: In this repeated-measures study, 100 female nurses (51 shift, 49 day workers) aged 25–50 wore actigraphy devices for 7–14 days to assess total sleep time (TST), sleep efficiency (SEF), and wake after sleep onset (WASO). Endothelial function was measured using EndoPAT (Reactive Hyperemia Index – RHI). Hemostatic markers included plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (VWF), heparanase and heparanase procoagulant activity assessed by ELISA and chromogenic assays in morning and evening. RESULTS: TST was not associated with any vascular outcomes. Poor sleep quality (low SEF, high WASO) was significantly associated with reduced RHI and elevated PAI-1 level, heparanase level, and heparanase procoagulant activity levels. Shift workers exhibited lower evening RHI and higher evening PAI-1 compared to day workers. Regression models revealed significant main effects of SEF and WASO on endothelial and coagulation markers, with some interactions depending on shift type and time of measurement. No significant associations were found for VWF. CONCLUSIONS: Impaired sleep quality, but not sleep duration, is associated with endothelial dysfunction and procoagulant activation, particularly among shift-working nurses. These findings suggest that sleep quality may play a critical role in vascular health and support the use of sleep-based interventions to reduce cardiovascular risk in shift work populations.

Sleep disturbances and shift work are associated with increased cardiovascular risk, possibly through disruptions in endothelial and hemostatic function. While prior studies link acute sleep deprivation to vascular dysfunction, the impact of chronic sleep quality and circadian misalignment on endothelial health in healthy individuals, particularly shift workers, remains underexplored. The aim of this study was to examine the association between objectively measured sleep quality and endothelial/hemostatic function in healthy female hospital nurses, comparing shift and day workers, and considering time-of-day variation. In this repeated-measures study, 100 female nurses (51 shift, 49 day workers) aged 25–50 wore actigraphy devices for 7–14 days to assess total sleep time (TST), sleep efficiency (SEF), and wake after sleep onset (WASO). Endothelial function was measured using EndoPAT (Reactive Hyperemia Index—RHI). Hemostatic markers included plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (VWF), heparanase and heparanase procoagulant activity assessed by ELISA, and chromogenic assays in morning and evening. TST was not associated with any vascular outcomes. Poor sleep quality (low SEF, high WASO) was significantly associated with reduced RHI and elevated PAI-1 level, heparanase level, and heparanase procoagulant activity levels. Regression models revealed significant main effects of SEF and WASO on endothelial and coagulation markers, with some interactions depending on shift type and time of measurement. No significant associations were found for VWF. Impaired sleep quality, but not sleep duration, is associated with endothelial dysfunction and procoagulant activation, particularly among shift-working nurses. These findings suggest that sleep quality may play a critical role in vascular health and support the use of sleep-based interventions to reduce cardiovascular risk in shift-working populations.