Abstract

BackgroundThe reactive hyperemia index (RHI), which is obtained from the measurement of peripheral arterial tonometry (PAT), is highly associated with the percentage change in the end-diastolic arterial diameter (%flow-mediated dilatation) at reactive hyperemia. Low RHI is reported to be a mortality risk in patients with a high risk of cardiovascular (CV) disease. CV events are thought to be induced by physical and mental stress, including long-term fatigue and lack of sleep. However, the relationship between fatigue, lack of sleep, and endothelial function has not yet been established.MethodsHealthy hospital workers (n = 13, 6 men and 7 women) with an average age of 31.6 years were assigned to this study after they provided written informed consent. During the study period, we conducted 72 measurements of reactive hyperemia-peripheral arterial tonometry (RH-PAT) in the morning before or after their duty. At each measurement of the RH-PAT, we recorded the participants’ hours of sleep and evaluated their degree of fatigue using a visual analog scale (VAS).ResultsAlthough the VAS was significantly less (36 ± 16% and 64 ± 12%, p < 0.001) and the hours of sleep were longer (6.0 ± 1.1 h and 2.3 ± 1.0 h, p < 0.001) before duty compared to those after duty, the RHI was comparable between them (2.12 ± 0.53 vs. 1.97 ± 0.50, p = 0.21). The VAS score was significantly higher in participants with low RHI (< 1.67) than in those with normal RHI (≥ 2.07) (59 ± 13% and 46 ± 21%, respectively, p < 0.05). However, binary logistic regression showed no significant association between low RHI and the VAS when adjusted for systemic blood pressure (SBP) and heart rate variability (HRV). In a simple regression analysis, the RHI was significantly correlated with the VAS score but not with sleep duration. A multiple linear regression analysis also showed no significant association between the RHI and VAS scores after adjustment for SBP and HRV.ConclusionsVascular endothelial function was not associated with overnight duty, hours of sleep, or degree of fatigue in healthy young adults. Since the RHI may be decreased in severe fatigue conditions through autonomic nerve activity, one should consider the physical and mental conditions of the examinee when evaluating the RH-PAT results.

Highlights

  • The reactive hyperemia index (RHI), which is obtained from the measurement of peripheral arterial tonometry (PAT), is highly associated with the percentage change in the end-diastolic arterial diameter (%flow-mediated dilatation) at reactive hyperemia

  • The RHI, Chalder Fatigue Question (CFQ), visual analog scale (VAS) scale, sleep duration, heart rate (HR), and heart rate variability (HRV) of the study participants were evaluated to analyze the changes in vascular endothelial function before and after duty

  • The results showed that the VAS score was independently associated with RHI in model 1 and remained independently associated with RHI when systemic blood pressure (SBP) was adjusted in model 2; no statistical significance was observed when SBP and HRV were adjusted in model 3 (Table 3)

Read more

Summary

Introduction

The reactive hyperemia index (RHI), which is obtained from the measurement of peripheral arterial tonometry (PAT), is highly associated with the percentage change in the end-diastolic arterial diameter (%flow-mediated dilatation) at reactive hyperemia. Low RHI is reported to be a mortality risk in patients with a high risk of cardiovascular (CV) disease. The relationship between fatigue, lack of sleep, and endothelial function has not yet been established. The role of the endothelium in the development of clinical cardiovascular disease (CVD) has been well established [1]. Endothelial dysfunction is the hallmark of the early stage of coronary artery disease [2]. If present in coronary arteries or peripheral vessels, it is an independent predictor of cardiovascular events. Given that endothelial dysfunction is reversible, early detection of this disorder may have therapeutic and prognostic implications [3]. Early detection of vascular damage before clinical CVD development has become the goal of prevention [4, 5]

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call