Abstract
OBJECTIVE: A growing body of literature has documented that job stress is associated with the development of cardiovascular disease. Nevertheless, the pathophysiological mechanism of this association remains unclear. Therefore, we tried to elucidate the relationship between job stress, heart rate variability and metabolic syndrome.
METHOD
The study design was cross-sectional, and 169 industrial workers were recruited. A structured-questionnaire was used to assess the general characteristics and job characteristics (work demand, decision latitude). Heart rate variability (HRV) was recorded using SA-2000 (medi-core). HRV was assessed by time-domain and by frequency-domain analyses. Time domain analysis was performed for SDNN (Standard Deviation of NN interval), and spectral analysis for low-frequency (LF), high-frequency (HF) and total frequency power. Metabolic syndrome was defined on the basis of clustering of risk factors, when three or more of the following cardiovascular risk factors were included in the fifth quintile: glucose, systolic blood pressure, HDL-cholesterol (bottom quintile), triglyceride and waist-hip ratio.
RESULTS
The results showed that job characteristics were not associated with cardiovascular risk factors. The high strain group had a less favorable cardiovascular risk profile with higher levels of blood pressure, glucose, homocysteine, and clotting factor than the lower strain group (low strain+passive+active group), but the difference was not statistically significant. The SDNN of HRV was significantly lower in the high strain group than in the low strain group. The prevalence of metabolic syndrome in the low strain, passive, active and high strain groups was 9.7%, 13.9%, 14.9% and 23.8%, respectively. In the high strain group, the metabolic syndrome was significantly related to a decreased SDNN. However, we could not find a significant association in LF/HF ratio.
CONCLUSION
This result suggests that decreased HRV does not play a role in the development of disease; however, it can induce cardiovascular abnormalities or dysfunctions related to the onset of heart disease among high risk groups.
Citations
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