Next Article in Journal
Prevalence and Risk Factors of Occupational Health Hazards among Health Care Workers of Northern Saudi Arabia: A Multicenter Study
Previous Article in Journal
Influencing Factors of Subjective Cognitive Impairment in Middle-Aged and Older Adults
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

Identification of a High-Risk Group of New-Onset Cardiovascular Disease in Occupational Drivers by Analyzing Heart Rate Variability

1
Division of Family Medicine, Department of Family and Community Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
2
Division of Occupational Medicine, Department of Family and Community Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
3
School of Medicine, National Defense Medical Center, Taipei 114, Taiwan
4
National Institute of Environmental Health Sciences, National Health Research Institutes, Miaoli 350, Taiwan
5
Institute of Environmental and Occupational Health Sciences, National Yang Ming Chiao Tung University, Taipei 112, Taiwan
6
Department of Healthcare Administration, Asia University, Taichung 413, Taiwan
*
Author to whom correspondence should be addressed.
Int. J. Environ. Res. Public Health 2021, 18(21), 11486; https://doi.org/10.3390/ijerph182111486
Submission received: 1 October 2021 / Revised: 28 October 2021 / Accepted: 29 October 2021 / Published: 31 October 2021

Abstract

:
Purpose: This cohort study evaluated the effectiveness of noninvasive heart rate variability (HRV) analysis to assess the risk of cardiovascular disease over a period of 8 years. Methods: Personal and working characteristics were collected before biochemistry examinations and 5 min HRV tests from the Taiwan Bus Driver Cohort Study (TBDCS) in 2005. This study eventually identified 161 drivers with cardiovascular disease (CVD) and 627 without between 2005 and 2012. Estimation of the hazard ratio was analyzed by using the Cox proportional-hazards model. Results: Subjects with CVD had an overall lower standard deviation of NN intervals (SDNN) than their counterparts did. The SDNN index had a strong association with CVD, even after adjusting for risk factors. Using a median split for SDNN, the hazard ratio of CVD was 1.83 (95% CI = 1.10–3.04) in Model 1 and 1.87 (95% CI = 1.11–3.13) in Model 2. Furthermore, the low-frequency (LF) index was associated with a risk of CVD in the continuous approach. For hypertensive disease, the SDNN index was associated with increased risks in both the continuous and dichotomized approaches. When the root-mean-square of the successive differences (RMSSDs), high frequency (HF), and LF were continuous variables, significant associations with hypertensive disease were observed. Conclusions: This cohort study suggests that SDNN and LF levels are useful for predicting 8 year CVD risk, especially for hypertensive disease. Further research is required to determine preventive measures for modifying HRV dysfunction, as well as to investigate whether these interventions could decrease CVD risk among professional drivers.

1. Introduction

Cardiovascular disease (CVD) is not only the leading cause of death in the world, but also a compensable diseases related to work [1,2]. Since the 1950s, many researchers have studied the occupational issues of professional drivers [3]. Male professional drivers have an elevated morbidity and mortality from myocardial infarction (MI), ischemic heart disease (IHD), coronary heart disease (CHD) [4,5,6], stroke [7], and arteriosclerosis, according to the brachial–ankle pulse wave velocity [8]. Some studies have indicated that professional drivers have an elevated risk of developing CVD due to a high workload and a psychosocial work environment, due to a highly demanding job, irregular shifts, overtime work, and limited meals and rest time [6,9,10,11]. Professional drivers living with CVD conditions are predisposed to work stress, triggering death by overwork. Therefore, early monitoring of a high-risk CVD group is important to design preventive measures and thus limit further health damage in the workplace.
The examination of heart rate variability (HRV) is a simple, noninvasive, and relatively inexpensive method for an epidemiological study with a large sample size [12,13,14,15,16,17,18]. HRV measures specifically reflect vagal activity and have been recommended by the Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (1996) [19]. The cardiovascular system is controlled by the nervous system, specifically, the autonomic nervous system (ANS) [18,19,20,21]. Table S1 (available as an online Supplementary Material) presents the definitions of HRV measures applied in our research [22,23].
Reduced HRV as a marker of autonomic dysfunction has been shown to be associated with a poor prognosis of CVD, as well as with MI incidence, CVD mortality, and death from other causes in the general population [24,25,26,27,28,29,30,31], Furthermore, decreased HRV at rest is associated with a poor prognosis of CVD [32], and reduced resting HRV is considered a risk marker for future cardiovascular and other stress-related diseases [33].
However, some problems have emerged in this research field, including small sample sizes, incomplete CVD data collection, and poor control for confounders, which have limited the evaluation of the independent predictive effect of HRV, and has not shown a clear causal relationship. Therefore, we adopted a cohort study design to assess the effectiveness of noninvasive HRV analysis to measure professional drivers’ autonomic function, and then investigated the relationship between HRV and the 8 year risk of CVDs.

2. Materials/Subjects and Methods

2.1. Study Population

A Taiwan Bus Drivers Cohort (TBDC) has previously been established [34] for a longitudinal follow-up study. We linked this cohort to Taiwan’s National Health Insurance Research Database (NHIRD) to obtain the medical information of these subjects. This study was approved by the Institutional Review Board of the National Health Research Institutes, Taiwan (NIRB File Number: EC1060516-E). The composition and operation of the review committee were established in accordance with the International Conference on Harmonization–Good Clinical Practice (ICH-GCP) guidelines. The authors confirm that all experiments were carried out in accordance with the relevant guidelines and regulations. Informed consent was obtained from all participants. A questionnaire was used to collect basic information and working patterns, including demographic characteristics, work conditions (year of first employment and bus driving experience), lifestyle habits, and job stress assessment. This study adopted a longitudinal design from 2005 to 2012, the questionnaire collected information on basic and working patterns and HRV, and two sets of biochemical measurements were conducted simultaneously (Supplementary Figure S1). This cohort was linked to Taiwan’s National Health Insurance Research Database (NHIRD) to obtain the CVD medical information of these subjects.
Figure 1 illustrates the procedures used in this study. The TBDC was created in 2006 and includes 1650 professional drivers from the largest transportation company in Taiwan. The Driving Hours Dataset between 2005 and 2007 was used to exclude subjects with a driving duration of fewer than 100 days (n = 613). Then, personal and working characteristics were collected before biochemistry examinations, and HRV tests were performed from 2007 to 2008. We excluded individuals with incomplete questionnaires or laboratory data (n = 249). Subsequently, we linked the remaining 788 drivers to the ambulatory care expenditures-by-visits and inpatient expenditures-by-admissions data from the NHIRD. The defining criteria for CVD cases were that bus drivers had had at least five recorded clinical visits within one year due to CVD, or at least one inpatient record because of CVD for the first-listed diagnosis code. The strict criteria increased the sensitivity and decreased the specificity for confirming CVD. We identified 161 drivers with CVD (International Classification of Diseases 9th Revision, ICD-9: 390–459) and 627 drivers without CVD from 2005 to 2012. Among the 161 drivers with CVD, 84 had a history of CVD before 2006. Finally, 77 incident CVD cases were defined. Meanwhile, CVD (excluding hypertensive disease) (ICD-9: 391, 392.0, 393–398, 410–414, 416, 420–429), IHD (ICD-9: 410–414), cerebrovascular disease (ICD-9: 430–438), and congestive heart failure (CHF) (ICD-9: 398.91, 422, 425, 428, 402.x1, 404.x1, 404.x3) were analyzed separately.

2.2. HRV and Biochemical Measurements

Each participant underwent a blood biochemistry test and noninvasive HRV examination in resting conditions with the ANS Analyzer (Medicore SA-3000P, Jamsil-dong, Songpa-gu, Seoul, Korea). The variability in heart rate over 5 min was analyzed by the method of time domain and frequency domain. This provided the degree of balance and activity of the ANS. The standard deviation of the normal-to-normal beats interval (SDNN) and the square root of the mean squared differences of successive N–N intervals (RMSSD) were used to compare the time domain indexes. Frequency domain methods, including very low frequency (VLF, 0.0033–0.04 Hz), low frequency (LF, 0.04–0.15 Hz), high frequency (HF, 0.15–0.4 Hz), and total power (TP) were used to determine the sympathetic and parasympathetic heartbeat rate modulations at rest. The physical stress index (PSI) reflected the load and pressure on the heart based on SDNN at the same time [35].
For the determination of total cholesterol (CHOL), this study employed the cholesterol oxidase method on an AU640 analyzer (Beckman Coulter Ltd., High Wycombe, UK). High-density lipoprotein cholesterol (HDL-C) levels were determined using the immunoinhibition method on the AU640 analyzer (Beckman Coulter Ltd., High Wycombe, UK). Triglyceride (TG) concentrations were determined using an enzymatic method on the AU640 analyzer (Beckman Coulter Ltd., High Wycombe, UK). Fasting blood glucose (FG) was conducted using the hexokinase method, also on the AU640 analyzer (Beckman Coulter Ltd., High Wycombe, UK).

2.3. Statistical Analysis

Logarithmical transformation was performed to approximate the normal distribution. This study also used a Cox proportional-hazards model to assess the effect of HRV parameters on the risk of CVD (hazard ratios (HRs) and 95% confidence intervals (CIs)) and to adjust for confounding variables. Standard median splits were used on HRV parameters (the continuous variables) to turn them into dichotomous variables. The risk factors we considered included age, job tenure, shift work, body mass index, drinking, smoking, exercise, and education. Moreover, clinical conditions such as systolic blood pressure, CHOL, TG, HDL, and fasting glucose were also considered. Age at first employment (≥45 vs. <45 years), time since first employment (years), shift work, body mass index (BMI; >30 vs. ≤30), drinking, smoking, exercise, and education were adjusted in Model 1. Next, we adjusted for clinical conditions, including systolic blood pressure, LnCHOL, LnTG, LnHDL, and Ln (fasting glucose) in Model 2. All analyses were performed using the Statistical Analysis System (SAS) software package (Version 9.3 for Windows; SAS Institute Inc., Cary, NC, USA).

3. Results

Demographic characteristics of the bus drivers are presented in Table 1. A total of 788 drivers and 5334.2 person-years were accumulated in this cohort. Almost half of the bus drivers were over 40 years old in their first employment (43.3%), more than half of the bus drivers (51.5%) had over 5 years of driving experience, and almost half were irregular shift-working drivers (47%). About 16% of the bus drivers were obese (BMI ≥ 30 kg/m2), more than half of the bus drivers had a smoking habit (57.5%), and 21.7% of the bus drivers had a drinking habit.
A comparison of HRV parameters between different cardiovascular diagnostic categories is shown in Table S2 (available as an online Supplementary Material). The cohort of 788 subjects included 49 people with CVD (not including hypertensive disease); 128 people with hypertensive disease; 35 people with IHD; 14 people with cerebrovascular disease; 8 people with diseases of the arteries, arterioles, and capillaries, as well as other diseases of the circulatory system; and 15 people with CHF.

3.1. HRV Indices and 8-Year CVD Risks

Table 2 lists the hazard ratios for CVD per single unit increment of HRV parameters (as continuous variables), as well as for dichotomized HRV parameters. For the 788 drivers with a known CVD history, an increased SDNN level had a negative association with the risk of CVD in the continuous approach in both models. The SDNN had a significant hazard ratio (per single unit increment) of 0.67 to 0.70. Regarding the dichotomized approach with a median split, a low SDNN level was associated with CVD (hazard ratio = 1.47; 95% CI = 1.04–2.07) in Model 1 and (1.44; 95% CI = 1.01–2.05) in Model 2.
Similar to the aforementioned findings, among the 704 drivers without a known CVD history at baseline, the SDNN index continued to exhibit a statistically significant association with the risk of CVD. In Model 2, a single unit increment in Ln SDNN was associated with a decrease of 44% in the hazard for CVD, with adjustments for demographics, working characteristics, and clinical risk factors (95% CI = 0.34–0.95, p = 0.031). Regarding the dichotomized approach with a median split, a low SDNN was associated with a hazard ratio of 1.83 (95% CI = 1.10–3.04) in Model 1 and 1.87 (95% CI = 1.11–3.13) in Model 2. Furthermore, the LF index exhibited associations with the risk of CVD in the continuous approach in both models.

3.2. HRV Indices and 8 Year Cardiovascular Diagnostic Risk Categories

Table 3 and Table S3 list the hazard ratios of HRV indices for cardiovascular diagnostic categories among the different driver groups with or without a known CVD history at baseline. After we excluded 84 cases of prevalent CVD before 2006 (Table 3), we found that the SDNN index was associated with increased risks of hypertensive disease in both the continuous and dichotomized approaches. A single unit increment in Ln SDNN was associated with a decrease of 65% in hypertensive disease in both models (Model 1: 95% CI = 0.19–0.66, p = 0.001; Model 2: 95% CI = 0.19–0.67; p = 0.002). Low levels of SDNN (0–30) were associated with increased risks of hypertensive disease in both models (Model 1: hazard ratio = 1.99; 95% CI = 1.03–3.84; p = 0.039; Model 2: hazard ratio = 2.02; 95% CI = 1.03–3.96; p = 0.041).
Meanwhile, a single unit increment in Ln RMSSD was associated with a decrease of 45–46% in hypertensive disease in the two models (Model 1: hazard ratio = 0.54; 95% CI = 0.31–0.92, p = 0.024; Model 2: hazard ratio = 0.55; 95% CI = 0.31–0.96; p = 0.035).
A single unit increment in Ln HF was associated with a decrease of 26–27% in hypertensive disease in two models (Model 1: hazard ratio = 0.73; 95% CI = 0.57–0.94, p = 0.015; Model 2: hazard ratio = 0.74; 95% CI = 0.57–0.96; p = 0.026). Ln LF had a significant hazard ratio of 0.76 for hypertensive disease in Model 1 (95% CI = 0.59–0.97; p = 0.027), which became nonsignificant in Model 2.
For CHF, Ln RMSSD only had a significant hazard ratio of 3.51, for which in Model 2: 95% CI = 1.03–12.0; p = 0.046.

4. Discussion

This study used a prospective professional cohort study to investigate the relationship between HRV and the risk of CVD in professional drivers without known CVD. The major finding of this study was that the SDNN and LF levels are useful for predicting the 8 year CVD risk even when adjusting for CVD risk factors. Furthermore, increased SDNN and LF levels elevated the risks for other CVD events, such as hypertensive disease.
Each unit increment in Ln SDNN was associated with a decrease of 65% in hypertensive disease in Model 2 (95% CI = 0.19–0.67, p = 0.002). Our results are consistent with a meta-analysis that indicated that the predicted risks of incident CVD of the 10th and 19th percentiles in SDNN compared with the 50th percentile were 1.50 (95% CI = 1.22, 1.83) and 0.67 (95% CI = 0.41, 1.09), respectively [36]. In general, the SDNN is the gold standard for the medical stratification of cardiac risk and predicts both CVD morbidity and mortality. However, this only applies when recorded over a 24 h period.
Furthermore, this study observed that the LF index was associated with the risk of CVD and hypertensive disease in a continuous approach. While sitting upright during resting conditions, the LF reflected parasympathetic nervous system activity and baroreflex activity, not sympathetic nervous system activity and cardiac sympathetic innervation [22]. A previous study demonstrated that a higher occupational workload resulted in reduced LF power, which indicates that a high workload is related to attenuating cardiac autonomic modulation during sleep. In contrast, enhanced sympathetic baroreceptor cardiac regulation during sleep in workers with a high level of physical leisure time activity was observed [37]. Bus drivers have a high workload and less leisure-time activity, which leads to the development of CVDs; thus, low LF power is reflected in advance.
Additionally, drivers with a low HRV may already suffer from silent CVD. Numerous overlapping risk factors exist for reduced HRV and CVD events [38]. However, the causal relationship of risk factors with the development of CVD or reduced HRV is still not completely understood. Work stress is associated with both CVD and reduced HRV [39]; however, we do not yet know whether work stress affects the development of CVD more than it contributes to reduced HRV. Further investigating the associations between psychosocial risk factors and HRV indices would be worthwhile [40,41]. Psychosocial conditions such as work stress, stressful life events, and mood disorders are emerging risk factors for CVD [42]. Risk factors are preceded by indicators of decreased vagal function; therefore, HRV was found to be a useful tool for studying work-related stress and the accompanying physiological effects. The SDNN was reported to be significantly lower among those categorized into a high-job-strain group than among those categorized into a low-job-strain group [43]. Amelsvoort [39] reported that a decreased SDNN level in shift workers indicates less favorable cardiovascular autonomic regulation. Moreover, numerous studies have indicated that a chronic autonomic imbalance with sympathetic dominance may partially explain the effects of work stress on CVD events [21]. Therefore, HRV could be used to screen workers at high risk of CVD, and preventive measures could be taken in advance.
This study had several advantages that included the large bus drivers cohort, the prospective design, the noninvasive marker of 5 min HRV measurements, confounders’ adjustment, and comprehensive CVD data collection. In addition, we fully admit that the method of this study has some limitations. First, only male bus drivers were included, which restricts the generalization of the results to females. Second, HRV may be influenced by the severity of CVD, respiratory patterns, circadian rhythm, as well as by the use of β-blockers or antidepressants [44,45,46,47]. Thus, analyses should be further stratified by the severity of diseases, such as MI or revascularization, as well as by ICD-10-PCS (Procedure Codes). In addition, a history of diabetes, cognitive disorders, severe lung diseases, and the use of β-blockers and antidepressants must be considered. Third, the current study design could not clarify which risk factors contributed more to reduced HRV and CVD events so that preventive measures can be taken in advance. The small number of subjects in these sub-categories is a restriction of this study. The statistical power may be too small to generalize the results to other subjects. Fourth, there is a possibility that the high false positive rate in this study could have caused incorrect results. Therefore, we used the strict criteria that CVD cases had to have at least five visits for the same diagnosis within 1 year, or were an inpatient with one or more admissions during the study period based on a clinical physician’s suggestion. This increased the sensitivity and decreased the specificity for CVD, but it could have underestimated the effect of our final result. Lastly, and most importantly, this study directly used commercial instruments and automated programs to analyze the change in heart rate during the short term by the method of time domain and frequency domain with an ANS Analyzer. This may obscure some meaningful signals in heart rate for arrhythmias or other CVD diseases. With the technological advances in big data analytics, a future study should be attempted to identify and interpret the computer identification of segments with aberrant patterns for CVD diseases.
In conclusion, this professional drivers’ cohort study concluded that the HRV parameters SDNN and LF are independent predictors of CVD and hypertensive disease, even after adjusting for risk factors. Further research is required to determine the preventive measures for modifying HRV dysfunction, as well as to investigate whether these interventions could reduce CVD risk in professional drivers.

Supplementary Materials

The following are available online at www.mdpi.com/article/10.3390/ijerph182111486/s1, Figure S1: Taiwan Bus Driver Cohort Study (TBDCS) schedule diagram, Table S1: Definition of HRV measures, Table S2: Compared HRV index for cardiovascular diagnostic categories in study population (n = 788), Table S3: Hazard ratios and 95% confidence intervals for cardiovascular diagnostic categories by HRV index in the study population (n = 788).

Author Contributions

Y.-C.W. designed the research, collected data, engaged in drafting the manuscript, and revised it critically. W.-T.W. conducted data collection and data analysis and interpretation, and helped to draft the manuscript and revise it critically. C.-C.W. collected data and participated in data analysis. Y.-H.Y. participated in data analysis, review, and editing. W.-T.W. conceived the study, participated in its design and coordination, and helped to draft the manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

The National Health Research Institutes of Taiwan (grants 98-EO-PP01, 99-EO-PP01, 00-EO-PP01, EO-101-PP-01, EO-102-PP-01, and EO-103-PP-01), and the Institute of Occupational Safety and Health of Taiwan (grants IOSH96-M102 and IOSH97-M102) supported this study. The funders had no role in the research design, data collection and analysis, manuscript preparation, or publication decision.

Institutional Review Board Statement

The study was conducted according to the guidelines of the Declaration of Helsinki, and approved by the Institutional Review Board of National Health Research Institutes (NIRB File Number: EC1060516-E).

Informed Consent Statement

The Institutional Review Board of the National Health Research Institutes, Taiwan, approved this study (NIRB File Number: EC1060516-E). The composition and operation of the review committee are established in accordance with the ICH-GCP guidelines. The authors confirm that all experiments were performed in accordance with relevant guidelines and regulations. After explaining the content in detail, informed consent was obtained from each participant.

Data Availability Statement

The data are not available, because we did not inform the participants of the data transparency nor declare the possibility on the institutional review board.

Acknowledgments

The authors are very grateful to the late Saou-Hsing Liou for his contribution to this article. All authors thank the drivers and administrators at the bus company for their participation and cooperation. The current analysis was based on data provided by the Collaboration Center of Health Information Application, Ministry of Health and Welfare, Executive Yuan, Taiwan.

Conflicts of Interest

The authors declare no conflict of interests.

Abbreviations

HRVheart rate variability
TBDCSTaiwan Bus Driver Cohort Study
CVDcardiovascular disease
SDNNstandard deviation of N–N intervals
LFlow frequency
RMSSDroot-mean-square of the successive differences
HFhigh frequency
MImyocardial infarction
IHDischemic heart disease
CHDcoronary heart disease
ANSautonomic nervous system
NHIRDTaiwan’s National Health Insurance Research Database
ICH-GCPInternational Conference on Harmonization–Good Clinical Practice
CHFcongestive heart failure
VLFvery low frequency
TPtotal power
PSIphysical stress index
CHOLtotal cholesterol
HDL-Chigh-density lipoprotein cholesterol
TGtriglycerides
FGfasting blood glucose
HRshazard ratios
CIsconfidence intervals
BMIbody mass index
SASStatistical Analysis System
ICD-9International Classification of Diseases 9th Revision
ICD-10International Classification of Diseases 10th Revision
PCSprocedure codes

References

  1. Hwang, W.J.; Hong, O. Work-related cardiovascular disease risk factors using a socioecological approach: Implications for practice and research. Eur. J. Cardiovasc. Nurs. 2012, 11, 114–126. [Google Scholar] [CrossRef]
  2. World Health Organization. Cardiovascular Diseases (CVDs). 2021. Available online: https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds) (accessed on 11 June 2021).
  3. Tse, J.L.M.; Flin, R.; Mearns, K. Bus driver well-being review: 50 years of research. Transport. Res. F-Traf. 2006, 9, 89–114. [Google Scholar] [CrossRef]
  4. Bigert, C.; Gustavsson, P.; Hallqvist, J.; Hogstedt, C.; Lewne, M.; Plato, N.; Reuterwall, C.; Schéele, P. Myocardial infarction among professional drivers. Epidemiology 2003, 14, 333–339. [Google Scholar] [CrossRef]
  5. Netterstrom, B.; Juel, K. Impact of Work-Related and Psychosocial Factors on the Development of Ischemic Heart-Disease among Urban Bus Drivers in Denmark. Scand. J. Work Environ. Health 1988, 14, 231–238. [Google Scholar] [CrossRef] [Green Version]
  6. Hartvig, P.; Midttun, O. Coronary heart disease risk factors in bus and truck drivers. A controlled cohort study. Int. Arch. Occup. Environ. Health. 1983, 52, 353–360. [Google Scholar] [CrossRef]
  7. Tuchsen, F.; Hannerz, H.; Roepstorff, C.; Krause, N. Stroke among male professional drivers in Denmark, 1994-2003. Occup. Environ. Med. 2006, 63, 456–460. [Google Scholar] [CrossRef] [Green Version]
  8. Chen, C.C.; Shiu, L.J.; Li, Y.L.; Tung, K.Y.; Chan, K.Y.; Yeh, C.J.; Chen, S.C.; Wong, R.H. Shift Work and Arteriosclerosis Risk in Professional Bus Drivers. Ann. Epidemiol. 2010, 20, 60–66. [Google Scholar] [CrossRef]
  9. Gimeno, D.; Benavides, F.G.; Mira, M.; Martinez, J.M.; Benach, J. External validation of psychological job demands in a bus driver sample. J. Occup. Health 2004, 46, 43–48. [Google Scholar] [CrossRef] [Green Version]
  10. Wang, P.D.; Lin, R.S. Coronary heart disease risk factors in urban bus drivers. Public Health 2001, 115, 261–264. [Google Scholar] [CrossRef]
  11. Tsai, S.S.; Lai, C.H.; Shih, T.S.; Lin, M.H.; Liou, S.H. High job strain is associated with inflammatory markers of disease in young long-haul bus drivers. J. Occup. Health Psychol. 2014, 19, 336. [Google Scholar] [CrossRef]
  12. Von Borell, E.; Langbein, J.; Despres, G.; Hansen, S.; Leterrier, C.; Marchant-Forde, J.; Marchant-Forde, R.; Minero, M.; Mohr, E.; Prunier, A.; et al. Heart rate variability as a measure of autonomic regulation of cardiac activity for assessing stress and welfare in farm animals—A review. Physiol. Behav. 2007, 92, 293–316. [Google Scholar] [CrossRef] [PubMed]
  13. Cowan, M.J. Measurement of Heart-Rate-Variability. West. J. Nurs. Res. 1995, 17, 32–48. [Google Scholar] [CrossRef] [PubMed]
  14. Liao, D.P.; Barnes, R.W.; Chambless, L.E.; Simpson, R.J.; Sorlie, P.; Heiss, G. Age, Race, and Sex-Differences in Autonomic Cardiac-Function Measured by Spectral-Analysis of Heart-Rate-Variability—The Aric Study. Am. J. Cardiol. 1995, 76, 906–912. [Google Scholar] [CrossRef]
  15. Tsuji, H.; Venditti, F.J.; Manders, E.S.; Evans, J.C.; Larson, M.G.; Feldman, C.L.; Levy, D. Determinants of heart rate variability. J. Am. Coll. Cardiol. 1996, 28, 1539–1546. [Google Scholar] [CrossRef] [Green Version]
  16. Berntson, G.G.; Bigger, J.T.; Eckberg, D.L.; Grossman, P.; Kaufmann, P.G.; Malik, M.; Nagaraja, H.N.; Porges, S.W.; Saul, J.P.; Stone, P.H.; et al. Heart rate variability: Origins, methods, and interpretive caveats. Psychophysiology 1997, 34, 623–648. [Google Scholar] [CrossRef]
  17. Greiser, K.H.; Kluttig, A.; Schumann, B.; Swenne, C.A.; Kors, J.A.; Kuss, O.; Haerting, J.; Schmidt, H.; Thiery, J.; Werdan, K. Cardiovascular diseases, risk factors and short-term heart rate variability in an elderly general population: The CARLA study 2002–2006. Eur. J. Epidemiol. 2009, 24, 123–142. [Google Scholar] [CrossRef] [PubMed]
  18. Harris, K.F.; Matthews, K.A. Interactions between autonomic nervous system activity and endothelial function: A model for the development of cardiovascular disease. Psychosom. Med. 2004, 66, 153–164. [Google Scholar] [CrossRef]
  19. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Heart rate variability: Standards of measurement, physiological interpretation and clinical use. Circulation 1996, 93, 1043–1065. [Google Scholar]
  20. Zheng, Z.H.; Zeng, Y.T.; Wu, J.Y. Increased neuroplasticity may protect against cardiovascular disease. Int. J. Neurosci. 2013, 123, 599–608. [Google Scholar] [CrossRef]
  21. Thayer, J.F.; Ahs, F.; Fredrikson, M.; Sollers, J.J.; Wager, T.D. A meta-analysis of heart rate variability and neuroimaging studies: Implications for heart rate variability as a marker of stress and health. Neurosci. Biobehav. R. 2012, 36, 747–756. [Google Scholar] [CrossRef]
  22. Shaffer, F.; Ginsberg, J.P. An Overview of Heart Rate variability Metrics and Norms. Front. Public Health 2017, 28, 258. [Google Scholar] [CrossRef] [Green Version]
  23. Tsuji, H.; Venditti, F.J.; Manders, E.S.; Evans, J.C.; Larson, M.G.; Feldman, C.L.; Levy, D. Reduced Heart-Rate-Variability and Mortality Risk in an Elderly Cohort—The Framingham Heart-Study. Circulation 1994, 90, 878–883. [Google Scholar] [CrossRef] [Green Version]
  24. Bilchick, K.C.; Fetics, B.; Djoukeng, R.; Fisher, S.G.; Fletcher, R.D.; Singh, S.N.; Nevo, E.; Berger, R.D. Prognostic value of heart rate variability in chronic congestive heart failure (veterans affairs’ survival trial of antiarrhythmic therapy in congestive heart failure). Am. J. Cardiol. 2002, 90, 24–28. [Google Scholar] [CrossRef]
  25. Dekker, J.M.; Schouten, E.G.; Klootwijk, P.; Pool, J.; Swenne, C.A.; Kromhout, D. Heart rate variability from short electrocardiographic recordings predicts mortality from all causes in middle-aged and elderly men—The zutphen study. Am. J. Epidemiol. 1997, 145, 899–908. [Google Scholar] [CrossRef] [Green Version]
  26. La Rovere, M.T.; Bigger, J.T.; Marcus, F.I.; Mortara, A.; Schwartz, P.J.; Investigators, A. Baroreflex sensitivity and heart-rate variability in prediction of total cardiac mortality after myocardial infarction. Lancet 1998, 351, 478–484. [Google Scholar] [CrossRef]
  27. Papaioannou, V.; Pneumatikos, I.; Maglaveras, N. Association of heart rate variability and inflammatory response in patients with cardiovascular diseases: Current strengths and limitations. Front. Physiol. 2013, 4, 174. [Google Scholar] [CrossRef] [Green Version]
  28. Janszky, I.; Ericson, M.; Mittleman, M.A.; Wamala, S.; Al-Khalili, F.; Schenck-Gustafsson, K.; Orth-Gomer, K. Heart rate variability in long-term risk assessment in middle-aged women with coronary heart disease: The Stockholm Female Coronary Risk Study. J. Intern. Med. 2004, 255, 13–21. [Google Scholar] [CrossRef] [Green Version]
  29. Stein, P.K.; Barzilay, J.I.; Chaves, P.H.M.; Mistretta, S.Q.; Domitrovich, P.P.; Gottdiener, J.S.; Rich, M.W.; Kleiger, R.E. Novel Measures of Heart Rate Variability Predict Cardiovascular Mortality in Older Adults Independent of Traditional Cardiovascular Risk Factors: The Cardiovascular Health Study (CHS). J. Cardiovasc. Electr. 2008, 19, 1169–1174. [Google Scholar] [CrossRef] [Green Version]
  30. Fyfe-Johnson, A.L.; Muller, C.J.; Alonso, A.; Folsom, A.R.; Gottesman, R.F.; Rosamond, W.D.; Whitsel, E.A.; Agarwal, S.K.; MacLehose, R.F. Heart Rate Variability and Incident Stroke The Atherosclerosis Risk in Communities Study. Stroke 2016, 47, 1452–1458. [Google Scholar] [CrossRef] [Green Version]
  31. Dekker, J.M.; Crow, R.S.; Folsom, A.R.; Hannan, P.J.; Liao, D.; Swenne, C.A.; Schouten, E.G. Low heart rate variability in a 2-minute rhythm strip predicts risk of coronary heart disease and mortality from several causes—The ARIC study. Circulation 2000, 102, 1239–1244. [Google Scholar] [CrossRef]
  32. Leino, J.; Virtanen, M.; Kahonen, M.; Nikus, K.; Lehtimaki, T.; Koobi, T.; Lehtinen, R.; Turjanmaa, V.; Viik, J.; Nieminen, T. Exercise-test-related heart rate variability and mortality The Finnish cardiovascular study. Int. J. Cardiol. 2010, 144, 154–155. [Google Scholar] [CrossRef] [PubMed]
  33. Weber, C.S.; Thayer, J.F.; Rudat, M.; Wirtz, P.H.; Zimmermann-Viehoff, F.; Thomas, A.; Perschel, F.H.; Arck, P.C.; Deter, H.C. Low vagal tone is associated with impaired post stress recovery of cardiovascular, endocrine, and immune markers. Eur. J. Appl. Physiol. 2010, 109, 201–211. [Google Scholar] [CrossRef] [Green Version]
  34. Wu, W.T.; Tsai, S.S.; Liao, H.Y.; Lin, Y.J.; Lin, M.H.; Wu, T.N.; Shih, T.S.; Liou, S.H. Usefulness of overnight pulse oximeter as the sleep assessment tool to assess the 6-year risk of road traffic collision: Evidence from the Taiwan Bus Driver Cohort Study. Int. J. Epidemiol. 2017, 46, 266–277. [Google Scholar] [CrossRef]
  35. Wu, W.T.; Wang, C.C.; Liou, S.H. Effects of nanoparticles exposure and PON1 genotype on heart rate variability. Environ. Res. 2019, 176, 108377. [Google Scholar] [CrossRef]
  36. Hillebrand, S.; Gast, K.B.; de Mutsert, R.; Swenne, C.A.; Jukema, J.W.; Middeldorp, S.; Rosendaal, F.R.; Dekkers, O.M. Heart rate variability and first cardiovascular event in populations without known cardiovascular disease: Meta-analysis and dose-response meta-regression. Europace 2013, 15, 742–749. [Google Scholar] [CrossRef]
  37. Hallman, D.M.; Jorgensen, M.B.; Holtermann, A. On the health paradox of occupational and leisure-time physical activity using objective measurements: Effects on autonomic imbalance. PLoS ONE 2017, 12, e0177042. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  38. Thayer, J.F.; Yamamoto, S.S.; Brosschot, J.F. The relationship of autonomic imbalance, heart rate variability and cardiovascular disease risk factors. Int. J. Cardiol. 2010, 141, 122–131. [Google Scholar] [CrossRef]
  39. Van Amelsvoort, L.G.P.M.; Schouten, E.G.; Maan, A.C.; Swenne, C.A.; Kok, F.J. Occupational determinants of heart rate variability. Int. Arch. Occup. Environ. Health 2000, 73, 255–262. [Google Scholar] [CrossRef]
  40. Solarikova, P.; Turonova, D.; Brezina, I.; Rajčáni, J. Heart rate variability in psychosocial stress: Comparison between laboratory and real-life setting. Act. Nerv. Super. Rediviva 2016, 58, 77–82. [Google Scholar]
  41. Lischke, A.; Jacksteit, R.; Mau-Moeller, A.; Pahnke, R.; Hamm, A.O.; Weippert, M. Heart rate variability is associated with psychosocial stress in distinct social domains. J. Psychosom. Res. 2018, 106, 56–61. [Google Scholar] [CrossRef]
  42. Mulle, J.G.; Vaccarino, V. Cardiovascular Disease, Psychosocial Factors, and Genetics: The Case of Depression. Prog. Cardiovasc. Dis. 2013, 55, 557–562. [Google Scholar] [CrossRef] [Green Version]
  43. Hernandez-Gaytan, S.I.; Rothenberg, S.J.; Landsbergis, P.; Becerril, L.C.; De Leon-Leon, G.; Collins, S.M.; Díaz-Vásquez, F.J. Job Strain and Heart Rate Variability in Resident Physicians Within a General Hospital. Am. J. Ind. Med. 2013, 56, 38–48. [Google Scholar] [CrossRef] [PubMed]
  44. Fang, Y.; Sun, J.T.; Li, C.; Poon, C.S.; Wu, G.Q. Effect of Different Breathing Patterns on Nonlinearity of Heart Rate Variability. In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society, Vancouver, BC, Canada, 20–25 August 2008; pp. 3220–3223. [Google Scholar] [CrossRef]
  45. Aronson, D.; Burger, A.J. Effect of beta-blockade on heart rate variability in decompensated heart failure. Int. J. Cardiol. 2001, 79, 31–39. [Google Scholar] [CrossRef]
  46. O’Regan, C.; Kenny, R.A.; Cronin, H.; Finucane, C.; Kearney, P.M. Antidepressants strongly influence the relationship between depression and heart rate variability: Findings from The Irish Longitudinal Study on Ageing (TILDA). Psychol. Med. 2015, 45, 623–636. [Google Scholar] [CrossRef] [Green Version]
  47. Collins, S.; Karasek, R. Reduced vagal cardiac control variance in exhausted and high strain job subjects. Int. J. Occup. Med. Environ. Health 2010, 23, 267–278. [Google Scholar] [CrossRef] [PubMed] [Green Version]
Figure 1. Study flow diagram in the Taiwan Bus Driver Cohort Study.
Figure 1. Study flow diagram in the Taiwan Bus Driver Cohort Study.
Ijerph 18 11486 g001
Table 1. Baseline characteristics of the study population.
Table 1. Baseline characteristics of the study population.
VariablesAll DriversPerson Years
n(%) sum (%)
Total subjects788100.05334.2100.0
Non-CVD drivers62779.65014.394.0
CVD drivers a16120.4319.96.0
CVD history before 2006 a,b8410.711.70.2
Age (years)
<358711.0666.512.5
35–4434043.12417.445.3
45–4919925.31339.625.1
≥5016220.6910.717.1
Age at first employment (years)
≤3217522.21320.624.8
33–3827234.51872.635.1
≥3934143.32141.140.1
Time since first employment (years)
≤215019.01091.820.5
2.1–523229.41647.230.9
5.1–816420.81059.919.9
>824230.71535.428.8
Shift work modes c
Day shifts only33842.92264.842.5
Irregular shift37047.02587.148.5
Evening and Night shift8010.2482.49.0
BMI (kg/m2)
<2529937.92166.640.6
25–29.935945.62361.844.3
≥3013016.5805.915.1
Marital status
Unmarried12415.7919.817.2
Married57773.23841.772.0
Others8711.0572.710.7
Education
≤Junior high school23529.81556.929.2
Senior high and vocational school49863.23396.263.7
University and College557.0381.17.1
Cigarette smoking
Current smokers27635.01808.733.9
Ex-smokers546.9337.46.3
Never smokers45357.53148.159.0
Missing5
Alcohol use
Yes61277.74240.579.5
No17121.71061.319.9
Missing5
Moderate exercise
Yes55770.73857.072.3
No22128.01397.326.2
Missing10
a The selection criteria for CVD (ICD-9-CM: 390–459) were at least five clinical visit records within a year or at least one inpatient record; b drivers who had a CVD history before 2006; c based on the Driving Hours Dataset.
Table 2. Hazard ratios and 95% confidence intervals for cardiovascular disease by HRV index in the study population.
Table 2. Hazard ratios and 95% confidence intervals for cardiovascular disease by HRV index in the study population.
All Drivers (n =788)Drivers (n = 704) a
Model 1 bModel 2 cModel 1 bModel 2 c
Independent Variables dHR95% CIp-ValueHR95% CIp-ValueHR95% CIp-ValueHR95% CIp-Value
1As a continuous (LnSDNN)0.670.480.930.0180.700.501.000.0470.570.350.950.0290.560.340.950.031
2As a categorical
variable: SDNN
(≤30 vs. >30)
1.471.042.070.0291.441.012.050.0441.831.103.040.0201.871.113.130.018
3As a continuous (LnRMSSD)0.830.621.100.1850.850.641.130.2640.830.541.280.3970.810.521.260.348
4As a categorical
variable: RMSSD (≤20 vs. >20)
1.340.951.890.0981.340.941.910.1041.340.812.200.2561.380.832.280.211
5As a continuous (LnLF)0.850.740.970.0160.880.761.020.0840.800.660.980.0310.790.640.980.032
6As a categorical
variable: LF
(≤380 vs. >380)
1.180.791.740.4201.140.761.690.5351.250.702.230.4451.250.702.250.453
7As a continuous (LnHF)0.910.791.040.1760.930.811.060.2830.840.691.030.0980.840.681.040.112
8As a categorical
variable: HF
(≤168 vs. >168)
1.050.721.540.7861.070.721.580.7430.980.581.670.9491.000.581.710.996
9As a continuous (LnLF/HF)0.900.761.060.2120.940.801.110.4860.930.731.180.5410.930.721.190.544
10As a categorical
variable: LF/HF
(≤3.5 vs. >3.5)
1.270.901.780.1731.160.821.630.4091.240.752.030.4051.200.721.970.486
a Excluded 84 drivers who had a CVD history from before 2006; b Model 1: Adjusted for age at first employment (≥45 vs. <45 years), body mass index (>30 vs. ≤30), education, drinking, smoking, exercise, time since first employment (years), and shift work; c Model 2: Same as Model 1, with additional adjustments for systolic blood pressure, LnCHOL, LnTG, LnHDL, and Ln (fasting sugar); d each independent variable (1–20) was separately included in the models.
Table 3. Hazard ratios and 95% confidence intervals for cardiovascular events by HRV index in the Scheme 704 a.
Table 3. Hazard ratios and 95% confidence intervals for cardiovascular events by HRV index in the Scheme 704 a.
Cardiovascular Disease (Not Including Hypertensive Disease)Hypertensive DiseaseIschemic Heart
Disease
Congestive Heart Failure (CHF)
Independent Variables dHR95% CIp-ValueHR95% CIp-ValueHR95% CIp-ValueHR95% CIp-Value
Model 1 b1As a continuous (LnSDNN)1.440.593.550.4230.350.190.660.0011.120.353.540.8512.460.649.420.188
2As a categorical
variable:
SDNN (≤30 vs. >30)
1.610.644.050.3161.991.033.840.0391.360.454.140.5841.960.3510.950.441
3As a continuous (LnRMSSD)2.061.014.210.0480.540.310.920.0242.020.815.030.1332.920.929.290.069
4As a categorical
variable: RMSSD (≤20 vs. >20)
0.800.341.910.6151.870.943.700.0740.640.231.790.3920.820.183.710.795
5As a continuous (LnLF)1.050.731.510.7830.760.590.970.0270.960.611.500.8551.300.642.660.470
6As a categorical
variable: LF
(≤380 vs. >380)
1.010.362.800.9881.310.622.740.4791.130.314.110.8520.420.072.730.366
7As a continuous (LnHF)0.990.691.420.9710.730.570.940.0151.150.731.800.5430.900.451.800.764
8As a categorical
variable: HF
(≤168 vs. >168)
0.710.281.770.4601.290.632.640.4920.660.221.980.4530.540.093.260.502
9As a continuous (LnLF/HF)1.090.711.670.7081.040.771.420.7860.780.471.320.3581.700.724.000.228
10As a categorical
variable: LF/HF
(≤3.5 vs. >3.5)
0.950.402.260.9011.020.561.850.9541.340.424.280.6210.770.173.530.740
Model 2 c11As a continuous (LnSDNN)1.700.644.520.2900.350.190.670.0021.040.303.660.9473.180.7513.470.117
12As a categorical
variable: SDNN
(≤30 vs. >30)
1.610.624.180.3322.021.033.960.0411.400.444.410.5681.940.3012.570.485
13As a continuous (LnRMSSD)2.171.034.590.0430.550.310.960.0352.300.885.980.0893.511.0312.020.046
14As a categorical
variable: RMSSD (≤20 vs. >20)
0.790.331.910.6001.920.963.870.0670.570.201.680.3100.550.093.420.519
15As a continuous (LnLF)1.020.681.510.9360.770.591.010.0570.900.551.470.6741.350.593.100.477
16As a categorical
variable: LF
(≤380 vs. >380)
1.030.362.910.9601.210.572.580.6201.190.324.410.7900.290.032.670.272
17As a continuous (LnHF)1.030.701.530.8800.740.570.960.0261.190.731.930.4820.890.411.950.774
18As a categorical
variable: HF
(≤168 vs. >168)
0.620.241.610.3301.280.612.660.5170.620.191.960.4120.460.063.350.445
19As a continuous (LnLF/HF)0.980.621.560.9321.080.791.480.6170.700.401.220.2071.720.674.430.261
20As a categorical
variable: LF/HF
(≤3.5 vs. >3.5)
0.950.392.310.9010.910.501.670.7621.440.454.630.5430.790.154.090.779
a Excluded 84 drivers who had CVD history before 2006; b Model 1: Adjusted for age at first employment (≥45 vs. <45 years), body mass index (>30 vs. ≤30), education, drinking, smoking, exercise, time since first employment (years), and shift work; c Model 2: As Model 1 with additional adjustments for systolic blood pressure, LnCHOL, LnTG, LnHDL, and LnAC; d Each independent variable (1–20) was separately included in the models.
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

Wang, Y.-C.; Wang, C.-C.; Yao, Y.-H.; Wu, W.-T. Identification of a High-Risk Group of New-Onset Cardiovascular Disease in Occupational Drivers by Analyzing Heart Rate Variability. Int. J. Environ. Res. Public Health 2021, 18, 11486. https://doi.org/10.3390/ijerph182111486

AMA Style

Wang Y-C, Wang C-C, Yao Y-H, Wu W-T. Identification of a High-Risk Group of New-Onset Cardiovascular Disease in Occupational Drivers by Analyzing Heart Rate Variability. International Journal of Environmental Research and Public Health. 2021; 18(21):11486. https://doi.org/10.3390/ijerph182111486

Chicago/Turabian Style

Wang, Ying-Chuan, Chung-Ching Wang, Ya-Hsin Yao, and Wei-Te Wu. 2021. "Identification of a High-Risk Group of New-Onset Cardiovascular Disease in Occupational Drivers by Analyzing Heart Rate Variability" International Journal of Environmental Research and Public Health 18, no. 21: 11486. https://doi.org/10.3390/ijerph182111486

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop