Skip Navigation LinksHome > December 2013 - Volume 55 - Issue 12 > Work Stress and the Long QT Syndrome: High Job Strain and Ef...
Journal of Occupational & Environmental Medicine:
doi: 10.1097/JOM.0000000000000026
Original Articles

Work Stress and the Long QT Syndrome: High Job Strain and Effort–Reward Imbalance at Work Associated With Arrhythmic Risk in the Long QT Syndrome

Hintsa, Taina PhD; Määttänen, I. MSc; Hintsanen, M. PhD; Swan, H. PhD; Toivonen, L.; Kontula, K.; Keltikangas-Järvinen, L.

Free Access
Continued Medical Education
Article Outline
Collapse Box

Author Information

From the Institute of Behavioural Sciences (Dr Hintsa and Mr Määttänen, Mr Hintsanen, and Ms Keltikangas-Järvinen), Helsinki Collegium for Advanced Studies (Ms Hintsanen), Department of Cardiology, Helsinki University Central Hospital (Mr Swan and Ms Toivonen), and Department of Medicine (Mr Kontula), University of Helsinki, Helsinki, Finland.

Address correspondence to: Taina Hintsa, PhD, Institute of Behavioural Sciences, University of Helsinki, PO Box 9, University of Helsinki, FIN-00014 Helsinki, Finland (

The study was supported by grants from the Academy of Finland, project 132729, and Ella and Georg Ehrnrooth Foundation (TH); Finnish Foundation for Cardiovascular Research (HS and KK); and the Sigrid Juselius Foundation (KK).

Authors Hintsa, Määttänen, Hintsanen, Swan, Toivonen, Kontula, and Keltikangas-Järviven have no relationships/conditions/circumstances that present potential conflict of interest.

The JOEM editorial board and planners have no financial interest related to this research.

Collapse Box


Objectives: To examine whether work stress is associated with a symptomatic status of the long QT syndrome (LQTS).

Methods: The sample comprised 173 KCNQ1, KCNH2, or SCN5A gene mutation carriers (70 symptomatic) and control groups of 203 relatives without the family mutation, and of 1209 population-based young Finns control subjects. Work stress was assessed using the Job Content Questionnaire and Occupational Stress Questionnaire.

Results: We found an association between the occurrence of symptoms in the LQTS and high work stress, higher job demands/effort, lower job control, and lower rewards compared with control subjects. We also found that symptomatic LQTS mutation carriers had higher work stress than asymptomatic LQTS mutation carriers.

Conclusions: Higher work stress is related to arrhythmic risk in the LQTS. It may be useful to incorporate assessment of work conditions and stress interventions into management of high-risk patients.

Back to Top | Article Outline
Learning Objectives

* Outline previous evidence on the contribution of stress to symptomatic long QT syndrome.

* Summarize the new findings on the relationship between work stress and the occurrence of symptomatic long QT syndrome.

* Discuss the study implications for management of workers at risk of symptomatic long QT syndrome.

The long QT syndrome (LQTS) is an inherited arrhythmic disorder that increases susceptibility to ventricular arrhythmias and sudden death.1–3 The syndrome is divided into subtypes, the three most common of which are LQT1, LQT2, and LQT3, in which mutations affect the potassium channel gene KCNQ1 or KCNH2, or the sodium channel gene SCN5A, respectively.4 Triggers that precipitate ventricular arrhythmias in the LQTS most typically include physical exercise and acute stress (LQT1), sudden arousal or startling auditory stimuli (LQT2), or rest or sleep (LQT3).5 It has been reported that sudden death is likely to result from an interaction between environmental conditions and a trigger.5 There is evidence suggesting that as the amount of environmental loading increases, the intensity of the trigger required to induce a cardiac event is likely to decrease.6–8

Environmental loading caused by stress seems to play a role in the symptomatic LQTS. It has been previously shown that stress-related factors outside work are related to the increased likelihood of having experienced cardiac events in the LQTS: it has been found that symptomatic LQTS mutation carriers report a higher level of depressive symptoms,9 have experienced more major stressful life events, and are more exhausted (chronically stressed) than asymptomatic LQTS mutation carriers or noncarrier relative control subjects.10 It has also been previously shown that LQTS mutation carriers are more sensitive to stress in terms of temperament than the general population.11,12 There is, however, no information on how work characteristics and work stress are related to clinical manifestation of the LQTS.

Two scientifically widely tested work stress models include Karasek's (1979) job demands–job control model (or job strain model) and Siegrist's (1996) effort–reward imbalance model.13–16 In Karasek's model, job demands refer to time pressures and an excessive work load, and job control refers to employees' opportunities to use social, organizational, and personal resources in their work tasks and environments.13,14 Job strain is assumed to result when job demands are high and job control is low.13

Siegrist's effort–reward imbalance model is based on social exchange theory, and emphasizes current social exchange processes in a work context.15,16 Efforts refer to demands and obligations of work such as time pressures and task difficulty. Rewards denote esteem rewards, monetary rewards, job security, and career development opportunities. If effort is not rewarded, an effort–reward imbalance may occur, resulting in a condition of high efforts and low rewards, which is assumed to induce work stress in the majority of the employees.15,16

Higher job strain and effort–reward imbalance have previously been related to an increased risk of cardiovascular disease.15,17–22 Higher effort–reward imbalance at work or lower reward has been shown to increase the risk of recurrent cardiac events.23 It is possible that work stress may also increase arrhythmic risk in the LQTS through altered autonomic function as autonomic tone and reflexes have been related to an increased risk of arrhythmias.24–26 Markers of reduced vagal activity, such as suppressed baroreflex sensitivity and heart rate variability, have been demonstrated to be predictors of cardiac mortality.24 It has been suggested that stress-inducing work characteristics may burden the vascular and nervous systems.27–30

Our first aim was to examine whether job strain, effort–reward imbalance at work, and their components (job demands/effort, job control, and rewards at work) are associated with the symptom status in the molecularly defined LQTS, and second, whether LQTS mutation carriers differ from the Finnish population in job strain or effort–reward imbalance. It was hypothesized that the occurrence of symptoms in the LQTS would be associated with higher perceived work stress, higher job demands/effort, lower job control, and lower rewards at work.

Back to Top | Article Outline



LQTS patients were recruited from the Finnish LQTS registry—which has included patients referred for molecular genetic studies at Helsinki University Hospital from all over the country since 1993—and who had also responded to a psychological questionnaire survey in 2006. Registry subjects who fulfilled the following criteria were included in this study: molecularly verified positive or negative mutation carrier status for the LQTS-causing mutation; the presence or absence of an LQTS-causing gene mutation, as verified by DNA analysis aged 16 to 65 years; permanent residency in Finland; and a written informed consent that conforms to the ethical guidelines of Helsinki University Central Hospital. All the patients in Finland with the molecular genetic diagnosis of the LQTS were included in the registry up to the year 2011. The diagnosis of the index patients of each family was made by their own cardiologist. Thereafter, cascade screening of the relatives was carried out.

Of this registry, 419 persons who worked full time in 2006 were available. Of them, 394 reported their education and occupation, which was required for this study. Because of the missing information on some other study variables, the final material comprised 376 participants, including 70 symptomatic and 103 asymptomatic LQTS mutation carriers, as well as 203 control subjects consisting of relatives of LQTS patients devoid of an LQTS-causing mutation. In addition, as controls we studied 1209 individuals derived from the Young Finns Study31,32 who had full information on all study variables. The analyses comparing symptomatic and asymptomatic LQTS mutation carriers and their unaffected relatives were additionally controlled for the use of β-blockers.

Back to Top | Article Outline
Job Strain

Job control was measured with a nine-item scale from the Karasek's Job Content Questionnaire.33 The responses of job control (Cronbach α = 0.88) were given on a five-point scale, ranging from 1 (strongly disagree) to 5 (strongly agree). Job demands (α = 0.64) were measured using a three-item scale from the Occupational Stress Questionnaire,34 which has been validated in Finland in 25,000 employees. The items were “Do you have to hurry to get your work done?” “Does your work have phases that are too difficult?” and “Is your work mentally straining?” The responses were given on a scale ranging from 1 (strongly disagree) to 5 (strongly agree). The linear job strain indicator was obtained by subtracting the job control score from the job demands score.35

Back to Top | Article Outline
Effort–Reward Imbalance

Because a standard long version of effort–reward imbalance measure by Siegrist15,16 was not available in this study, a shorter measure that has been used previously in Finnish work stress studies was applied.36,37 Effort and reward were measured with three-item scales from the Occupational Stress Questionnaire,34,38 which are similar to the items of the original effort–reward imbalance questionnaire. The number of items in the proxy measure was lower than that in the original measure (effort, 3 vs 6; reward, 3 vs 11). Effort (Cronbach α = 0.64) was measured with the same three items from the Occupational Stress Questionnaire as job demands. Reward (α = 0.61) was measured with three items: “Do you get help and support from your superior if needed?” “How do your coworkers get along with each other in the workplace?” and “How satisfied are you with your current employment?” Responses to the effort and reward items were given on a five-point scale; the higher the value, the higher the effort and reward. A mean value was calculated. Effort–reward imbalance was calculated by dividing efforts by rewards. Values of more than 1 indicate that efforts are higher than expected rewards, indicating a stressful condition at work.16,39

Education was measured by total years of education. Socioeconomic status was reported and classified as manual (semiskilled and unskilled manual occupations), nonmanual (clerical and skilled manual occupations), and upper nonmanual (managerial and professional occupations).

Back to Top | Article Outline


The main demographic characteristics as well as the mean data on the job strain and effort–reward imbalance analyses are summarized in Table 1. LQTS mutation carriers and noncarrier relative controls were older than the young Finns control group. The majority of the symptomatic LQTS patients were women (81.4%). More than half of the LQTS subjects and their relative control subjects reported their occupational class as manual (semiskilled and unskilled occupations).

Table 1
Table 1
Image Tools

Table 2 presents logistic multinomial regression analyses comparing symptomatic and asymptomatic LQTS mutation carriers and their nonaffected relatives (control subjects). Analyses controlling for age, sex, education, and occupation showed an association of the symptom status of the LQTS with higher job strain (odds ratio [OR], 1.72; 95% confidence interval [CI], 1.27 to 2.34; P 0.001) and higher effort–reward imbalance (OR, 3.92; 95% CI, 1.66 to 9.24; P 0.002) compared with control subjects. We found that of the work characteristics, higher job demands (OR, 1.72; 95% CI, 1.16 to 2.57; P 0.007), lower job control (OR, 0.46; 95% CI, 0.46 to 0.99; P 0.046), and lower rewards at work (OR, 0.59; 95% CI, 0.40 to 0.86; P 0.007) were associated with the occurrence of symptoms in the LQTS independently of age, sex, education, and occupation compared with relative control subjects. Controlling additionally for the use of β-blockers and smoking did not essentially change the results. Asymptomatic LQTS mutation carriers did not differ from control subjects in job demands/effort, job control, or rewards at work.

Table 2
Table 2
Image Tools

Table 3 presents binary logistic regression analyses comparing symptomatic and asymptomatic LQTS mutation carriers. Analyses controlling for age, sex, education, and occupation showed an association of high job strain (OR, 1.52; 95% CI, 1.06 to 2.17) and high effort–reward imbalance (OR, 5.66, 95% CI, 1.75 to 18.27) in LQTS mutation carriers with arrhythmic events compared with LQTS mutation carriers without arrhythmic events. Controlling additionally for the use of β-blockers did not essentially change the results. Comparing symptomatic LQTS mutation carriers with asymptomatic LQTS mutation carriers, we found that lower rewards at work (OR, 0.59, 95% CI 0.37 to 0.95; P 0.031) were related to the occurrence of symptoms in the LQTS.

Table 3
Table 3
Image Tools

As we have previously found stress-related differences between the general Finnish population and LQTS mutation carriers,11,40 we compared symptomatic and asymptomatic LQTS mutation carriers with the controls consisting of the Young Finns Study subjects in job strain and effort–reward imbalance. Table 4 presents the results of multinomial logistic regression. Analyses controlling for age, sex, education, and occupation showed an association of higher job strain (OR, 1.51; 95% CI, 1.13 to 2.02; P = 0.006) and higher effort–reward imbalance (OR, 1.86; 95% CI, 1.00 to 3.46; P = 0.049) in symptomatic LQTS mutation carriers compared with young Finns control subjects. This pattern was not found for asymptomatic LQTS mutation carriers.

Table 4
Table 4
Image Tools
Back to Top | Article Outline


We examined whether job strain and effort–reward imbalance and their components (job demands/effort, job control, rewards at work) are associated with the symptom status in the LQTS. We found that higher work stress indexed by job strain and effort–reward imbalance was associated with the occurrence of symptoms in the LQTS. Of the components of job strain and effort–reward imbalance, higher job demands, lower job control, and lower rewards at work were all related to history of symptoms in the LQTS. In addition, the symptomatic, but not the asymptomatic, LQTS mutation carriers differed in both job strain and effort–reward imbalance from the general Finnish population.

Higher job strain was associated with history of LQTS symptoms independently of age, sex, education, and occupation. Taking β-blocker medication into account in the analyses did not attenuate the association. Previous evidence has shown that job strain is a major risk for cardiovascular disease,18,41 and job strain has been associated with a significantly increased risk of recurrent coronary heart disease events.42 These results add to the literature by showing an association between job strain and the risk of arrhythmias in the LQTS.

Reduced capacity of cardiac vagal control may play a major role in increasing the risk of arrhythmic events of LQTS patients under stress. Job strain has previously been associated with pathogenic cardiovascular regulation.27 Vagal tone has the primary influence on cardiovascular recovery, and vagal rebound is associated with alterations in the baroreflex sensitivity.43 In the study of Collins et al,27 among healthy men, an increased sympathetic and decreased vagal activity was observed during the workday in the high-strain group. Job strain has also been related to greater systolic pressor responses to phenylephrine, which mimics the effects of noradrenaline, whereas lower job control has been associated with the higher level of plasma noradrenaline.44,45

Lower values of baroreflex sensitivity, measured by the phenylephrine method, have been related to the lower risk for life-threatening arrhythmias.26 This suggests that when strong autonomic reflexes result in rapid increases in the heart rate, the probability of arrhythmic events increases. There is evidence of reduced vagal cardiac control and variability in high-strain job and exhausted subjects.46 High job strain subjects have reduced vagal cardiac control capacity, and exhausted subjects have additional reductions in such capacity.46 It has been previously shown that symptomatic LQTS mutation carriers report more chronic stress, manifesting with a higher level of exhaustion than the asymptomatic LQTS mutation carriers.10 As both higher exhaustion and higher job strain are related to suppressed parasympathetic activity and control of the heart rate,46 LQTS mutation carriers with high job strain might be at an increased risk for arrhythmias because of individual and environmental loading.

Of the work characteristics, higher job demands/effort at work were observed among symptomatic LQTS patients than among relative control subjects and asymptomatic LQTS mutation carriers. The association between job strain and the occurrence of symptoms in the LQTS seems to be mainly due to higher job demands rather than lower job control because job demands were more robustly associated with symptomatic status of the LQTS. This differs from previous studies reporting no association between job demands and the parasympathetic nervous system, or between job demands and baroreflex sensitivity.27,45

Lower job control was related to the symptomatic LQTS compared with relative control subjects when adjusting for age, sex, education, and occupation, but this association became nonsignificant when β-blocker treatment was taken into account. There was, however, no significant difference between symptomatic and asymptomatic LQTS mutation carriers in their job control. Our finding linking lower job control with potential arrhythmic risk is in accordance with previous findings on job control, altered autonomic function, and baroreflex sensitivity. Thus, it has been previously shown that those with lower job control have lower diastolic baroreflex sensitivity45 and reduced cardiac vagal control.27

We also found that higher effort–reward imbalance was related to the occurrence of symptoms in the LQTS. Effort–reward imbalance was 3.3-fold among symptomatic LQTS mutation carriers compared with their nonaffected relatives, and more than 5-fold compared with asymptomatic LQTS mutation carriers. These findings are in line with a previous study showing that effort–reward imbalance at work is positively associated with the occurrence of coronary events.22 Higher effort–reward imbalance has previously been related to lower vagal cardiac control.47,48 Higher effort–reward imbalance has been associated with both reduced parasympathetic activity in samples consisting only or mainly of women,49,50 but not in men.49 The previous studies have reported ORs ranging from 1.22 to 8.98 for the association between high effort–reward imbalance and elevated risk of cardiovascular disease incidence22 that are in accordance with the ORs found in this study.

Lower rewards at work were associated with symptomatic LQTS status, which is in line with a previous studies reporting that lower rewards at work are related to the higher heart rate and reduced vagal activity49 and that lower rewards are associated with increased risks of recurrent coronary heart disease events among workers who had returned to work after a first myocardial infarction.23 Lower rewards at work have been related to the higher heart rate and reduced vagal activity in a population-based sample although there was no association between effort and cardiac measures.49 We show here that lower reward at work was related to the symptom status in the LQTS.

The clinical importance of this study comes from the finding that higher work stress is related to the risk of arrhythmic events in the LQTS. Being chronically stressed at work may alter the autonomic nervous function, in particular suppress parasympathetic activation, and may secondly prevent LQTS mutation carriers from relaxing after work or during days of rest. This process may eventually lead to fatigue or exhaustion. Therefore, it could be beneficial to enquire into work conditions during clinical management of LQTS patients if regarded necessary. Accordingly, it may be important to initiate stress interventions at work and refer the patient to psychological assistance when needed.

There are some limitations in the study that need to be considered when interpreting the results. The use of only self-report measures may bias the results. Work stress was self-reported in a cross-sectional study, which is a limitation compared to that from prospective data. Therefore, prospective studies are needed in the future. Another limitation is a potential bias because of nonresponse to the work stress questionnaire. It is possible that persons who did not respond were not interested to participate because they did not experience stress at work. It is, however, equally likely that persons who did not respond were not able to respond because of being excessively stressed at work. Furthermore, using a proxy measure for effort–reward imbalance may have influenced the findings. Rewards at work are measured in a more versatile way in the original measure of effort–reward imbalance and each of them consists of several items, whereas the proxy measure used in this study measured rewards at work only with three items. The reliability of the reward scale was, however, within an acceptable range. It is recommended to use the original effort–reward imbalance measure in the future studies whenever possible. There are also significant strengths in this study. The sample of the study consisted of DNA-verified Finnish LQTS mutation carriers as well as two control groups, one consisting of unaffected relatives of the patients and the other of a population-based control material. Work stress was measured with two work stress questionnaires, which have been widely validated in cardiovascular research and which reflect two of the most well-known work stress models.

Back to Top | Article Outline


Work stress is associated with the occurrence of symptoms in the LQTS. Reduced vagal tone because of chronic exhaustion may be the mechanism that increases the risk of arrhythmias. Measures to reduce chronic stress and avoidance of exhaustion should be considered as lifestyle modifications that could reduce the risk of cardiac events in the LQTS. Therefore, assessment of current work conditions and informing the patient about dealing with work stress should be part of the clinical management of at least of high-risk LQTS patients. In addition, addressing the work conditions of LQTS mutation carriers and initiating stress interventions at work when needed would be important.

Back to Top | Article Outline


1. Schwartz PJ, Periti M, Malliani A. Fundamentals of clinical cardiology: the long QT syndrome. Am Heart J. 1975;89:378–390.

2. Schwartz PJ, Priori SG, Locati EH, et al. Long QT syndrome patients with mutations of the SCN5A and HERG genes have differential responses to Na+ channel blockade and to increases in heart rate. Implications for gene-specific therapy. Circulation. 1995;92:3381–3386.

3. Swan H, Toivonen L, Viitasalo M. Rate adaptation of QT intervals during and after exercise in children with congenital long QT syndrome. Eur Heart J. 1998;19:508–513.

4. Splawski I, Shen J, Timothy KW, et al. Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2. Circulation. 2000;102:1178–1185.

5. Schwartz PJ, Priori SG, Spazzolini C, et al. Genotype-phenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias. Circulation. 2001;103:89–95.

6. Reich P, DeSilva RA, Lown B, et al. Acute psychological disturbances preceding life-threatening ventricular arrhythmias. JAMA. 1981;246:233–235.

7. Keefe DL, Schwartz J, Somberg JC. The substrate and the trigger: the role of myocardial vulnerability in sudden cardiac death. Am Heart J. 1987;113:218–225.

8. Willich SN, Maclure M, Mittleman M, et al. Sudden cardiac death. Support for a role of triggering in causation. Circulation. 1993;87:1442–1450.

9. Hintsa T, Keltikangas-Järvinen L, Puttonen S, et al. Depressive symptoms in the congenital long QT syndrome. Ann Med. 2009;41:516–521.

10. Hintsa T, Puttonen S, Toivonen L, et al. A history of stressful life events, prolonged mental stress and arrhythmic events in inherited long QT syndrome. Heart. 2010;96:1281–1286.

11. Määttänen I, Hintsa T, Toivonen L, et al. Cloninger's temperament traits and inherited long QT syndrome. J Psychosom Res. 2011;71:245–249.

12. Määttänen I, Keltikangas-Järvinen L, Swan H, et al. Stress proneness in molecularly defined long qt syndrome: a study using temperament assessment by behavioural inhibition system scale. Stress Health. 2012;29:150–155.

13. Karasek RA. Job demands, job decision latitude, and mental strain: implications for job redesign. Admini Sci Quart. 1979;24:285–308.

14. Karasek RA, Theorell T. Healthy Work: Stress, Productivity and The Reconstruction of Working Life. New York, NY: Basic Books; 1990.

15. Siegrist J. Adverse health effects of high-effort/low-reward conditions. J Occup Health Psychol. 1996;1:27–41.

16. Siegrist J, Starke D, Chandola T, et al. The measurement of effort-reward imbalance at work: European comparisons. Soc Sci Med. 2004;58:1483–1499.

17. van der Doef M, Maes S. The job-demand-control-(support) model and psychological wellbeing: a review of 20 years of empirical research. Work Stress. 1999;13:87–114.

18. Belkic KL, Landsbergis PA, Schnall PL, et al. Is job strain a major source of cardiovascular disease risk? Scand J Work Environ Health. 2004;30:85–128.

19. Hintsa T, Shipley M, Gimeno D, et al. Do pre-employment influences explain the association between psychosocial factors at work and coronary heart disease? The Whitehall II study. Occup Environ Med. 2010;67:330–334.

20. Hintsanen M, Kivimäki M, Elovainio M, et al. Job strain and early atherosclerosis: the Cardiovascular Risk in Young Finns Study. Psychosom Med. 2005;67:740–747.

21. Kivimäki M, Leino-Arjas P, Luukkonen R, et al. Work stress and risk of cardiovascular mortality: prospective cohort study of industrial employees. BMJ. 2002;325:857–861.

22. van Vegchel N, de Jonge J, Bosma H, et al. Reviewing the effort-reward imbalance model: drawing up the balance of 45 empirical studies. Soc Sci Med. 2005;60:1117–1131.

23. Aboa-Eboule C, Brisson C, Maunsell E, et al. Effort-reward imbalance at work and recurrent coronary heart disease events: a 4-year prospective study of post-myocardial infarction patients. Psychosom Med. 2011;73:436–447.

24. La Rovere MT, Pinna GD, Hohnloser SH, et al. Baroreflex sensitivity and heart rate variability in the identification of patients at risk for life-threatening arrhythmias: implications for clinical trials. Circulation. 2001;103:2072–2077.

25. Schwartz PJ, Vanoli E, Stramba-Badiale M, et al. Autonomic mechanisms and sudden death. New insights from analysis of baroreceptor reflexes in conscious dogs with and without a myocardial infarction. Circulation. 1988;78:969–979.

26. Schwartz PJ, Vanoli E, Crotti L, et al. Neural control of heart rate is an arrhythmia risk modifier in long QT syndrome. J Am Coll Cardiol. 2008;51:920–929.

27. Collins SM, Karasek RA, Costas K. Job strain and autonomic indices of cardiovascular disease risk. Am J Ind Med. 2005;48:182–193.

28. van der Palen J, Doggen CJ, Beaglehole R. Variation in the time and day of onset of myocardial infarction and sudden death. N Z Med J. 1995;108:332–334.

29. Douglas AS, Dunnigan MG, Allan TM, et al. Seasonal variation in coronary heart disease in Scotland. J Epidemiol Community Health. 1995;49:575–582.

30. Schwartz PJ, La Rovere MT. ATRAMI: a mark in the quest for the prognostic value of autonomic markers. Autonomic tone and reflexes after myocardial infarction. Eur Heart J. 1998;19:1593–1595.

31. Raitakari OT, Juonala M, Rönnemaa T, et al. Cohort profile: the cardiovascular risk in Young Finns Study. Int J Epidemiol. 2008;37:1220–1226.

32. Åkerblom HK, Uhari M, Pesonen E, et al. Cardiovascular risk in young Finns. Ann Med. 1991;23:35–40.

33. Karasek RA. Job Content Questionnaire and User's Guide. Revision 1.1. Lowell, MA: University of Massachusetts; 1985.

34. Elo A-L, Leppänen A, Lindström K, et al. Occupational Stress Questionnaire: User's Instructions (Reviews 19). Helsinki: Finnish Institute of Occupational Health; 1992.

35. Landsbergis PA, Schnall PL, Warren K, et al. Associations between ambulatory blood pressure and alternative formulations of job strain. Scand J Work Environ Health. 1994;20:349–363.

36. Hintsa T, Hintsanen M, Jokela M, et al. Divergent influence of different type A dimensions on job strain and effort-reward imbalance. J Occup Environ Med. 2010;52:1–7.

37. Hintsa T, Kivimäki M, Elovainio M, et al. Preemployment family factors as predictors of effort/reward imbalance in adulthood: a prospective 18-year follow-up in the Cardiovascular Risk in Young Finns Study. J Occup Environ Med. 2007;49:659–666.

38. Elo A-L, Leppänen A, Lindström K, et al. Miten Käytät Työstressikyselyä (Työterveyshuolto 17)? How to Use Occupational Stress Questionnaire? Helsinki: Työterveyslaitos, Finnish Institute of Occupational Health; 1990.

39. Niedhammer I, Tek M-L, Starke D, et al. Effort-reward imbalance model and self-reported health:cross-sectional and prospective findings from the GAZEL cohort. Soc Sci Med. 2004;58:1531–1541.

40. Määttänen I, Keltikangas-Järvinen L, Pulkki-Råback L, et al. Stressful work involvement and inherited long QT syndrome. BJMMR. 2012;2:31–38.

41. Steptoe A, Kivimäki M. Stress and cardiovascular disease. Nat Rev Cardiol. 2012;9:360–370.

42. Aboa-Eboule C, Brisson C, Maunsell E, et al. Job strain and risk of acute recurrent coronary heart disease events. JAMA. 2007;298:1652–1660.

43. Mezzacappa ES, Kelsey RM, Katkin ES, et al. Vagal rebound and recovery from psychological stress. Psychosom Med. 2001;63:650–657.

44. Ziegler MG, Nelesen RA, Mills PJ, et al. The effect of hypoxia on baroreflexes and pressor sensitivity in sleep apnea and hypertension. Sleep. 1995;18:859–865.

45. Thomas KS, Nelesen RA, Ziegler MG, et al. Job strain, ethnicity, and sympathetic nervous system activity. Hypertension. 2004;44:891–896.

46. 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.

47. Vrijkotte TG, van Doornen LJ, de Geus EJ. Effects of work stress on ambulatory blood pressure, heart rate, and heart rate variability. Hypertension. 2000;35:880–886.

48. Hanson EK, Godaert GL, Maas CJ, et al. Vagal cardiac control throughout the day: the relative importance of effort-reward imbalance and within-day measurements of mood, demand and satisfaction. Biol Psychol. 2001;56:23–44.

49. Hintsanen M, Elovainio M, Puttonen S, et al. Effort-reward imbalance, heart rate, and heart rate variability: the Cardiovascular Risk in Young Finns Study. Int J Behav Med. 2007;14:202–212.

50. Uusitalo A, Mets T, Martinmaki K, et al. Heart rate variability related to effort at work. Appl Ergon. 2011;42:830–838.

Copyright © 2013 by the American College of Occupational and Environmental Medicine


Article Tools