Association Between Work-Related Stress and Coronary Heart Disease: A Review of Prospective Studies Through the Job Strain, Effort-Reward Balance, and Organizational Justice Models.

Abstract

HomeJournal of the American Heart AssociationVol. 7, No. 9Association Between Work‐Related Stress and Coronary Heart Disease: A Review of Prospective Studies Through the Job Strain, Effort‐Reward Balance, and Organizational Justice Models Open AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citations ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toOpen AccessReview ArticlePDF/EPUBAssociation Between Work‐Related Stress and Coronary Heart Disease: A Review of Prospective Studies Through the Job Strain, Effort‐Reward Balance, and Organizational Justice Models Jaskanwal D. Sara, MBChB, Megha Prasad, MD, Mackram F. Eleid, MD, Ming Zhang, MD, R. Jay Widmer, MD, PhD and Amir Lerman, MD Jaskanwal D. SaraJaskanwal D. Sara Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, MN Search for more papers by this author , Megha PrasadMegha Prasad Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, MN Search for more papers by this author , Mackram F. EleidMackram F. Eleid Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, MN Search for more papers by this author , Ming ZhangMing Zhang Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, MN Search for more papers by this author , R. Jay WidmerR. Jay Widmer Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, MN Search for more papers by this author and Amir LermanAmir Lerman Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, MN Search for more papers by this author Originally published27 Apr 2018https://doi.org/10.1161/JAHA.117.008073Journal of the American Heart Association. 2018;7:e008073IntroductionWork‐related stress is an example of a psychosocial risk factor that has become of interest in today's ever‐demanding, fast‐paced, and globalized society, although its link to adverse health and in particular coronary heart disease (CHD) is incompletely understood. In this review, we will outline the need to identify novel risk factors for cardiovascular disease (CVD) and the potential role of psychosocial risk factors, such as work stress; describe the theoretical frameworks by which work stress may influence health; review evidence provided by observational studies for the link between work stress and CHD; and explore potential mechanisms that may play a role in this relationship and evaluate the evidence for potential therapeutic interventions in this area.The Need to Identify Novel Risk Factors for CVDCVDs are the leading cause of death in both men and women of every major ethnic group in the United States, of which CHD is the most prevalent.1 In 2014, >600 000 Americans were estimated to have a new coronary event and ≈300 000 had a recurrent event.2 Between 2013 and 2030, medical costs of CHD are projected to increase by ≈100%,3 highlighting a growing health and socioeconomic problem. Nevertheless, CHD may be preventable,4 and preventative strategies are cost‐effective.5 Identification of at‐risk groups and appropriately addressing risk factors form the cornerstone of successful management, and can be achieved using multivariable risk‐prediction algorithms,6, 7, 8, 9 of which the most widely used in clinical practice are the Framingham‐based models. These scores assign weights to different levels of traditional risk factors, such as age, total cholesterol, and systolic blood pressure, which are combined to generate an absolute probability of developing CHD within a specified time frame. Framingham‐based risk prediction models are well established, practical, and easy to use, supported by large amounts of data and in most cohorts discriminate risk well, after calibration, where necessary.10 Nevertheless, Framingham‐based scores are limited by incorporating a limited number of risk factors, such as age, hypertension, diabetes mellitus, dyslipidemia, and smoking, which have been identified from historically based population studies.11 Alternative tools to assist in risk prevention have been developed, including the American Heart Association's Life's Simple 7, which identifies a construct of ideal cardiovascular health characterized by ideal health behaviors: nonsmoking, body mass index (BMI) <25 kg/m2, physical activity at goal levels, pursuit of a diet consistent with current guideline recommendations, and ideal health factors (untreated total cholesterol <200 mg/dL, untreated blood pressure <120/<80 mm Hg, and fasting blood glucose <100 mg/dL).12 Although these individual concepts are well supported in the literature, the Life's Simple 7 focuses exclusively on “conventional cardiovascular risk factors,” which in themselves account for between 58% and 72% of all incident cases of CHD.13 Alternative nonconventional risk factors may account for some of this gap and are becoming increasingly important, particularly as the effects of previously implemented attempts at managing conventional risk factors are being seen. For example, a recent time trend analysis showed that patients presenting to the catheterization laboratory with CHD had better blood pressure and lipid profiles between 2006 and 2010, compared with between 1994 and 1999,14 which may reflect improved uptake of primary and secondary preventative strategies, such as smoking cessation.15 There was also a higher proportion of patients taking risk‐modifying cardiovascular medication.16 Furthermore, in one study of young adults hospitalized with their first myocardial infarction, <25% would have qualified for lipid‐lowering therapy based on guidelines available at the time,17 further demonstrating the limitation of current risk‐based algorithms. Thus, there is a need to identify and account for novel risk factors not currently accounted for in traditional risk prevention models. The increasing awareness of social and psychological determinants of health18 has opened up novel avenues in which the contribution of these risk factors to the cause, development, and outcome of CHD19, 20, 21 is becoming increasingly understood.One review concluded “there is strong and consistent evidence of an independent causal association between depression, social isolation and lack of quality social support and the causes and prognosis of CHD” and that the “increased risk contributed by these psychosocial factors is of similar order to more conventional CHD risk factors such as smoking, dyslipidemia and hypertension.”22 Similarly, in their review of the literature, Krantz and McCeney found compelling evidence to suggest an association between acute and chronic stress, depression, social support, and socioeconomic status with the development of CHD,23 which was in keeping with the findings of Strike and Steptoe in their review of epidemiologic data.24Evidence linking work stress and the development of CHD remains unclear however. Of the workforce, 10% to 40% struggle with work‐related stress, and at least one third of these experience severe chronic psychosocial stress.25 In one national study performed in France, up to 2% of a working population were affected by illnesses attributable to work‐related stress, which cost society up to 1975 million Euros.26 It is, therefore, important to examine this potential association in greater depth, particularly because work‐related stress is potentially modifiable.Theoretical Frameworks Linking Work Stress to CHDEvaluating “work stress” as a potential risk factor for CHD is challenging, given its subjectivity and the difficulty associated with synthesizing its significant components into comparable metrics. Social scientists have tackled this issue by constructing simplified frameworks by which a seemingly abstract concept, such as work stress, can be appreciated in an objective way. Investigators have since adopted these frameworks in their studies and in doing so have been able to generate useful comparisons that help determine the role work stress plays in CHD. In one of these frameworks, work stress can be characterized from the perspective of “job strain,” as per the job strain model, also known as the demand‐control model27, 28 (Figure 1). This states that work associated with high psychological demands, such as intense and time‐critical tasks, and low control in areas such as decision authority, skill discretion, and learning opportunities is associated with high job strain27 and, in turn, high work stress. Several studies that have demonstrated an association between high job strain and an increased risk of CVD have shown that both high demands and low control are required to convey increased risk,27, 28, 29 whereas others have shown that low job control was more important than high job demand and is itself an independent predictor of CVD risk.30, 31, 32 There remains much controversy in the literature as to whether the relationship between job demand and control is additive or multiplicative, or if there is a buffering effect. In the latter, once levels of job control reach or exceed a certain threshold, the deleterious effects of demands are supposedly negated, although to date the precise relationship has not yet been clarified.33, 34, 35 Furthermore, a third component of the job strain model has been suggested (namely, social support in the workplace),36 which evaluates the contribution of support provided by one's colleagues and supervisors in the workplace. Once again, the buffer theory postulates that social support above a certain threshold level protects against the adverse effects of high job strain.34, 37Download PowerPointFigure 1. Outline of the “Job Strain,” “Effort‐Reward Imbalance,” and “Organizational Justice” psychosocial models underlying the potential relationship between work‐related stress and coronary heart disease. Individuals with high job strain, effort‐reward imbalance, or organizational injustice may be at an increased risk of coronary heart disease directly or through mediating factors, such as hypertension, high cholesterol, or maladaptive behaviors.The effort‐reward imbalance model (Figure 1) centers on the idea that the balance between one's perceived or actual effort into a particular job with one's actual or perceived rewards in terms of salary, recognition, and opportunities for career progression will influence one's risks for adverse health outcomes.38, 39 Although studies have shown an association between job strain and CVD mortality,40 evidence linking job effort‐reward imbalance to CVD mortality has been more sparse. Furthermore, studies that have been able to show an association have typically shown that, of the 2 constituent parts, low reward is the more important predictor of events.31 Another component of this model, personality traits, such as overcommitment, are seldom evaluated in work stress related studies, nor is their precise role, interactive or otherwise, clearly defined in the literature.41Further research into work stress has led to the development of a third framework, known as the organizational justice model42 (Figure 1). This model operates under the precept that justice is a fundamental value to the organization of society and to individual social interactions,43 and enduring perceived unfairness within the workplace can contribute to work stress.44 The model consists of 3 separate entities: distributive justice, which refers to the fairness associated with decision outcomes and the distribution of resources that may be tangible, such as pay, or intangible, such as praise; procedural justice, which is linked to distributive justice in that it relates to the fairness of the processes that lead to outcomes, such that when individuals believe they have a voice in the process or that these processes are consistent, accurate, and without bias, procedural justice is enhanced; and interactional justice, which, in turn, is linked to procedural justice and relates to informational justice, which focuses on explanations provided to people as to why certain procedures were used, and interpersonal justice, which reflects the degree to which people are treated with politeness, dignity, and respect by those performing procedures. The organizational justice model was developed later, and it is, therefore, less well established than the job strain and effort‐reward imbalance models; it has been examined in fewer studies. Although these models integrate and combine multiple different facets of working life, they remain limited in that they cannot account for all possible psychosocial and biological factors that may coexist and contribute to work stress and its relationship with CHD and adverse health in general. The precise interplay of extraneous psychosocial and biological factors with work stress and CHD is challenging to encapsulate in the form of descriptive models, which are designed to help simplify seemingly abstract and potentially subjective concepts into understandable and comparable constructs. Further investigation is required to better delineate these relationships. This review focuses on the 3 aforementioned models of work stress and does not evaluate the individual role of other work‐related factors, such as working shift patterns, whose relationship with CHD may be as important or potentially even more so than that of the 3 models evaluated.Work Stress and CHDWe searched PubMed for potentially relevant articles published from January 1, 1970, through December 31, 2017, using the following key search terms: work stress, occupational stress, job stress, coronary artery disease, ischemic heart disease, and CVD. Searches were enhanced by scanning bibliographies of identified articles, and relevant articles were selected for review. Studies included for selection in this review required the following criteria: characterization of work stress using at least 1 of the 3 aforementioned established and validated work‐stress models (namely, the job strain, effort‐reward imbalance, and organizational justice models); defined outcomes of incident CHD/ischemic heart disease, characterized by angina or myocardial infarction, or of mortality related to CHD; provided a quantitative estimate and confidence interval (CI) of relative risk for incident CHD or CHD mortality and used a prospective causative cohort study design, because randomized controlled trials are not practical for this study question and prospective cohort studies represent the next best level of evidence and can allow inference of causality. Cross‐sectional and case‐control studies were excluded, as were studies that evaluated the impact of multiple individual isolated facets of the work environment, such as emotional demands, role clarity, career possibilities, and working overtime. Although they relate to adverse psychosocial elements of the working environment, and some have been shown to be associated with an increased risk of CHD,45 they do not encapsulate work‐related stress per se as a wider construct in the same ways that the 3 models selected for this review do. Indeed, work stress can be linked to a wide variety of psychosocial risk factors, some of which may coexist with work stress, but may not necessarily correlate with work‐related stress incurred on a day‐to‐day basis, or form an acceptable measurable synthesis of its relevant constituent parts. Working long hours, for example, has been shown to be associated with CHD,46 but individuals working long hours, or shift work, may not necessarily have work stress. Similarly, the authors of the job strain model stated that “cardiovascular risk results not from a single factor, but from the joint effects of the psychological demands of the work situation and the range of decision‐making freedom with respect to task organization and skill usage,”27 suggesting an understanding that work stress cannot be usefully characterized by focusing on individual work‐ related factors. The purpose of the current review was to examine the relationship between work stress in of itself, as a broad construct, synthesizing multiple relevant, yet unique, aspects of working life and CHD and not to investigate all individual psychosocial elements related to the working environment.Often, separate articles were identified that presented data from the same study cohort (eg, with different periods of follow‐up or event rates). In these cases, unless the independent or dependent variables were significantly different, only the study presenting the most comprehensive data was included. Articles containing no original data, including reviews and meta‐analyses, were also excluded to avoid redundancy, particularly because those identified47, 48, 49, 50, 51, 52 included cohort studies that were individually selected for this review. A further issue with meta‐analyses for work stress is that concepts, such as job strain, effort‐reward imbalance, and organizational injustice, are typically characterized in a median or quartile split across the population investigated. As Burr et al outlined in their Letter to the Editor, whether certain individuals are identified as having job strain, and therefore have work stress, depends on who else is in the sample.53 This is problematic when work demand, control, and other work environment related characteristics vary between jobs and across countries. If the prevalence of job strain varies between populations and is inherently dependent on the distribution of demands and control within that population, combining data from different populations as part of a meta‐analysis can become challenging. This is highlighted in a review by Szerencsi et al, in which the authors showed that studies undertaken in the United States yielded ≈ 26% lower estimates compared with studies conducted in Scandinavian countries when determining the relative risk of CVD using the job strain model.54Figure 2 highlights the countries from which the 23 prospective cohort studies31, 39, 40, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74 that satisfied our inclusion criteria were performed and summarizes the estimate of risk (relative risk and CI) for incident CHD/CVD death associated with work stress in each study. Where studies provided a multivariable adjusted estimate of risk, this was preferentially included over an unadjusted estimate. All studies identified were undertaken in industrialized economically developed nations from North America, Western Europe, Scandinavia, and Japan. These nations would likely lend themselves to broad similarities in the types of jobs their populations do and have democratic political systems that would likely result in greater oversight and regulation of working environments and individual worker rights. As such, the results generated by these studies are likely to represent select populations in which working life is relatively more homogeneous compared with that found in nations with developing economies and alternative political systems. Thus, the results obtained from the studies included in this review may not necessarily be generalizable to workers in other nations, highlighting the need for further studies to be performed in different regions of the world. In addition, the lack of studies performed in developing nations with emerging economies and distinct social and cultural norms skews our understanding of work stress and its implications on CHD and adverse health. Studies performed in developing nations would enrich our understanding of this question and may allow the development of newer frameworks that factor in other aspects of working life and society not included in established models. Furthermore, studies from developing nations may uncover unique methods that local populations use to help mitigate work stress that could, in turn, help in the development of novel interventions that may be useful in managing work stress and its adverse health consequences.Download PowerPointFigure 2. Illustration of the global distribution of prospective cohort studies evaluating the potential association between work‐related stress and coronary heart disease (CHD) or cardiovascular disease (CVD) mortality. Twenty‐three prospective cohort studies were identified up until December 2017. Studies that provided a quantitative estimate of the association between work stress and incident CHD or CVD events/mortality and characterized work stress using the job strain, effort‐reward imbalance, or organizational injustice model were included. CI indicates confidence interval; IHD, ischemic heart disease; JACE, Job Stress, Absenteeism and Coronary Heart Disease In Europe study; MONICA, Multinational Monitoring of Trends and Determinants in Cardiovascular Disease; NHANES, National Health and Nutrition Examination Survey; and RR, relative risk.Among the 23 studies identified, 17 evaluated work stress through the “job strain” framework only, 2 made use of the “effort‐reward imbalance” framework only, 2 evaluated both models separately, and 2 evaluated the organizational injustice model. Fourteen studies evaluated incident CHD or ischemic heart disease as their primary outcome, whereas the remaining 9 evaluated the incidence of CVD events or death. Eleven studies found no significant association between work stress and incident CHD/CVD. Among the 12 that did find an association, the relative risk (95% CI) for the association between work stress and incident CHD varied between 1.22 (1.01–1.46) and 4.53 (1.43–14.3), whereas that for the association between work stress and CVD events and death varied between 1.53 (1.08–1.97) and 1.92 (1.15–3.21). Both studies evaluating the organizational justice model found a significant association between work stress and incident CHD or CVD death, as did all 4 studies using the effort‐reward balance model, whereas of the 19 studies using the job strain model, 8 found a positive relationship. Thus, almost as many studies found an association between work stress and CHD as those that did not, and although one study demonstrated a >4‐fold increase in risk of incident CHD in patients experiencing work stress, the great variability in the results from the studies reflects differences in study design, number of patients included, follow‐up duration, and definitions of the exposures and outcomes. Several of these studies used CVD as the outcome of interest, which includes non–CHD‐related pathological conditions, such as cerebral vascular disease, which makes direct comparisons between studies difficult. Along the same lines, studies that evaluated CVD or CHD events and death look at “hard” outcomes that are easier to define accurately than more subjective definitions of CHD, such as a history of new‐onset chest pain consistent with angina, with the former definition likely to generate more conservative estimates of risk. Using different outcome variables defined in different ways raises difficulties when trying to compare and/or combine results from individual studies. Furthermore, the absence of randomization of the exposure variable in all the studies leads to problems with confounding and makes it difficult to derive a causal relationship between work stress and CHD with certainty. In addition, the studies included in this review represent a relatively homogeneous group and share many similarities in study design, in part because they are all prospective causative studies, but also because the nature of this particular study question is limited in the number of study designs it can lend itself to. Important differences in sample size, demography, length of follow‐up, and which exposure and outcome variables were used are highlighted in Figure 2. Herein, we outline some additional key issues related to study design that we believe are best illustrated through critiquing the 2 studies by Kuper et al61 and Kivimaki et al,31 which both included an assessment of the job strain and effort‐reward imbalance model, and are therefore more comprehensive studies that collectively highlight important methodological considerations common to all studies included in this review.The Whitehall Study was one of the earlier cohorts to be evaluated for the relationship between work stress and CHD, and in one study, Kuper et al examined this association among 10 308 (67% men, aged 35–55 years) civil servants in London, England.61 This study followed a prospective cohort design in which subjects completed questionnaires at baseline (1985–1988) and on 2 subsequent follow‐up visits (1989–1990 and 1991–1993) consisting of questions asking about job control, job demand, and social support at work. In addition, questions derived from the previously validated Rose Questionnaire75 were used to assess for new angina or severe pain across the chest, a new diagnosis of ischemic heart disease, or any coronary event. The subjects’ managers also completed a questionnaire at baseline, providing an independent assessment of employee job strain. The investigators demonstrated that men and women with low job control had a higher risk for newly reported CHD at follow‐up compared with those with high control and that the odds ratio (95% CI) between men and women did not vary significantly (1.55 [1.20–2.01] versus 1.74 [1.15–2.64]). Furthermore, the investigators found that low job control had a cumulative effect on newly reported CHD rates, with subjects with low control on both follow‐up occasions having the highest odds of new CHD (odds ratio, 1.93 [95% CI, 1.34–2.77]). This association could not be explained away by employment grade or conventional CVD risk factors. A dose‐response relationship between job strain and the relative risk for acute myocardial infarction has been demonstrated in other studies.31, 76 Last, there was no significant association between job demand and social support in the work environment with newly reported CHD.The previously described study highlights some of the design characteristics and methodological issues commonly encountered by other studies included in Figure 2. Although this study included a relatively large sample size (it was overall the sixth largest study included in this review; the largest study included 35 471 subjects, whereas 6 studies included <1000 subjects) and used a prospective design, one of its major limitations relates to the generalizability of the results. The British civil servants included in this study comprise “white collar” workers and are not comparable to manual laborers working in “blue collar” jobs. Moreover, the outcomes used in this study were subjectively determined by each employee and may correlate poorly to actual CHD, a problem encountered in other studies using a survey‐based approach to quantify outcomes. Studies relying on objective determinants of the outcome variable, such as myocardial infarction, identified from clinical records may arrive at more accurate conclusions, particularly because subjects who report experiencing job strain may have an inherent disposition making them more likely to report physical symptoms, such as chest pain/tightness, that may have organic causes but could also represent a psychosomatic process. All studies included in Figure 2 also made use of written surveys and/or direct in‐person interviews with employees and sometimes managers as well when characterizing work stress as the exposure variable. This poses another problem because not only does this method involve a subjective component that may be influenced by the interpretation of each question and the interviewing style of the questioner, among other factors, but there is also a possibility of responder bias. Those subjects who choose to participate in studies by responding to surveys, taking part in interviews, and then engaging with follow‐up are likely to be systematically different to those who do not respond or follow up, who may in general be less health conscious or too “stressed” at work to find time to participate in studies. A unique quality of this study was that the investigators evaluated the cumulative effect of job stress with an independent assessment of the impact that work stress had on CHD at multiple follow‐up points. There was also an independent assessment of job strain provided by questionnaires answered by managers as well as a subjective assessment of job strain completed by employees. Although these correlated poorly with each other (correlation coefficient, 0.41), both measures were associated with newly reported CHD, demonstrating that objective measures of work strain may be as important as those reported by the individual workers.Other problems related to the studies included in Figure 2 relate to the fact that previous studies have shown that psychosocial stressors have a tendency to coexist and cluster such that individuals from lower socioeconomic status backgrounds tend to also have poorer social support and education levels as well as a higher prevalence of conventional CVD risk factors and certain “maladaptive” psychological traits24 compared with their counterparts from higher socioeconomic status backgrounds. Thus, when one social factor, such as higher socioeconomic status, is shown to be associated with lower rates of CHD,77 it can be challenging to determine if any coexisting variable is, in fact, playing a role, and if so, to what extent. Randomization is a useful technique in experimental studies that can balance covariates between groups exposed and not exposed to the variable of interest, although to date no randomized trial has been published evaluating the relationship between work stress and CHD, likely because of the practical difficulty of “assigning” a group to work stress. As such, a significant problem with the studies included in this review is discriminating whether work stress itself is responsible for the identified effect on CHD. Part of the increased risk of