Objective: A high level of work stress has been associated with cardiovascular disease. However, the pathophysiological mechanisms underlying this association remain unclear. This study examined the effect of work stress on a cluster of metabolic and hemostatic risk factors. Methods: Blood was collected three times, on the first third, and fifth day of a work week, from 124 middle-aged, white-collar workers. Metabolic measures were insulin, glucose, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and total cholesterol. Hemostatic measures were fibrinogen, tissue-type plasminogen activator activity, tissue-type plasminogen activator antigen, and type 1 plasminogen activator inhibitor antigen. Chronic work stress was defined according to Siegrist's model as 1) a combination of high effort and low reward at work (effort-reward imbalance) or 2) high overcommitment (an exhaustive work-related coping style). Results: Overcommitment, but not imbalance or the imbalance-overcommitment interaction, was associated with an impaired fibrinolytic system, as reflected in decreased tissue-type plasminogen activator activity levels and increased type 1 plasminogen activator inhibitor antigen levels on all three measurement occasions. After controlling for body mass index, total cholesterol, triglycerides, high-density lipoprotein/low-density lipoprotein cholesterol ratio, glucose, and insulin, the relation between overcommitment and the fibrinolytic factors was attenuated but remained significant. Conclusions: The results suggest that individuals with an exhaustive coping style at work have an impaired fibrinolytic capacity that is possibly due to the effects of chronic stress on insulin resistance.
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