This revised proposal is a continuation and extension of a study of the association between occupational stress ('job strain', evaluated by the Karasek Job Content Survey) and hypertensive cardiovascular disease, evaluated principally by ambulatory blood pressure (ABP) and left ventricular mass index (LVMI). It was originally a case control study in which cases (hypertensive subjects) were found to be more likely to be exposed to job strain than normotensive controls, with an odds ratio of 2.75, and to have a greater LVMI. This effect was independent of other known risk factors for hypertension. It has been extended as a prospective study of 314 men and women studied at 9 worksites during Waves of observation over 5 years. Preliminary results from Waves 1 and 2 show a longitudinal association between persistent job strain and progressive elevation of ABP. In this continuation, we propose to increase the sample size by 100 subjects and to add a 4th Wave of observation. In Wave 3 we are adding a new outcome measure-ultrasound examination of the carotid artery, which can detect early structural changes and atherosclerosis. We will also monitor physical activity continuously during ABP monitoring using an Actigraph monitor. A new focus will be on social support, which has been shown to relate to cardiovascular morbidity, possibly via an interaction effect with job strain. We will evaluate how its availability and perceived satisfaction interact with job strain and our outcome measures. The effects of job strain on urinary catecholamines and cortisol will also be examined in 210 subjects, to test the hypothesis that job strain is associated with an overactivity of both the sympathetic nervous system and adrenocortical system, by analogy with Frankenhaueser's Effort-Distress model. In Wave 4 we will also perform reactivity testing, in order to examine correlations between reactivity, atherosclerosis, and other cardiovascular variables. The proposed research should determine whether sequential linkages exist between major psychosocial factors (job strain and lack of social support), mechanisms mediating cardiovascular damage (elevated ABP and sympathoadrenal activation), and resultant preclinical cardiovascular disease (left ventricular hypertrophy and carotid atherosclerosis).
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