Ambulatory Blood Pressure and Behavior

BACKGROUND:

The causes of essential hypertension remain unknown, but it is generally agreed that both genetic and environmental factors are important. Of the latter, the two leading contenders are nutrition including sodium intake and weight gain, and psychosocial stress. It is probable that no single factor is responsible, and that hypertension is most likely to develop when a number of factors act in unison, so that different mechanisms operate in different individuals. It also seems probable that there may be two different components to the development of hypertension, with differing time courses. First, there are a number of mechanisms which produce rapid changes of blood pressure, which are not necessarily sustained for very long. Prime among these are the sympathetic nervous system and the renin-angiotensin system. Although derangements of both have been described in patients with essential hypertension, neither can on its own explain the overall mechanism. Secondly, there is also a slowly occurring hypertrophy of the arterial wall, which occurs partly in response to the transient increases of pressure, but also acts as a positive feedback loop, serving to amplify them. It seems probable that a number of different mechanisms may be involved in the first process, possibly including the effects of psychosocial stress and nutrition, but that the slow mechanism may be the final common path which maintains and amplifies the development of hypertension independently of the initiating causes. While the relevance of behavioral factors, or stress in hypertension is commonly accepted by the lay public, it has found much less acceptance among their physicians. This is perhaps not surprising, because stress is so hard to quantify on a scientific basis, particularly when it is borne in mind that there is still no agreement about the role of sodium intake, which is comparatively easy to quantify, in the development of hypertension. The treatment of patients with mild hypertension is a major public health issue. There are two possible strategies to counter the costs and side effects of universal pharmacological treatment, namely, defining high risk patients and finding safer methods of treatment. Patients with white coat hypertension show elevations of blood pressure only in the clinic situation. If it can be demonstrated that individuals with white coat hypertension are not at increased risk and do not exhibit the physiological and biochemical characteristics normally associated with early hypertension, such individuals will not necessarily require drug treatment but may be treated by desensitization. Also, the studies on job strain may enable identification of some environmental risk factors which may have an adverse effect on certain individuals' blood pressure. If job strain does influence blood pressure, it presents the possibility of an entirely new non-pharmacological method of preventing or treating hypertension, through manipulation of the work environment.

DESIGN NARRATIVE:

When the study was initiated in 1984, five interdisciplinary studies were conducted. Study 1 followed 1,500 hypertensive patients who had ambulatory blood pressures recorded over the last ten years, to determine whether ambulatory blood pressure improved the prediction of morbid events relative to clinic blood pressures. Study 2 evaluated factors contributing to white coat hypertension, and whether it could be treated behaviorally. Study 3 compared the reactivity to beta-adrenergic stimulation and to behavioral tasks in normals and patients with hypertension or depression. Study 4 tested the Job Strain Model in the laboratory by investigating the interactive effects on blood pressure of varying levels of workload or task difficulty and decision latitude or degree of personal control during a challenging behavioral task. Generalization of this measure of reactivity was assessed by comparison with ambulatory blood pressure recordings. Study 5, in a cohort study of 400 subjects, determined whether individuals in high-strain jobs showed greater elevations of blood pressure over five years than those in low-strain jobs.

The study was renewed for one year in 1993 as a continuation and extension of the 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 was extended as a prospective study of 314 men and women studied at 9 worksites during Waves of observation over five years. Preliminary results from Waves 1 and 2 showed a longitudinal association between persistent job strain and progressive elevation of ABP.

In the renewal, the investigators increased the sample size by 100 subjects and added a 4th Wave of observation. In Wave 3, they added a new outcome measure-ultrasound examination of the carotid artery, which detected early structural changes and atherosclerosis. They also monitored physical activity continuously during ABP monitoring using an Actigraph monitor. A new focus wass on social support, which had been shown to relate to cardiovascular morbidity, possibly via an interaction effect with job strain. The investigators evaluated how its availability and perceived satisfaction interacted with job strain and their outcome measures. The effects of job strain on urinary catecholamines and cortisol were also examined in 210 subjects, to test the hypothesis that job strain was associated with an overactivity of both the sympathetic nervous system and adrenocortical system, by analogy with Frankenhaueser's Effort-Distress model. In Wave 4 they also performed reactivity testing, in order to examine correlations between reactivity, atherosclerosis, and other cardiovascular variables. The research helped to determine whether sequential linkages existed 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).

The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.