Job strain and electrocardiograph assessed pathophysiologic mechanisms

The goal of this dissertation was to assess the effect of stress in the work environment on cardiovascular health through assessment of electrocardiograph data. The hypothesis was that psychosocial stress from work affects cardiac regulation in a pathogenic manner. The demand/control model was used to quantify work stress. Cardiac regulation was measured by components of electrocardiogram output: high frequency power (HFP) which represents the parasympathetic autonomic nervous system (ANS); the ratio of low to high frequency power (lo/hi), residual heart rate as well as QT interval variability (QTVI) as measures of sympathetic activity. Thirty-six males between the ages of 35 and 59 years and free of known heart disease were selected from a larger longitudinal study of healthy subjects and cardiovascular risk based on responses to a subset of questions from the Job Content Questionnaire (JCQ). Subjects were monitored with an ambulatory Holter electrocardiograph. Monitoring began on the morning of a workday followed for 48 continuous hours through the following rest day. Subjects were classified as high and low job strain based on occupational code, responses to the Job Content Questionnaire (JCQ) and a workday diary. High strain subjects exhibited lower parasympathetic activation during the entire 48-hour monitoring period, while measures of sympathetic activation were elevated in the high strain subjects on the workday. Multilevel modeling demonstrated that strain reported on the ambulatory diary was significantly associated with reductions in parasympathetic activity within-subjects. JCQ assessed decision latitude had a significant effect on this relationship with greater within-subject reductions in parasympathetic activity with low decision latitude. One implication of this study is that demands seem associated with short-term alterations in cardiac regulatory control with long-term changes in parasympathetic activity being associated with job control. Preliminary results support the use of ECG data for further analysis of Karasek's Stress Disequilibrium Model. However, longitudinal studies on larger populations in a wide variety of occupations are needed to fully explore the methods and theories presented. Implications of findings for physiological linkages between strain and disease, testing new job strain based cardiac regulatory hypotheses, as well as for future studies of occupational monitoring are discussed.