AIMS: Low socioeconomic status is associated with increased cardiovascular disease risk. We hypothesized that psychobiological pathways, specifically slow recovery in blood pressure and heart rate variability following mental stress, partly mediate social inequalities in risk.
METHODS AND RESULTS: Participants were 123 men and 105 women in good health aged 47-58 years drawn from the Whitehall II cohort of British civil servants. Grade of employment was the indicator of socioeconomic status. Cardiovascular measures were monitored during performance of two behavioural tasks, and for 45 min following stress. Post-stress return of blood pressure and heart rate variability to resting levels was less complete after 45 min in the medium and low than in the high grade of employment groups. The odds of failure to return to baseline by 45 min in the low relative to the high grade of employment groups were 2.60 (95% CI 1.20-5.65) and 3.85 (1.48-10.0) for systolic and diastolic pressure, respectively, and 5.19 (1.88-18.6) for heart rate variability, adjusted for sex, age, baseline levels and reactions to tasks. Subjective ratings of task difficulty, involvement and stress did not differ by socioeconomic status.
CONCLUSIONS: Lower socioeconomic status is associated with delayed recovery in cardiovascular function after mental stress. Impaired recovery may reflect heightened allostatic load, and constitute a mechanism through which low socioeconomic status enhances cardiovascular disease risk.

Shift workers encounter an increased risk of cardiovascular disease compared to their day working counterparts. To explore this phenomenon, the effects of one week of simulated night shift on cardiac sympathetic (SNS) and parasympathetic (PNS) activity were assessed. Ten (5m; 5f) healthy subjects aged 18-29 years attended an adaptation and baseline night before commencing one week of night shift (2300-0700 h). Sleep was recorded using a standard polysomnogram and circadian phase was tracked using salivary melatonin data. During sleep, heart rate (HR), cardiac PNS activity (RMSSD) and cardiac SNS activity (pre-ejection period) were recorded. Night shift did not influence seep quality, but reduced sleep duration by a mean of 52 +/- 29 min. One week of night shift evoked a small chronic sleep debt of 5 h 14 +/- 56 min and a cumulative circadian phase delay of 5 h +/- 14 min. Night shift had no significant effect on mean HR, but mean cardiac SNS activity during sleep was consistently higher and mean cardiac PNS activity during sleep declined gradually across the week. These results suggest that shiftwork has direct and unfavourable effects on cardiac autonomic activity and that this might be one mechanism via which shiftwork increases the risk of cardiovascular disease. It is postulated that sleep loss could be one mediator of the association between shiftwork and cardiovascular health.

OBJECTIVE: This study examined the effects of exposure to job strain on independent predictors of cardiovascular disease (ambulatory blood pressure, heart rate, and heart rate variability).
METHODS: The participants comprised a homogeneous group of 159 healthy female nurses [mean age 35.9 (SD 8.5) years]. The choice of this population minimized variance attributable to gender, socioeconomic status, and work characteristics. Job demands, decision latitude, and social support were measured with the Karasek job content questionnaire, which was administered twice with an average interval of 12.2 months. The nurses’ scores for job demands and decision latitude on both occasions were used to define their job-strain category. Ambulatory blood pressure, heart rate, and heart rate variability were assessed on a workday and a day of leisure.
RESULTS: No effect on the ambulatory levels of blood pressure, heart rate, or heart rate variability was found for job strain by itself or in interaction with social support. In addition, job strain was not associated with differences in short-term or long-term physiological recovery during sleep after a workday or a day of leisure. High job demand was associated with higher systolic blood pressure at work and with higher diastolic blood pressure at work, but the latter association was found only when decision latitude was concurrently high, rather than low.
CONCLUSIONS: High job strain among young female nurses is not associated with an unfavorable ambulatory cardiovascular profile. The robust effect of job strain on male health appears to be less apparent for women.

In this paper, a new model for adaptive artifact cancelation in impedance cardiography (ICG) signals is presented. It is a hybrid model based on wavelet decomposition and an adaptive filter. A novel feature of this model is the implementation of reference-free adaptive artifact cancellers (AAC). For this implementation, the reference signal is constructed using a wavelet transformation. During critical conditions the filter weights may be negative and cause an imbalance in the convergence. To overcome this problem, we introduce non-negative adaptive algorithms in the proposed artifact canceller. To accelerate the performance of the AAC, we propose exponential non-negative and normalized non-negative algorithms to update the filter coefficients. The computational complexity of the filtering section in a remote health care system is important to avoid inter-symbol interference of the incoming samples. This can be achieved by combining sign-based algorithms with the adaptive filtering section. Finally, several AACs are developed using variants of the non-negative algorithms and performance measures are computed and compared. All of the proposed AACs are tested on actual ICG signals. Among the AACs evaluated, sign regressor normalized non-negative LMS (SRN3LMS) based adaptive artifact canceller achieves highest signal to noise ratio (SNR). The SNR achieved by this algorithm in baseline wander artifact elimination is 8.5312 dBs, in electrode muscle artifact elimination is 7.5908 dBs and in impedance measurement artifact elimination is 8.4231 dBs.