Age, job characteristics and coronary health

Background: Workplace demographics are changing in many European countries with a higher proportion of older workers in employment. Research has shown that there is an association between job strain and cardiovascular disease, but this relationship is unclear for the older worker. Aims: To investigate the association between job strain and a coronary event comparing younger and older male workers. Methods: Cases with a first-time coronary event were recruited from four coronary/intensive care units (1999-2001). Matched controls were recruited from the case's general practitioner surgery. Physical measurements were taken and self-administered questionnaires completed with questions on job characteristics, job demands and control. Unconditional logistic regression was carried out adjusting for classical cardiovascular risk factors. Results: There were 227 cases and 277 matched controls. Age stratified analyses showed a clear difference between younger (= 50 years) workers with regard to the exposure of job strain (job demands and control) and the association between these factors and cardiovascular disease. Older workers who had a coronary event were four times as likely to have high job strain [OR = 4.09 (1.29-13.02)] and more likely to report low job control [ OR = 0.83 (0.72-0.95)]. Conclusions: Job control emerged as a potential protective factor for heart disease and this evidence was stronger in the older male worker. Nevertheless, they were significantly more likely to have job strain. These results suggest that older workers may be more susceptible to job strain.

Assessing the immune phenotype of cardiac syndrome x: a prospective study of biomarkers

Cardiac Syndrome X (CSX), the presence of angina pectoris with objective signs of myocardial ischaemia despite angiographically normal epicardial coronary arteries, appears to be due to coronary microvascular dysfunction and is known to be associated with an elevation of several inflammatory biomarkers, suggesting a possible role for inflammation in its pathogenesis. We aimed to further characterise this relationship by prospectively analysing a wide variety of molecular biomarkers in a cohort of CSX patients thereby charting the changes in biomarkers throughout the natural history of CSX from its initial diagnosis to eventual disease quiescence. We found that CSX patients, when compared to healthy controls, have a persistent low-grade systemic inflammatory response characterised by an elevation of Tumour Necrosis Factor and Interferon-gamma, regardless of the presence of contemporaneous signs or symptoms of disease activity. Interleukin-6 and C-reactive Protein (CRP) are only elevated when patients have clinical evidence of disease activity and may be state markers in CSX. Moreover, CRP levels appear to correlate with signals of disease severity such as the time taken to develop symptoms during exercise stress testing. We have also demonstrated that the enzyme Indoleamine-2,3- dioxygenase is upregulated in active disease thus providing a possible explanation for the increased burden of psychological disease encountered in CSX. Analysis of the microRNA transcriptome showed that miR-143 is significantly under-expressed in CSX patients. This could allow phenotype switching in vascular smooth muscle cells with the resultant vascular remodelling causing reduced vessel responsiveness to local rheological stimuli and reduced luminal diameter with consequent increased microvascular resistance during times of increased myocardial oxygen demand, thereby limiting maximal hyperaemia during exercise. Our findings corroborate many previous hypotheses regarding the role of inflammation in CSX, generate new insights into possible pathogenic mechanisms and offer new therapeutic targets for the future management of this important cardiological condition.