The interaction between systemic inflammation and psychosocial stress in the association with cardiac troponin elevation: A new approach to risk assessment and disease prevention.
We have previously shown that there is a complex and dynamic biological interaction between acute mental stress and acute release of inflammatory factors into the blood stream in relation to heart disease. We now hypothesize that the presence of chronic psychosocial stress may modify the weight of single test results for inflammation as a predictor of heart disease. Using a cross-sectional design, 500 participants free from heart disease drawn from the Whitehall II study in UK in 2006-2008 were tested for plasma fibrinogen as an inflammatory factor, financial strain as a marker of chronic psychosocial stress, coronary calcification measured using computed tomography, and for plasma high-sensitivity cardiac troponin T (HS-CTnT) as a marker of cardiac risk. Fibrinogen concentration levels above the average were associated with a 5-fold increase in the odds of HS-CTnT positivity only among individuals with financial strain (N=208, OR=4.73, 95%CI=1.67 to 13.40, P=0.003). Fibrinogen was in fact not associated with HS-CTnT positivity in people without financial strain despite the larger size of that subsample (n=292, OR=0.84, 95%CI=0.42 to 1.67, P=0.622). A test for interaction on the full sample (N=500) showed a P value of 0.010 after adjusting for a range of demographics, health behaviours, traditional cardiovascular risk factors, psychosocial stressors, inflammatory cytokines, and coronary calcification. In conclusion, elevated fibrinogen seems to be cardio-toxic only when is combined with financial strain. Chronic psychosocial stress may modify the meaning that we should give to single test results for inflammation. Further research is needed to confirm our results.
London School of Hygiene & Tropical Medicine, Keppel Street, London WC1E 7HT, United Kingdom; Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, United Kingdom. Electronic address: antonio.lazzarino@lshtm.ac.uk.
Antonio Ivan
AI
Lazzarino
School of Sport, Exercise, and Health Sciences, National Centre for Sport & Exercise Medicine, Loughborough University, LE11 3TU, United Kingdom.
Mark
M
Hamer
Chemical Pathology, Clinical Blood Sciences, St George's Healthcare NHS Trust, Blackshaw Road, Tooting, London SW17 0QT, United Kingdom.
David
D
Gaze
Chemical Pathology, Clinical Blood Sciences, St George's Healthcare NHS Trust, Blackshaw Road, Tooting, London SW17 0QT, United Kingdom.
Paul
P
Collinson
Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow G12 8TA, United Kingdom.
Ann
A
Rumley
Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow G12 8TA, United Kingdom.
Gordon
G
Lowe
Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, United Kingdom.
Andrew
A
Steptoe
D015415:Biomarkers / Q000097:blood; D002114:Calcinosis; D002318:Cardiovascular Diseases / Q000097:blood / Q000517:prevention & control; D003430:Cross-Sectional Studies; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D018570:Risk Assessment; D013315:Stress, Psychological / Q000097:blood* / Q000523:psychology; D020107:Troponin T / Q000097:blood*; D006113:United Kingdom
D015415:Biomarkers; D020107:Troponin T; D005340:Fibrinogen
Allostasis; Atherosclerosis; Cardiovascular diseases; Fibrinogen; Neuroendocrinology; Psychological stress; Socioeconomic factors; Troponin T
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