Abstract
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.
Highlights
Inflammation is recognised as a fundamental determinant of atherosclerosis and cardiovascular disease (CVD), which are labelled as inflammatory conditions (Epstein and Ross, 1999; Libby and Theroux, 2005; Libby, 2013)
The mechanisms involved in these complex pathways of causation have yet to be clarified genetically and phenotypically, there have been attempts to add markers of stress and inflammation when performing cardiovascular risk assessments (Macleod et al, 2007; Schnohr et al, 2015; Fiscella et al, 2009; Pearson et al, 2003; Ioannidis and Tzoulaki, 2012)
We evaluated the extent of multicollinearity among covariates by computing one-to-one correlation coefficients and by examining variance inflation factors (VIF) (“Regression with Stata Web Book: Chapter 2 - Regression Diagnostics,”, n.d.)
Summary
Inflammation is recognised as a fundamental determinant of atherosclerosis and cardiovascular disease (CVD), which are labelled as inflammatory conditions (Epstein and Ross, 1999; Libby and Theroux, 2005; Libby, 2013).Chronic psychosocial stressors such as anxiety and depression are associated with inflammation (Dimsdale, 2008; Lazzarino et al, 2013a, 2013b, 2013c; Steptoe and Vögele, 1991) and with heart disease with an effect size that is comparable to that of the traditional risk factors such as high blood pressure, cholesterol, smoking, etc. (Brotman et al, 2007; Dimsdale, 2008; Steptoe and Kivimäki, 2012; Kivimäki et al, 2012).⁎ Corresponding author at: Room 142b, London School of Hygiene & Tropical Medicine, Keppel Street, London WC1E 7HT, United Kingdom. the mechanisms involved in these complex pathways of causation have yet to be clarified genetically and phenotypically, there have been attempts to add markers of stress and inflammation when performing cardiovascular risk assessments (Macleod et al, 2007; Schnohr et al, 2015; Fiscella et al, 2009; Pearson et al, 2003; Ioannidis and Tzoulaki, 2012). Inflammation is recognised as a fundamental determinant of atherosclerosis and cardiovascular disease (CVD), which are labelled as inflammatory conditions (Epstein and Ross, 1999; Libby and Theroux, 2005; Libby, 2013) Chronic psychosocial stressors such as anxiety and depression are associated with inflammation (Dimsdale, 2008; Lazzarino et al, 2013a, 2013b, 2013c; Steptoe and Vögele, 1991) and with heart disease with an effect size that is comparable to that of the traditional risk factors such as high blood pressure, cholesterol, smoking, etc. A finding of elevated inflammation would be clinically unfavourable only if it is coupled with chronic psychosocial stress, and favourable if it is due to a healthy stress response in an individual with good psychosocial adaptation These dynamics make single tests for inflammation further difficult to interpret when not impossible
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