Inflammatory response to acute mental stress is associated with altered cortisol reactivity and telomere shortening in patients with coronary artery disease
(English)Manuscript (preprint) (Other academic)
Background: Psychological stress and inflammation are both important risk factors for coronary artery disease (CAD). Susceptibility to mental stress-induced inflammation has been little explored in patients with CAD. Here, we investigated whether stress-induced inflammatory response, more precisely neutrophil activation, was associated with cortisol reactivity, leukocyte telomere length (TL) and carotid atherosclerotic burden in CAD.
Methods: Sixty-four patients with stable CAD underwent a laboratory stress test. Matrix metalloproteinase (MMP)-9, MMP-8, tissue inhibitors (TIMP)-1 and -2, myeloperoxidase (MPO) and salivary cortisol were measured before and 20 min after stress. Leukocyte TL was assessed as well as basal cortisol levels, background psychological factors and atherosclerosis in carotid arteries.
Results: The variation in stress-induced release of neutrophil markers was substantial. Patients were therefore divided into lower and upper tertiles depending on changes in serum MMP-9, T1: -12 %, T3: +27 %, with corresponding changes in MMP-8 and MPO. Clinical or psychological characteristics did not differ between groups, neither did basal levels of neutrophil markers or cortisol. Cardiovascular reactivity during stress was similar in T1 and T3, while cortisol declined after stress only in T3 (-30 %). Leukocyte TL was shorter in T3 than in T1, 0.78 vs 0.88, p = 0.006. Moreover, presence of plaques in right carotid artery differed between T1 and T3, 66 % vs 100 %, p = 0.004.
Conclusion: Stress-induced neutrophil activation in CAD patients was associated with altered cortisol reactivity, leukocyte telomere attrition and increased subclinical atherosclerosis. Data suggest that mental stress testing can identify high-risk patients in need of novel prevention and treatment strategies.
Stress, inflammation, matrix metalloproteinase, telomere length, cortisol, coronary artery disease
Cell and Molecular Biology
IdentifiersURN: urn:nbn:se:liu:diva-114326OAI: oai:DiVA.org:liu-114326DiVA: diva2:789275