Petra H. Wirtz

Background: The health promoting effects of positive psychological factors in cardiovascular disease (CVD) are gaining increasing attention. Key factors such as optimism, mindfulness, positive affect, and life satisfaction have been linked to a lower incidence of CVD. While these effects are often explained by favorable health behaviors, potential biological mechanisms are insufficiently explored. Objectives: We aimed to to investigate independent associations between positive psychological factors and prospective changes in intermediate biological coronary heart disease (CHD) risk factors in CHD-patients, hypertensives (HT), and normotensive controls (NT). Methods: At baseline, 200 men (CHD=86,HT = 61,NT = 53) completed questionnaires on positive psychological factors and had blood samples collected. As CHD-risk factors lipid profiles (TC/HDL-ratio), blood glucose (HbA1c), coagulation (fibrinogen, D-dimer), and inflammation markers (CRP, IL-6, TNF-α) were measured. At 3-year follow-up, blood sample were collected from 126 men (NT = 34,HT = 37,CHD=55). Results: At baseline, the groups differed in positive affect only [F(2,197) = 3.63, p = .028], with highest levels in NT and lowest levels in CHD. Prospectively, higher baseline positive affect ( p = .026) and life satisfaction ( p = .026) were associated with lower CHD-risk over time. Specifically, higher baseline positive affect predicted lower increase in coagulation markers ( p = .010), particularly fibrinogen (ß=-0.37, p = .003), while higher baseline life satisfaction predicted lower increase in inflammation markers, especially IL-6 (ß=-.38, p = .005). Neither optimism nor mindfulness were linked to change in CHD-risk factors over time. Conclusion: Positive affect and life-satisfaction may benefit cardiovascular health by favorably affecting coagulation and inflammation, with potential implications for CHD prevention and intervention strategies.

Background: The mineralocorticoid hormone aldosterone plays a key role in blood pressure regulation and the development of cardiovascular disease. However, the biological mechanisms that underly prospective associations with negative health outcomes are not fully understood. We compared the awakening response of biologically active salivary aldosterone (AldAR) between male participants with coronary heart disease (CHD), essential hypertension (EHT), and normotension (NT) and additionally examined prospective associations with biological CHD risk factors. Methods: At baseline, 60 CHD patients, 40 EHT and 44 NT repeatedly assessed the AldAR over two consecutive days. In 97 participants, prospective CHD risk was assessed by changes from baseline to follow-up 2.95 ± 0.07 ( SEM ) years later in the pro-inflammatory measures interleukin (IL)-6, tumor necrosis factor-alpha (TNF-α), and acute phase protein C-reactive protein (CRP), as well as blood lipids in terms of total cholesterol (tChol), high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol. Potential confounding variables were controlled. Results: Whereas NT showed the regular AldAR, EHT had higher overall aldosterone levels ( p ’s < .010, with confounders: p ’s < .065) but a flattened AldAR ( p = .89). Moreover, CHD patients showed the regular AldAR but on a lower level as compared to NT ( p = .002, with confounders: p = .075). Greater AldAR area under the curve independently predicted greater increases in overall inflammatory ( p ’s ≤ .032) and lipid CHD risk markers ( p ’s ≤ .089). Significantly greater increases were found for LDL cholesterol (ß = .24, p = .037; with confounders: p ’s ≤ .067), and tChol (ß = .26, p = .032; with confounders: p ’s ≤ .064). A trend for an association was found for IL-6 (ß = .22, p = .068; with confounders: p ’s ≤ .079). Conclusions: We found evidence for altered AldAR in CHD and EHT with higher AldAR predicting higher CHD risk, particularly in relation to systemic inflammation and dyslipidemia. Elevated AldAR levels may contribute to the pathogenesis of atherosclerotic cardiovascular disease.

Psychosocial stress has been proposed to induce a redistribution of immune cells, but a comparison with an active placebo-psychosocial stress control condition is lacking so far. We investigated immune cell redistribution due to psychosocial stress compared to that resulting from an active placebo-psychosocial stress but otherwise identical control condition. Moreover, we tested for mediating effects of endocrine parameters and blood volume changes. The final study sample comprised 64 healthy young men who underwent either a psychosocial stress condition (Trier Social Stress Test; TSST; n = 38) or an active placebo-psychosocial stress control condition (PlacTSST; n = 26). Immune cell counts and hemoglobin, epinephrine, norepinephrine, ACTH, renin, and aldosterone levels, as well as those of saliva cortisol, were determined before and up to 30 min after the TSST/PlacTSST. The TSST induced greater increases in total leukocyte, monocyte, and lymphocyte levels as compared to the PlacTSST (p’s ≤ 0.001), but in not granulocyte counts. Neutrophil granulocyte counts increased in reaction to both the TSST and PlacTSST (p’s ≤ 0.001), while eosinophil and basophil granulocyte counts did not. The psychosocial stress-induced increases in immune cell counts from baseline to peak (i.e., +1 min after TSST cessation) were independently mediated by parallel increases in epinephrine (ab’s ≤ −0.43; 95% CIs [LLs ≤ −0.66; ULs ≤ −0.09]). Subsequent decreases in immune cell counts from +1 min to +10 min after psychosocial stress cessation were mediated by parallel epinephrine, renin, and blood volume decreases (ab’s ≥ 0.17; 95% CIs [LLs ≥ 0.02; ULs ≥ 0.35]). Our findings indicate that psychosocial stress specifically induces immune cell count increases in most leukocyte subpopulations that are not secondary to the physical or cognitive demands of the stress task. Increases in the number of circulating neutrophil granulocytes, however, are not psychosocial stress-specific and even occur in situations with a low probability of threat or harm. Our findings point to a major role of epinephrine in mediating stress-induced immune cell count increases and of epinephrine, renin, and blood volume changes in mediating subsequent immune cell count decreases from +1 min to +10 min after psychosocial stress cessation.

Introduction: While the effectiveness of cognitive-behavioral stress management trainings (SMTs) is well-documented, the underlying mechanisms, especially in an occupational context, are not fully understood. We tested whether SMT-induced improvements in stress management skills, particularly in the mastery of changing cognitions, may explain beneficial SMT effects.Methods: Our non-randomized controlled trial comprised 108 employees of a German health insurance company, with 65 of them participating in a cognitive-behavioral SMT and 43 participating in an alternative control training (AT). As outcome variables, we repeatedly assessed stress-related (functional stress management skills, relaxation, stress reactivity, exhaustion), work-related (job dissatisfaction), and specific-context-related (social support, trait anger) measures at baseline, 2 weeks, and 3 months after the trainings. Functional stress management skills and, in particular, a subscale assessing perceived mastery of changing cognitions (“cognitive-strategies-and-problem-solving”) were tested as mediators of change.Results: Repeated measures (M)AN(C)OVAs and complementary multigroup latent difference models confirmed improvements in all outcomes in the SMT-group compared to the AT-group (p's ≤ 0.015). Multivariate mediation path analyses revealed that, regarding mechanisms of change, the subscale cognitive-strategies-and-problem-solving was identified as the most important mediator for all outcomes (95% CIs for expected increases in SMT- vs. AT-group = [lower limits (LLs) ≥ 0.004]; 95% CIs for expected decreases in the SMT- vs. AT-group = [upper limits(ULs) ≤ −0.078]) except for job dissatisfaction.Discussion: Our findings confirm that employees can effectively learn to master stress reduction techniques and consequently lower the resulting burden. Moreover, beneficial SMT effects seem to result from improvements in functional stress management skills, particularly in the ability to change cognitions. This points to the importance of training cognitive techniques.

Background: While aldosterone plays an important role in blood pressure regulation, its role in essential hypertension (EHT) remains unclear. Here, we systematically investigated the secretion of biologically-active free aldosterone in saliva in response to awakening (AldAR) and during the day (AldDay) in EHT compared to normotensive controls (NT).Methods: In 30 men with EHT and 30 age-matched NT, AldAR saliva samples were collected immediately after awakening and 15, 30, 45, and 60 min thereafter and AldDay samples were collected from 08:30–22:00 h on two consecutive days.Results: Over the course of the day, men with EHT had higher repeated AldDay levels compared to NT (p = .002) with higher concentrations in the morning hours (p's ≤ .047), a steeper decline over the course of the day (p's ≤ .018), and similar concentrations in the evening (p's ≥ .21). Regarding AldAR, we observed higher concentrations in EHT at awakening (p = .017) and borderline higher concentrations at 15 min (p = .086). No differences were found 30–60 min after awakening (p's ≥ .34). Analyses with repeated and aggregated AldAR levels resulted in borderline significantly higher free aldosterone in EHT (p's ≤ .077). Complementary analyses confirmed linear associations between higher blood pressure and higher AldAR and AldDay levels.Conclusions: Our data point to elevated salivary free aldosterone secretion in EHT over the course of the day, particularly in the morning hours. As the free aldosterone fraction is considered biologically active, our data may point to a biological mechanism underlying EHT.