Relationship between a Self-Reported History of Depression and Persistent Elevation in C-Reactive Protein after Myocardial Infarction.

Background: Elevated levels of C-reactive protein (CRP) are associated with both an increased risk of cardiovascular disease (CVD) and depression. We aimed to test the hypothesis that a self-report history of depression is associated with a smaller decrease in CRP levels from hospital admission to 3-month follow-up in patients with acute myocardial infarction (MI). Methods: We assessed 183 patients (median age 59 years; 84% men) with verified MI for a self-report history of lifetime depression and plasma CRP levels within 48 h of an acute coronary intervention and again for CRP levels at three months. CRP values were categorized according to their potential to predict CVD risk at hospital admission (acute inflammatory response: 0 to <5 mg/L, 5 to <10 mg/L, 10 to <20 mg/L, and ≥20 mg/L) and at 3 months (low-grade inflammation: 0 to <1 mg/L, 1 to <3 mg/L, and ≥3 mg/L). Additionally, in a subsample of 84 patients showing admission CRP levels below 20 mg/L, changes in continuous CRP values over time were also analyzed. Results: After adjustment for a range of potentially important covariates, depression history showed a significant association with a smaller decrease in both CRP risk categories (r = 0.261, p < 0.001) and log CRP levels (r = 0.340, p = 0.005) over time. Conclusions: Self-reported history of depression may be associated with persistently elevated systemic inflammation three months after MI. This finding warrants studies to test whether lowering of inflammation in patients with an acute MI and a history of depression may improve prognosis.

C-reactive protein as a predictor of posttraumatic stress induced by acute myocardial infarction.

BACKGROUND: Acute coronary syndrome (ACS) may cause clinically relevant posttraumatic stress disorder symptoms (PTSS). An inflammatory state might be one mechanism linking PTSS with poor prognosis after ACS. We tested the hypothesis that a change in C-reactive protein (CRP) between hospital admission and 3-month follow-up is an independent predictor of ACS-triggered PTSS. METHODS: We assessed 183 patients (median age 59 years; 84% men) with verified myocardial infarction (MI) within 48 h of an acute coronary intervention and three months post-MI for self-rated PTSS. 14 (7.7%) patients fulfilled definition criteria for PTSS caseness. CRP values were categorized according to the predicted risk of cardiovascular disease (CVD) at hospital admission (acute inflammatory response): 0 to <5 mg/L, 5 to <10 mg/L, 10 to <20 mg/L, and ≥ 20 mg/L; and at 3-month follow-up (low-grade inflammation): 0 to <1 mg/L, 1 to <3 mg/L, and ≥ 3 mg/L. Additionally, in a subsample of 84 patients with CRP levels below 20 mg/L at admission, CRP values were log-transformed. RESULTS: After adjustment for covariates, less of a reduction or an increase of log CRP values between admission and 3-month follow-up predicted PTSS caseness (OR 6.25, 95% CI 1.25, 31.38), and continuous PTSS (unstandardized B = 0.21, 95% CI 0.07, 4.19; p = 0.043). Less reduction in CRP risk categories predicted both PTSS caseness (OR 4.14, 95% CI 1.89, 9.06) and continuous PTSS (B = 1.80, 95% CI 1.09, 2.51; p < 0.001). CONCLUSIONS: Persistently heightened inflammation seems to be predictive for the development of PTSS three months after ACS, so interventions to lower inflammation might be warranted.

Acute stress disorder and C-reactive protein in patients with acute myocardial infarction.

Background Myocardial infarction-triggered acute stress disorder (ASD) and subclinical inflammation associate with the development of posttraumatic stress disorder, and worsen the prognosis of myocardial infarction patients. We examined the relationship between ASD severity and C-reactive protein levels in patients with acute myocardial infarction. Methods We assessed 190 patients (median age 59 years; 83% men) with a verified myocardial infarction within 48 h of an acute coronary intervention. Circulating levels of C-reactive protein were categorized according to their prognostic risk for cardiovascular disease: 0 to <5, 5 to <10, 10 to <20, and ≥ 20 mg/l. Patients completed the ASD-Scale (ASDS) for myocardial infarction-triggered symptoms and questionnaires for demographic factors, health behaviours, cardiac-related variables and psychosocial characteristics. Results The ASDS sum score was positively associated with C-reactive protein categories in the bivariate analysis ( r = 0.20, p < 0.01). Significant relationships with C-reactive protein also emerged for dissociation ( r = 0.25, p < 0.001) and avoidance ( r = 0.19, p < 0.01), but not for arousal and re-experiencing. Similarly, C-reactive protein levels ≥ 20 mg/l versus < 20 mg/l were predicted by the ASDS sum score, and the dissociation, avoidance and arousal subscores (all p-values < 0.05) in the fully adjusted binary regression analyses. C-reactive protein levels ≥ 20 mg/l were also independently predicted by male gender, body mass index, lower education, and lower left ventricular ejection fraction and higher white blood cell count. Conclusions Higher levels of myocardial infarction-triggered ASD symptoms associate with a greater inflammatory response in patients with acute myocardial infarction independently of important covariates. The findings suggest a link between myocardial infarction-triggered ASD symptoms and a heightened acute phase response with a potential impact on cardiovascular disease prognosis.

The associations of cumulative adverse childhood experiences and irritability with mental disorders in detained male adolescent offenders.

BACKGROUND: Adverse childhood experiences (ACEs) and psychiatric disorders are common in juvenile detainees. Emotional dysregulation resulting from cumulated ACEs may be characterized by symptoms of irritability. The present study examined whether the accumulation of ACEs, irritability, or both predicted mental disorders in incarcerated adolescents with and without controlling for one another and for socio-demographic factors. METHODS: One hundred thirty male detained juvenile offenders (aged 13.8-19.5 years) were assessed by structured clinical interviews and a self-reporting scale for irritability. Univariate and multivariate regression models were used to examine the shared and distinct associations of ACEs and irritability with psychiatric diagnoses. RESULTS: A total of 75 % of the participants reported more than one ACE. The ACE total score was positively related to self-reported irritability. The ACE total score predicted depressive disorders, suicidality, post-traumatic stress disorder (PTSD), and anxiety disorders. Irritability was positively related to depressive disorders, suicidality, disruptive behavior disorder (DBD), substance use disorder (SUD), and attention deficit hyperactivity disorder (ADHD). These associations remained significant in multivariate models. CONCLUSIONS: This study provides evidence for the predictive impact of self-reported ACEs and irritability with regard to adolescent psychiatric disorders in young male inmates. Both variables differed in their predictive power for PTSD, internalizing, and externalizing disorders indicating the need for specific therapeutic interventions. Taking a close look at their trauma history seems to be of special importance for juveniles suffering from PTSD and anxiety disorders. For delinquent adolescents with DBD, ADHD and SUD, the training of emotion regulation techniques appears most promising. Approaches focusing on both, ACEs and emotion-focused contents may be implemented in the treatment of depressive disorders and suicidality.

Preliminary Evidence for a Compromised T-Cell Compartment in Maltreated Children with Depression and Posttraumatic Stress Disorder.

OBJECTIVE: Adverse childhood experiences, such as maltreatment, and affective disorders are associated with a proinflammatory state and/or variably compromised counts in lymphocyte subsets in adults. Animal models of social stress indicate that recent thymic emigrant cells (RTE), which maintain the T-cell compartment, are affected. METHODS: In this study, we examined the association between lymphocyte subsets, and depression and posttraumatic stress disorder (PTSD) among 16 maltreated children (aged 6-17 years) 1-3 years after the intervention by the Child Protection Team and among 14 healthy age-matched controls. The participants completed psychological assessment and had blood drawn for fluorescent-activated cell sorting analysis. RESULTS: Among maltreated children and adolescents, depression was associated with lower counts of RTEs and T-helper cells after controlling for age. We found additional trends and large effect sizes with regard to the percentages of these cells, as well as for related lymphocyte subsets. Similar effects were found for PTSD, i.e. lower counts of naïve T cells, which was also supported by a trend for their percentage. Compared to controls, maltreated participants with a clinical level of depression had decreased percentages of RTEs, with a similar trend for PTSD. CONCLUSION: Limited by the nature of a pilot study and the small sample size, these preliminary findings of a compromised T-cell compartment related to psychiatric symptoms in maltreated children and adolescents need to be further studied; particularly the role of RTEs needs further evaluation.

Neurogenic inflammation in stress-induced termination of murine hair growth is promoted by nerve growth factor.

Recently, we have revealed the existence of a "brain-hair follicle axis" in murine skin and have identified the neuropeptide substance P (SP) as a key mediator of stress-induced hair growth inhibition in vivo. Published evidence suggests that increased numbers of SP-immunoreactive sensory fibers, as seen in the dermis of stressed mice in anagen-catagen transition, are a result of transient high levels of nerve growth factor (NGF). Thus, we now aimed at dissecting the role of NGF in stress-triggered hair growth termination in our murine model. By real time PCR and immunohistochemistry, stress-exposed mice showed an up-regulation of NGF and its low-affinity receptor p75NTR; the NGF high-affinity receptor TrkA was moderately down-regulated. On neutralization of NGF, premature onset of catagen, apoptosis, and increased number/activation of perifollicular mast cells and antigen-presenting cells, which reflects the skin response to stress, was significantly abrogated. Stress or subcutaneous injection of recombinant NGF (to mimic stress) resulted in an increased percentage of SP(+) neurons in dorsal root ganglia, as measured by retrograde tracing. Taken together, these data suggest that NGF is a central element in the perifollicular neurogenic inflammation that develops during the murine skin response to stress and antagonizing NGF may be a promising therapeutic approach to counter the negative effect of stress on hair growth.