Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease.

OBJECTIVE: Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF). METHODS: The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment. RESULTS: Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS. CONCLUSION: Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.

Association of 5-HTTLPR/rs25531 with depressive symptoms in patients with coronary heart disease: A prospective study.

BACKGROUND: 5-HTTLPR/rs25531 is suspected to be involved in the pathogenesis of both coronary heart disease (CHD)1 and depression. We aimed to investigate the role of 5-HTTLPR/rs25531 in the development of depressive symptoms among CHD patients in a longitudinal design. METHODS: N = 265 participants with CHD diagnosis were included while hospitalized in a department of cardiology and genotyped for the 5-HTTLPR/rs25531. Depressive symptoms were measured using the Patient Health Questionnaire (PHQ-9)7 at baseline and after 6 and 12 months. Binary logistic regression models were used to analyze the association of 5-HTTLPR/rs25531 with the prevalence of depressive symptoms at each time point as well as with the incidence and persistence of depressive symptoms at follow-up. RESULTS: "LALA" genotype was associated with a higher prevalence of depressive symptoms 12 months after study inclusion. "LALA" genotype was associated with a higher incidence of depressive symptoms 6 and 12 months after study inclusion. There was no association of 5-HTTLPR/rs25531 with the persistence of depressive symptoms. LIMITATIONS: Inclusion criteria did not demand a particular cardiac event at baseline, which aggravated the interpretation of the time-specific results. The majority of the participants was of male gender which could cause bias. The present study only vaguely differentiated between ethnical groups which might cause bias regarding nationality-dependent allele distributions. CONCLUSION: The present study suggests a time-dependent association of the "LALA" genotype with depressive symptoms in CHD patients. 5-HTTLPR/rs25531 might be an important marker to detect risk groups for later onset depressive symptoms among CHD patients.

Association of FKBP5 genotype with depressive symptoms in patients with coronary heart disease: a prospective study.

Depression and coronary heart disease (CHD) are prevalent and often co-occurring disorders. Both have been associated with a dysregulated stress system. As a central element of the stress system, the FKBP5 gene has been shown to be associated with depression. In a prospective design, this study aims to investigate the association of FKBP5 with depressive symptoms in CHD patients. N = 268 hospitalized CHD patients were included. Depressive symptoms were measured using the Hospital Anxiety and Depression Scale (HADS-D) at four time points (baseline, and after 1 month, 6 months, and 12 months). The functional FKBP5 single-nucleotide polymorphism (SNP) rs1360780 was selected for genotyping. Linear regression models showed that a higher number of FKBP5 C alleles was associated with more depressive symptoms in CHD patients both at baseline (p = 0.015) and at 12-months follow-up (p = 0.025) after adjustment for confounders. Further analyses revealed that this effect was driven by an interaction of FKBP5 genotype with patients' prior CHD course. Specifically, only in patients with a prior myocardial infarction or coronary revascularization, more depressive symptoms were associated with a higher number of C alleles (baseline: p = 0.046; 1-month: p = 0.026; 6-months: p = 0.028). Moreover, a higher number of C alleles was significantly related to a greater risk for dyslipidemia (p = .016). Our results point to a relevance of FKBP5 in the association of the two stress-related diseases depression and CHD.

Association between heart-focused anxiety, depressive symptoms, health behaviors and healthcare utilization in patients with coronary heart disease.

OBJECTIVE: To analyze the association between heart-focused anxiety, depressive symptoms, health behaviors and healthcare utilization in patients with coronary heart disease (CHD). METHODS: N = 1007 patients with CHD were recruited in hospital and followed for one year in a two-site cohort study. Heart focused anxiety (Cardiac Anxiety Questionnaire [CAQ] with the three subscales fear, attention, and avoidance), depressive symptoms (depression module from the Patient Health Questionnaire [PHQ-9]), health behaviors and healthcare utilization (smoking status, alcohol consumption, physical activity, outpatient physician/psychotherapist visits) were assessed six months after the initial hospitalization. Multiple regression models were used for statistical analysis. RESULTS: About one third of the sample exhibited clinically significant CAQ scores. Higher CAQ-avoidance scores were associated with current smoking (OR = 1.62; 95%CI: 1.33-1.98), reduced alcohol intake (OR = 0.83; 95%CI: 0.71-0.98), non-participation in a coronary exercise group (OR = 1.76; 95%CI: 1.42-2.17), less regular physical activity (OR = 2.69; 95%CI: 2.32-3.12), and more frequent contact to general practitioners (GPs; b = 0.07, SE: 0.03). CAQ-attention was associated with non-smoking (OR = 0.51; 95%CI: 0.37-0.70), exercise group participation (OR = 0.69; 95%CI: 0.51-0.94), more frequent regular physical activity (OR = 0.55; 95%CI: 0.44-0.68), and more frequent contact to specialists for internal medicine (b = 0.09, SE: 0.04). CAQ-fear was not associated with any of the health behavior or healthcare use measures. Depressive symptoms were associated with reduced regular physical activity (OR = 1.05; 95%CI: 1.02-1.08) and increased contact to mental care specialists (b = 0.03, SE: 0.01) and GPs (b = 0.02, SE: 0.01). CONCLUSIONS: Heart-focused anxiety and depressive symptoms may impede secondary prevention in patients with CHD and increase outpatient healthcare utilization.

[Diagnostic Accuracy of German Depression Screenings in Patients with Coronary Heart Disease]. / Erkennungsgüte dreier deutschsprachiger Screeninginstrumente für Depression bei hospitalisierten Patienten mit koronarer Herzerkrankung.

OBJECTIVE: To compare the diagnostic accuracy of German depression screening instruments in patients with coronary heart disease (CHD). METHODS: 1019 CHD patients completed the Patient Health Questionnaire (PHQ-9 and PHQ-2) and the Hospital Anxiety and Depression Scale (HADS-D). The Composite International Diagnostic Interview served as reference standard for "any depressive disorder" and "major depression". RESULTS: The accuracy of the PHQ-9 and the HADS-D was comparable according to the area under the curve, and both were superior to the PHQ-2. The optimal cut-off according to the Youden index (maximum sum of sensitivity and specificity) was 7 for both instruments. At this optimal cut-off, the PHQ-9 had a higher sensitivity compared to the HADS-D, but a lower specificity (below 68). Results remained similar when patients who reported that they currently underwent treatment for depression were excluded. CONCLUSION: The PHQ-9 and the HADS-D have comparable overall diagnostic accuracy in CHD patients. In line with previous screening studies with CHD patients, the optimal cut-offs were below the cut-offs that are recommended in the literature.

Serum brain-derived neurotrophic factor and stability of depressive symptoms in coronary heart disease patients: A prospective study.

OBJECTIVE: Brain-derived neurotrophic factor (BDNF) supports neurogenesis, angiogenesis, and promotes the survival of various cell types in the brain and the coronary system. Moreover, BDNF is associated with both coronary heart disease (CHD) and depression. The current study aims to investigate whether serum BDNF levels are associated with the course of depressive symptoms in CHD patients. METHODS: At baseline, N=225 CHD patients were enrolled while hospitalized. Of these, N=190 (84%) could be followed up 6 months later. Depressive symptoms were assessed both at baseline and at the 6-months follow-up using the Patient Health Questionnaire (PHQ-9). Serum BDNF concentrations were measured using fluorometric Enzyme-linked immunosorbent assays (ELISA). RESULTS: Logistic regression models showed that lower BDNF levels were associated with persistent depressive symptoms, even after adjustment for age, sex, smoking and potential medical confounders. The incidence of depressive symptoms was not related to lower BDNF levels. However, somatic comorbidity (as measured by the Charlson Comorbidity Index) was significantly associated with the incidence of depressive symptoms. CONCLUSIONS: Our findings suggest a role of BDNF in the link between CHD and depressive symptoms. Particularly, low serum BDNF levels could be considered as a valuable biomarker for the persistence of depressive symptoms among depressed CHD patients.