title: Antidepressive treatment as a modulator of inflammatory process in patients with heart failure: effects on proinflammatory cytokines and acute phase protein levels.
abstract: BACKGROUND
  Depression has been associated with increased inflammatory process. Although anti-depressive medication has anti-inflammatory effect in major depression, its role in patients with heart failure (HF) is unknown. In the present study we evaluated the impact of antidepressive medication on the expression of proinflammatory cytokines and acute phase response proteins, in patients with HF and major depression.
  
  
  METHODS
  The study population consisted of 250 patients with HF (154 suffering from major depression). Patients with major depression were under selective serotonin reuptake inhibitors (SSRIs, n=120) or tricyclic antidepressants (TCA) and/or serotonin/norepinephrine reuptake inhibitors (SNRIs) (n=34), for at least 6 months.
  
  
  RESULTS
  Levels of TNF-alpha, IL-6, CRP and fibrinogen were not significantly different between HF patients with depression under treatment and those without depression (p=NS for all). However, TNF-alpha and CRP levels were significantly lower in patients receiving TCA/SNRI compared to patients receiving SSRIs or those without depression (p<0.05 for all). Similarly, patients under TCA/SNRI had significantly lower heart rate compared to those treated with SSRIs or those without depression. In multivariate analysis, treatment with SNRI/TCA was an independent predictor for log(TNF-alpha) (beta=0.036(SE:0.016) and log(CRP) (beta=0.099(SE:0.048), p=0.041).
  
  
  CONCLUSIONS
  In the present study we demonstrate for the first time that treatment of patients with HF and major depression with TCAs/SNRIs, is associated with lower levels of TNF-alpha and CRP, suggesting that the type of antidepressive treatment may have a significant effect on the underlying inflammatory process.
authors.affiliation: 1st Cardiology Department, Athens University Medical School, Athens, Greece. tousouli@med.uoa.gr
authors.forename: Dimitris
authors.initials: D
authors.lastname: Tousoulis
authors.forename: Apostolos
authors.initials: A
authors.lastname: Drolias
authors.forename: Charalambos
authors.initials: C
authors.lastname: Antoniades
authors.forename: Carmen
authors.initials: C
authors.lastname: Vasiliadou
authors.forename: Kyriakoula
authors.initials: K
authors.lastname: Marinou
authors.forename: George
authors.initials: G
authors.lastname: Latsios
authors.forename: Elli
authors.initials: E
authors.lastname: Stefanadi
authors.forename: Panagiota
authors.initials: P
authors.lastname: Gounari
authors.forename: Gerasimos
authors.initials: G
authors.lastname: Siasos
authors.forename: Nikos
authors.initials: N
authors.lastname: Papageorgiou
authors.forename: Athanasios
authors.initials: A
authors.lastname: Trikas
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism*; D000929:Antidepressive Agents, Tricyclic / Q000627:therapeutic use*; D002097:C-Reactive Protein / Q000378:metabolism; D003430:Cross-Sectional Studies; D003865:Major Depressive Disorder / Q000150:complications / Q000188:drug therapy / Q000276:immunology; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006333:Heart Failure / Q000150:complications* / Q000276:immunology*; D006801:Humans; D007107:Immune System / Q000187:drug effects; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009638:Norepinephrine / Q000378:metabolism; D011446:Prospective Studies; D017367:Selective Serotonin Reuptake Inhibitors / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000209:Acute-Phase Proteins; D000929:Antidepressive Agents, Tricyclic; D002097:C-Reactive Protein; D005340:Fibrinogen; D015850:Interleukin-6; D009638:Norepinephrine; D017367:Selective Serotonin Reuptake Inhibitors; D014409:Tumor Necrosis Factor-alpha; C508600:IL6 protein, human