title: Elevated stress-hemoconcentration in major depression is normalized by antidepressant treatment: secondary analysis from a randomized, double-blind clinical trial and relevance to cardiovascular disease risk.
abstract: BACKGROUND
  Major depressive disorder (MDD) is an independent risk factor for cardiovascular disease (CVD); the presence of MDD symptoms in patients with CVD is associated with a higher incidence of cardiac complications following acute myocardial infarction (MI). Stress-hemoconcentration, a result of psychological stress that might be a risk factor for the pathogenesis of CVD, has been studied in stress-challenge paradigms but has not been systematically studied in MDD.
  
  
  METHODS
  Secondary analysis of stress hemoconcentration was performed on data from controls and subjects with mild to moderate MDD participating in an ongoing pharmacogenetic study of antidepressant treatment response to desipramine or fluoxetine. Hematologic and hemorheologic measures of stress-hemoconcentration included blood cell counts, hematocrit, hemoglobin, total serum protein, and albumin, and whole blood viscosity.
  
  
  RESULTS
  Subjects with mild to moderate MDD had significantly increased hemorheologic measures of stress-hemoconcentration and blood viscosity when compared to controls; these measures were correlated with depression severity. Measures of stress-hemoconcentration improved significantly after 8 weeks of antidepressant treatment. Improvements in white blood cell count, red blood cell measures and plasma volume were correlated with decreased severity of depression.
  
  
  CONCLUSIONS
  Our secondary data analyses support that stress-hemoconcentration, possibly caused by decrements in plasma volume during psychological stress, is present in Mexican-American subjects with mild to moderate MDD at non-challenged baseline conditions. We also found that after antidepressant treatment hemorheologic measures of stress-hemoconcentration are improved and are correlated with improvement of depressive symptoms. These findings suggest that antidepressant treatment may have a positive impact in CVD by ameliorating increased blood viscosity. Physicians should be aware of the potential impact of measures of hemoconcentration and consider the implications for cardiovascular risk in depressed patients.
authors.affiliation: Department of Psychiatry and Behavioral Sciences, Leonard M. Miller School of Medicine, University of Miami, Miami, Florida, USA. mali@miami.edu
authors.forename: Ma-Li
authors.initials: ML
authors.lastname: Wong
authors.forename: Chuanhui
authors.initials: C
authors.lastname: Dong
authors.forename: Karin
authors.initials: K
authors.lastname: Esposito
authors.forename: Sarika
authors.initials: S
authors.lastname: Thakur
authors.forename: Weiqing
authors.initials: W
authors.lastname: Liu
authors.forename: Robert M
authors.initials: RM
authors.lastname: Elashoff
authors.forename: Julio
authors.initials: J
authors.lastname: Licinio
mesh_terms: D000328:Adult; D000368:Aged; D000928:Antidepressive Agents / Q000627:therapeutic use*; D001798:Blood Proteins / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000453:epidemiology*; D003865:Major Depressive Disorder / Q000188:drug therapy*; D004311:Double-Blind Method; D005260:Female; D006400:Hematocrit; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013315:Stress, Psychological / Q000150:complications*
chemical_list: D000928:Antidepressive Agents; D001798:Blood Proteins; D006454:Hemoglobins