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

Ma Li Wong, Chuanhui Dong, Karin Esposito, Sarika Thakur, Weiqing Liu, Robert M. Elashoff, Julio Licinio

Research output: Contribution to journalArticle

19 Citations (Scopus)

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. Findings: 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.

Original languageEnglish
Article numbere2350
JournalPLoS One
Volume3
Issue number7
DOIs
StatePublished - Jul 16 2008

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antidepressants
Major Depressive Disorder
blood viscosity
Antidepressive Agents
cardiovascular diseases
clinical trials
Cardiovascular Diseases
Clinical Trials
Depression
Blood Viscosity
Blood
signs and symptoms (animals and humans)
risk factors
Plasma Volume
pharmacogenomics
Mexican Americans
Psychological Stress
blood cell counts
myocardial infarction
Cells

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

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. / Wong, Ma Li; Dong, Chuanhui; Esposito, Karin; Thakur, Sarika; Liu, Weiqing; Elashoff, Robert M.; Licinio, Julio.

In: PLoS One, Vol. 3, No. 7, e2350, 16.07.2008.

Research output: Contribution to journalArticle

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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. Findings: 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.",
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