Relation of depressive mood to plasminogen activator inhibitor, tissue plasminogen activator, and fibrinogen levels in patients with versus without coronary heart disease.
The increased risk of coronary heart disease (CHD) associated with depression is well documented. We hypothesized that impaired fibrinolysis is involved in this link. To explore the association of depressive mood and/or vital exhaustion with various measurements of fibrinolysis activity, 231 men (40 to 65 years old; 123 without CHD and taking no medication and 108 with documented CHD), completed the Center of Epidemiologic Studies Depression Scale and the Maastricht Questionnaire for vital exhaustion. Using classic cut-off points (Center of Epidemiologic Studies Depression Scale score >or=17, Maastricht Questionnaire score >or=8), 6.5% and 9.8% of subjects without CHD and 38% and 48.1% of those with CHD were classified as depressed and exhausted, respectively. Patients with CHD were older, had a higher body mass index, and higher levels of total cholesterol, glucose, plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator (t-PA) antigen, and fibrinogen; 47% were treated for hypertension. Depressed subjects had higher levels of PAI-1 activity (p = 0.006) and exhausted patients had higher levels of PAI-1 activity (p = 0.011) and fibrinogen (p = 0.009). After adjusting for clinical condition (with or without CHD), smoking, hypertension, triglyceride concentration, and body mass index, PAI-1 activity remained higher in depressed subjects (p = 0.03). This association persisted after further adjustment for vital exhaustion or for t-PA antigen and fibrinogen levels. t-PA antigen and fibrinogen levels were not associated with depressive mood in multivariate analyses. No fibrinolytic variable was associated with vital exhaustion in multivariate analyses. In conclusion, depressive mood, but not vital exhaustion, is associated with higher levels of PAI-1 activity, suggesting a possible impairment of fibrinolysis and indicating a potential additional mechanism by which depressive mood may act as a cardiovascular risk factor.
Lahlou-Laforet
Khadija
K
Department of C-L Psychiatry, Faculté de Médecine, Université Paris-Descartes, AP-HP, Hôpital Europeén Georges Pompidou, France. khadija.lahlou-laforet@hop.egp.aphp.fr
Alhenc-Gelas
Martine
M
Pornin
Maurice
M
Bydlowski
Sarah
S
Seigneur
Etienne
E
Benetos
Athanase
A
Kierzin
Jean-Michel
JM
Scarabin
Pierre-Yves
PY
Ducimetiere
Pierre
P
Aiach
Martine
M
Guize
Louis
L
Consoli
Silla M
SM
D000328:Adult; D000368:Aged; D003327:Coronary Disease / Q000097:blood*; D003863:Depression / Q000097:blood*; D005221:Fatigue / Q000097:blood; D005340:Fibrinogen / Q000032:analysis*; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D011569:Psychiatric Status Rating Scales; D011795:Surveys and Questionnaires; D010959:Tissue Plasminogen Activator / Q000097:blood*
D017395:Plasminogen Activator Inhibitor 1; D005340:Fibrinogen; D010959:Tissue Plasminogen Activator