Dissertation committee:
Δημόπουλος Μελέτιος-Αθανάσιος, Καθηγητής, Ιατρική Σχολή, ΕΚΠΑ
Σταματελόπουλος Κίμων, Αναπληρωτής Καθηγητής, Ιατρική Σχολή, ΕΚΠΑ, Επιβλέπων
Δάλλα Χριστίνα, Αναπληρώτρια Καθηγήτρια, Ιατρική Σχολή, ΕΚΠΑ
Πρωτογέρου Αθανάσιος, Αναπληρωτής Καθηγητής, Ιατρική Σχολή, ΕΚΠΑ
Κουζούπης Αναστάσιος, Αναπληρωτής Καθηγητής, Ιατρική Σχολή, ΕΚΠΑ
Μανιός Ευστάθιος, Αναπληρωτής Καθηγητής, Ιατρική Σχολή, ΕΚΠΑ
Γαβριατοπούλου Μαρία, Επίκουρη Καθηγήτρια, Ιατρική Σχολή, ΕΚΠΑ
Summary:
Depression is a condition that affects more than 300 million people worldwide. It is well known that major depression increases the risk of cardiovascular disease, and several pathways have been suggested in order to explain this association, such as sympathetic nervous activation, unbalanced immune response, neuroendocrine changes. Accumulating data suggest that depression is associated with endothelial dysfunction and arterial stiffening, which may mediate development of hypertension and increased cardiovascular risk. The effect of antidepressant treatment on these vascular parameters has not been elucidated.
The aim of this research is to assess the effect of antidepressant therapy on endothelial function and arterial stiffness in patients with major depression.
Sixty-nine patients with major psychotic depression, according to DSM-IV-TR, suitable for treatment with citalopram and risperidone, were initially enrolled. Vascular assessment was performed at the Laboratory and the patients were matched 1:1 with control subjects without depression. Forty-nine of the recruited patients continued with the prospective part of the study, and were deemed by the treating psychiatrist to receive combination of citalopram and risperidone, in titrated doses, for a period of 6 months. Thirty-seven of them completed the 6-month treatment, while 12 patients denied treatment, or were non-compliant, nonetheless they agreed to be followed for the same time period. This group of patients was used as controls in further analysis. Vascular function was assessed at baseline and at the end of follow-up, by assessment of flow-mediated dilatation (FMD), carotid-femoral pulse wave velocity (PWV) and estimation of aortic pressure waveforms, reflected waves and augmentation index (AI). During the follow-up visit, response to antidepressant therapy was also assessed in the group of treated patients (n=37, improvement in 24 patients and no improvement in 13).
Results show that the 69 initially enrolled patients with psychotic depression, presented worse endothelial function as compared to controls without depression, matched for traditional cardiovascular risk factors. Moreover, aortic and peripheral blood pressure, PWV, FMD and AI (p < 0.05 for all comparisons) were significantly improved in the group that received treatment. In this group, only responders to treatment (n = 24) presented significant improvements in all hemodynamic and vascular parameters (p < 0.05 for all comparisons), irrespectively of traditional cardiovascular risk factors, treatment with vasoactive medication and the observed blood pressure lowering.
In conclusion, patients who respond to therapy for major psychotic depression present sustained improvement in vascular function. Given that depressed patients are considered to be at high cardiovascular risk and are often non-compliant with treatment, the results of the present thesis support the importance of close vigilance of patient adherence to treatment, as well as regular assessment of the efficacy of antidepressant therapy.
