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Abstract
Although it is recognized that patients with major depressive disorder (MDD) are at increased risk of developing cardiovascular disease (CVD) the mechanisms responsible remain unknown. Endothelial dysfunction is one of the first signs of CVD. Using two techniques, flow-mediated dilatation in response to reactive hyperemia and laser Doppler velocimetry with iontophoresis, we examined endothelial function in the forearm before and after serotonin-specific reuptake inhibitor (SSRI) treatment in 31 patients with MDD. Measurement of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, soluble P-selectin, and noradrenaline in plasma was also performed. Prior to treatment, markers of endothelial and vascular function and platelet reactivity were within the normal range. Following SSRI therapy (95 ± 5 days) symptoms of depression were reduced (paired difference between pre- and post-treatment Hamilton rating −18 ± 1, P < 0.001) with 19 patients recovered and 4 remitted. There occurred no significant change in markers of endothelial or vascular function following SSRI therapy. The improvement in Hamilton depression rating in response to therapy could be independently predicted by the baseline arterial plasma noradrenaline concentration (r2 = 0.36, P = 0.003). In this cohort of patients with MDD, SSRI therapy did not influence endothelial function or markers of vascular or platelet reactivity. Patient response to SSRI therapy could be predicted by the initial circulating level of noradrenaline, with noradrenaline levels being lower in responders.
Highlights
The link between cardiovascular disease (CVD) development and major depressive disorder (MDD) is well described [1,2,3]
Contrary to some previous reports, we found that antidepressant therapy was not associated with any change in endothelial function or of markers of vascular function or platelet reactivity
There occurred a significant reduction in the plasma level of noradrenaline following serotonin-specific reuptake inhibitor (SSRI) treatment and that the improvement in Ham-D score following SSRI therapy was associated with the plasma noradrenaline level at baseline
Summary
The link between cardiovascular disease (CVD) development and major depressive disorder (MDD) is well described [1,2,3]. The mechanisms linking MDD and CVD development remain to be unequivocally determined previous studies have provided some evidence of sympathetic nervous activation, endothelial dysfunction, and increased platelet reactivity in patients with MDD. Endothelial function was shown to be improved in patients with coronary heart disease and symptoms of depression following 20 weeks of sertraline treatment [8], a shorter period of therapy with either of these, sertraline, fluoxetine, or paroxetine, in women with no history of CVD was associated with no improvement in endothelial function [9]. Given the equivocal nature of these results, in this study, we aimed to examine endothelial function, in otherwise healthy patients with MDD, prior to and following serotonin-specific reuptake inhibitor (SSRI) treatment using two different techniques, flowmediated dilatation in response to reactive hyperemia to examine endothelial function in large vessels in the forearm, and, in small vessels, laser Doppler velocimetry (LDV) with iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP) [10]. Blood samples were obtained to examine markers of vascular function and platelet reactivity
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