| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2932881 | International Journal of Cardiology | 2010 | 9 Pages |
BackgroundSelective serotonin reuptake inhibitors (SSRIs) exert cardioprotective effects. We examined whether SSRIs a) modulate endothelial cell expression of vascular cell adhesion molecule (VCAM-1), intracellular adhesion molecule (ICAM-1) and adhesiveness to U937 monocytes, b) reduce the circulating levels of these adhesion molecules in vivo.MethodsWe assessed the effect of SSRIs, (citalopram, fluvoxamine and fluoxetine), on TNF-alpha-induced expression of VCAM-1 and ICAM-1 in human aorta endothelial cells and adhesiveness to U937 monocytes. Cells were incubated with TNF-alpha in the absence and in the presence of SSRIs concentrations from 10− 7 M to10− 4 M and the VCAM-1 and ICAM-1 expression was quantified by cell-ELISA. The TNF-alpha-stimulated adhesiveness to U937 monocytes was also assessed. Twenty five patients with chronic heart failure and depression were randomized to receive sertaline 50 mg, p.o., o.d. (n = 13) or placebo. At baseline and 3-months after treatment, we measured VCAM-1and ICAM-1 plasma levels.ResultsSSRIs decreased the TNF-alpha-induced endothelial expression of VCAM-1 at concentration range 10− 7 M to 10− 4 M (p < 0.05). ICAM-1 expression was decreased in the presence of fluvoxamine and fluoxetine at concentrations from10− 7 M to 10− 4 M (p < 0.05) and in the presence of citalopram at concentrations from 10− 7 M to 10− 5 M (p < 0.05). All SSRIs inhibited the TNF-alpha-stimulated adhesiveness to U937 cells at 10− 5 M and 10− 4 M (p < 0.05). Compared to baseline, there was a greater reduction in ICAM-1 and VCAM-1 levels post-sertaline than post placebo in heart failure patients (p < 0.05).ConclusionSSRIs may exhibit an anti-inflammatory activity on endothelial cells and reduce circulating VCAM-1 and ICAM-1 in vivo, a mechanism which may partly mediate their cardioprotective effects.
