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Updated: May 16, 2026

Measuring the Carotid to Femoral Pulse Wave Velocity (Cf-PWV) to Evaluate Arterial Stiffness
Published on: May 3, 2018
Depression treatment selectively modifies arterial stiffness in older participants
Angelo Scuteri1, Anna Modestino, Francesca Fedullo
1UOC Geriatria, IRCCS INRCA, POR Roma, Italy. angeloelefante@interfree.it
Background:
Depression is emerging as an independent cardiovascular disease risk factor. We investigated whether treating depression in older participants impacted on arterial stiffness, a known cardiovascular disease risk factor and a clinical marker of arterial aging.
Methods:
Seventy-five participants with pulse wave velocity (PWV), the gold standard measure for arterial stiffness, at baseline and at 12-month follow-up were included. Depressed patients were randomized to escitalopram (10mg/d) or to duloxetine (60mg/d). In patients without depression, no antidepressant therapy was started. The psychologist and the doctor measuring PWV were both unaware of antidepressant treatment.
Results:
At study entry, no difference in PWV were observable in the three groups of participants. A significant time × drug interaction term (p < .05) was observed for the impact of antidepressant therapy on PWV by analysis of covariance analysis. After 12 months of therapy, duloxetine treatment resulted in a significant (+21%) and escitalopram treatment in a not significant (6%) PWV increase. These changes in PWV were accompanied by a similar increase in blood pressure and LDL cholesterol in the two treated groups. However, duloxetine resulted in a significant 10% greater heart rate after 12 months that was not observable in participants treated with escitalopram nor in not-depressed older participants. Multiple regression models revealed that a drug-specific effect on PWV persisted after controlling for cardiovascular risk factor levels.
Conclusion:
Duloxetine but not escitalopram significantly increased PWV in older depressed participants after 12 months of treatment. The effect was not fully explained by concomitant changes in traditional cardiovascular risk factors known to significantly impact arterial stiffness.
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