Background: A growing body of evidence links depression with cardiovascular events, but the mechanisms responsible remain unknown.
Aims: To investigate the role of the autonomic nervous system and inflammation in the link between coronary heart disease and major depressive disorder (MDD); and, cardiac risk modification following pharmacological treatment of depression.
Methods: We examined cardiac baroreflex function, heart rate variability, pulse pressure and high sensitivity C-reactive protein (hsCRP), all of which impact on cardiac risk, pre- and post- treatment in 25 patients with MDD, with no history of coronary heart disease, and in 15 healthy subjects. Treatment consisted of selective serotonin reuptake inhibitors for approximately 12 weeks.
Results: No significant differences were observed between untreated MDD patients and healthy subjects in blood pressure, heart rate, baroreflex sensitivity, heart rate variability or pulse pressure. HsCRP was significantly elevated in patients with MDD prior to treatment (p = 0.025). Moreover, while pharmacotherapy was effective in alleviating depression, surprisingly, all of these parameters were modified (p < 0.05) in a manner likely to increase cardiac risk.
Conclusion: This study demonstrated higher hsCRP plasma levels in patients with MDD. Following treatment vagal activity was reduced, manifest in reductions in baroreflex sensitivity and heart rate variability, accompanied by increases in pulse pressure and plasma hsCRP levels. Mechanisms possibly responsible for generating cardiac risk in patients treated with SSRIs may need to be therapeutically targeted to reduce coronary heart disease incidence in this population.
