We aim to determine why patients with depression are at an elevated risk for the development
of coronary heart disease, and resolve whether the severity of a patient's depression has a
counterpart in demonstrable abnormalities in brain chemistry. Studies will be completed in 28
patients with depression; both males and females. Patients will be studied both untreated and
during administration of a selective serotonin re-uptake inhibitor (SSRI) antidepressant.
They will be either newly diagnosed with depression, untreated patients suffering a recent
relapse, or patients seeking to switch from a non-SSRI antidepressant due to non-response.
The turnover of chemical messengers in the brain will be estimated by high internal jugular
venous blood sampling and DNA will be isolated and examined from blood cells. Immune function
will also be assessed. Whole body and cardiac sympathetic nervous activity will be
determined, as well as microneurographic recording of muscle sympathetic nervous activity.
It is hypothesised that patients with depression and no existing demonstrable cardiac disease
demonstrate:
Alterations in brain monoaminergic neurotransmitter turnover, resulting in sympathetic
nervous activation and dysregulation of the baroreflex control to both the heart (vagal) and
muscle vasoconstrictor sympathetic nerves; and Exhibit enhanced platelet reactivity
predisposing them to thrombogenesis and myocardial ischaemia.
Therapeutic intervention with an SSRI will modify cardiac sympathetic function, baroreflex
sensitivity or platelet reactivity in a fashion likely to reduce cardiac risk.
Phase:
N/A
Details
Lead Sponsor:
Baker Heart Research Institute
Collaborator:
National Health and Medical Research Council, Australia