DEPRESSION AS A RISK FACTOR FOR ISCHEMIC HEART DISEASE

Project: Research project

Project Details

Description

DESCRIPTION (Adapted from the Applicant's Abstract): The training and
research components of this application for a Scientist Development Award
for New Minority Faculty are designed to prepare the applicant for a career
as an independent investigator at the interface of the basic and clinical
sciences. The career development plan, modeled after the Ph.D. program in
biological sciences, will provide the scientific knowledge base and specific
laboratory techniques required to conduct the proposed research. Supervised
case management in addition to tutorials in hematology, cardiology, and
psychiatric assessment will develop the applicant's clinical skills.

The research plan focuses on the relationship between major mood disorders
and thrombotic disease. Not only are platelets a source of vasoactive
mediators that regulate vascular tone, but they also play a role in
intravascular thrombus formation and dynamic coronary constriction that
results in myocardial ischemia. There is considerable evidence that
patients with ischemic heart disease (IHD) and concurrent major depression
have a less favorable prognosis than patients with IHD alone. Recent
studies have revealed that major depression is a very significant risk
factor for death after myocardial infarction and stroke and not simply a
nonspecific emotional response to cardiovascular illness. The overall
objective of the proposed work is to investigate further this interaction
between major depression and the hemostatic system, especially major
depression. The research aims are to determine: 1) whether depressed
patients without cardiovascular disease exhibit exaggerated platelet
reactivity under basal conditions, 2) whether platelet responsiveness to
orthostatic challenge and standard inducers of aggregation are altered in
patients with major depression, and 3) if pharmacologic treatment of
depressed patients with paroxetine (a potent and selective serotonin
reuptake inhibitor) is associated with alteration of platelet responsiveness
to orthostatic challenge, and to standard inducers of aggregation. To
accomplish these aims, platelet function and severity of depression willbe
evaluated longitudinally before and after treatment with either placebo or
paroxetine. Additionally, the in vitro activity of paroxetine on platelet
activity will be evaluated. Future investigators would expand these
findings to depression by evaluation and treatment of depressed patients at
risk for IHD (e.g., those with hypertension, hyperlipidemia, etc...) and
patient post-myocardial infarction with comorbid depression. These studies
will provide novel information on the biological basis for the apparent
increased vulnerability of depressed patients to IHD.
StatusFinished
Effective start/end date2/1/971/31/02

Funding

  • National Institute of Mental Health: $138,849.00
  • National Institute of Mental Health
  • National Institute of Mental Health
  • National Institute of Mental Health
  • National Institute of Mental Health: $142,242.00

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