Depression is frequently seen in cardiac patients. It has been shown that depression often has a negative impact on the course of coronary disease. More recently, research has demonstrated that some antidepressants can be used safely to treat depressed coronary patients. Although the majority of patients improve substantially with antidepressant treatment, a significant proportion do not respond to antidepressants. This project seeks to better understand why depression does not improve equally well in all patients. Ultimately, the hope is to improve the treatments available to people affected by both cardiac disease and depression, and to help select the best type of treatment in advance for each individual based on his or her personal history, and biological characteristics.
In this study 140 patients who have had a recent hospitalization for an acute coronary syndrome and who have major depression will all receive 12 weeks of treatment with the antidepressant citalopram and regular clinical management visits from a mental health professional. The objective is to examine the characteristics of depressed cardiac patients who do and do not show an improvement in depression with citalopram treatment. There is evidence that the causes of depression may be different in some people with cardiac disease than in individuals who do not have heart problems, and these differences may be at least partially involved in determining response to antidepressant treatment. Inflammation, one of the body's responses to the development of atherosclerosis (hardening of the arteries and blockages in the heart) may be particularly important in producing depression in cardiac patients. There may also be changes in the body's metabolism of tryptophan, a protein that is involved in making serotonin, and levels of serotonin are often low in depression. Other factors thought to influence the development of depression include childhood experiences and personality factors. Heredity and family history also seem to play a role in some people with depression and heart disease. Finally, some patients experience sleep apnea, interruptions in breathing while they are asleep, that can contribute to both cardiac disease and depression.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
7
All patients will take citalopram once daily. Medication will be commercial tablets of 20 mg or 40 mg. All patients will start on a half dose of 10 mg and, if there are no severe side effects, will be increased to 20 mg after 1 week, and if the HAMD-24 at 6 weeks is not \< 8, the dose will increase to 40 mg.
Centre de recherche du CHUM
Montreal, Quebec, Canada
Montreal Heart Insitute
Montreal, Quebec, Canada
Changes from baseline to 12 weeks in depression levels on the 24-item Hamilton Depression Rating Scale (HAMD-24)
Administered centrally by telephone
Time frame: 12 weeks
Changes from baseline to 12 weeks in depression levels on the Inventory of Depressive Severity Clinician Version (IDS-C)
Administered centrally by telephone
Time frame: 12 weeks
Changes from baseline to 12 weeks in self-reported depression symptoms on the Beck Depression Inventory-II (BDI-II)
self-report
Time frame: 12 weeks
Changes from baseline to 12 weeks in Inflammatory markers
e.g. Tumor necrosis factor-alpha (TNF-alpha), Interleukin-6 (IL-6), Interleukin-10 (IL-10), C-Reactive Protein (CRP), Soluble intercellular adhesion molecule-1 (s-ICAM1)
Time frame: 12 weeks
Changes from baseline to 12 weeks in kynurenine levels
Time frame: 12 weeks
Changes from baseline to 12 weeks in tryptophan levels
Time frame: 12 weeks
Changes from baseline to 12 weeks in neopterin levels
Time frame: 12 weeks
Changes from baseline to 12 weeks in cognitive function
scores on the Trail Making Tests A and B, Digit Symbol Substitution Test, Rey Auditory Verbal Learning Test
Time frame: 12 weeks
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