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        Post-Stroke Treatment With Antidepressants Appears To Reduce Death Rate

        IOWA CITY, IA -- September 30, 2003 -- Antidepressant treatment for people who have had stroke -- whether the patients are depressed or not -- appears to increase their chances of living longer, according to a University of Iowa study.

        The antidepressants may reduce mortality by decreasing the number of cardiovascular events such as heart attack and recurrent stroke occurring during the follow-up period of both depressed and non-depressed patients who had a stroke. The study involved 104 patients who randomly were assigned to receive nortriptyline (Aventyl or Pamelor), fluoxetine (Prozac) or placebo (inactive substance) for three months after their stroke, and mortality data investigators obtained nine years later. The findings appear in the October issue of the American Journal of Psychiatry.

        The relatively small study must be considered preliminary, but the findings are significant, said Ricardo Jorge, M.D., UI assistant professor of psychiatry and the study's co-investigator.

        "The study implications are impressive because they indicate patients with stroke may benefit from prevention strategies that use antidepressants to improve recovery and also reduce mortality," Jorge said. "The findings also are important when you take into account that post-stroke depression is so frequent."

        Post-stroke depression can occur during the first two years after a stroke. Approximately one in five people who have a stroke develop major depression, while another one in five survivors have less severe depression.

        Robert G. Robinson, M.D., the Paul W. Penningroth Professor of Psychiatry, head of the department, and the study's principal investigator, and colleagues previously found that many patients with post-stroke depression who receive antidepressants can improve their activities of daily living (such as bathing oneself or keeping a checkbook) and cognitive function (such as memory and the ability to solve problems).

        Robinson and colleagues' previous analysis also showed that stroke patients with depression die at a faster rate than stroke patients who are not depressed, and this higher death rate has been linked to cardiovascular events.

        The current analysis used the initial data from the previous research and mortality data obtained nine years later. Half of the patients who received antidepressants actually were depressed at the start of the study (27 of 53), and 46.4 percent of patients receiving placebo were depressed at baseline (13 of 28). Of the 104 patients in the study, 23 did not complete their initial assignment to take either one of the antidepressants or the placebo for 12 weeks.

        The researchers found that nearly 68 percent of the patients who received all 12 weeks of antidepressant treatment were alive after nine years (36 of 53 patients), compared with about 36 percent of patients who received 12 weeks of the inactive substance (10 of 28 patients).

        Analysis of the causes of death revealed that patients who received antidepressants were less likely to die from cardiovascular problems than patients who did not receive antidepressants. Thirty percent of the patients, depressed or not, who received antidepressants and died within nine years died from cardiovascular causes. In contrast, nearly 55 percent of patients who did not receive adequate antidepressant therapy and died during the same period died from cardiovascular causes.

        Jorge said antidepressants may provide protective effects in several ways, both behaviorally and physiologically. For one, depressed patients may not comply with treatments. For example, a person who is depressed after a stroke and has diabetes may poorly control their diabetes by failing to eat properly and failing to take medications. However, a non-depressed person with diabetes may be more attentive to these important self-care measures.

        Depression also may be associated with changes in platelet function. Platelets play a role in blood clotting and in the progress of arterial disease. Jorge and colleagues will study how antidepressants may affect platelet function in patients who have had a stroke.

        Jorge added that scientific literature also indicates depression can cause changes in blood pressure and heart rate, making depressed patients prone to serious heart attacks. "Antidepressants may modify the way a person reacts to stress and, thus, reduce the frequency of these complications," he said.

        The UI study included a number of Iowans, representing primarily whites. Jorge said this limitation may mean the findings are not applicable to other groups of patients who strokes. He said future studies will need to include a large number of patients to determine whether antidepressants have a definite positive effect on people with stroke.

        Jorge said that the incidence, or rate, at which people get strokes in western societies has been relatively stable for the past few years because of prevention and control of conditions such as hypertension (high blood pressure) and other cardiovascular risk factors. However, as the population in the United States ages, the total number of strokes will eventually increase, requiring a renewed effort in implementing primary and secondary prevention strategies.

        The study was funded by a grant from the National Institute of Mental Health.


        SOURCE: University of Iowa Health Science Relations



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