Letters to the Editor
Re: Depression, Stroke Diagnosis, and SSRI Discontinuation Syndrome
Dear Editor:
I read with great interest Dr Ramasubbu’s and Dr Patten’s article on the effects of depression on stroke morbidity and mortality (1), as well as Dr Ramasubbu’s letter in the same issue about minor strokes related to paroxetine discontinuation (2). Together, these reports provoke much thought about the role of selective serotonin reuptake inhibitors (SSRIs) in preventing stroke and the complications of stroke. Dr Ramasubbu reported an association between depressive symptoms and increased risk of stroke morbidity and mortality (1). Alternatively, in addition to an association with SSRI discontinuation syndrome, withdrawal of antidepressants such as paroxetine may create a clinical picture similar to a minor stroke. In their double-blind, placebo-controlled study of sertraline and the prevention of depression in stroke patients, Rassmussen and others reported that the prophylactic use of sertraline prevented the development of depression in poststroke patients (3). They also reported that patients given sertraline experienced fewer cardiovascular and noncardiovascular adverse events than patients treated with placebo. While there is room for much speculation about the mechanism by which SSRIs reduce the risk of stroke and cardiovascular events, a factor that may bear further consideration is the direct effect of SSRIs on platelets. SSRIs induce reduced platelet adhesion and activity, as has been noted by Musselman and colleagues (4). Further clinical evidenced is summarized by Dalton and others (5). In a community-based study, Dalton found that SSRIs, but not non-SSRIs, were associated with significantly increased risk of gastrointestinal bleeding, particularly with the concomitant use of nonsteroidal antiinflammatory drugs.
In essence, depression, which is a well-established risk factor for the development of cardiovascular disease (6), can now be considered as a risk factor for cerebrovascular disorders. The SSRIs’ ability to inhibit platelet adhesion, independent of their effect on mood, may be the causative agent. Whether response to depression is necessary for this added benefit has not been established.
If these observations are supported by further studies, we now also have another factor to consider in the selection of antidepressants. Patients who may be at increased risk for cardiovascular or cerebrovascular events may be better served by SSRIs as a drug of first choice. Alternatively, a non-SSRI agent may be the drug of first choice in the treatment of depression for those patients who are on nonsteriodal antiinflammatory drugs.
References
1. Ramasubbu R, Patten SB. Effect of depression on stroke morbidity and mortality. Can J Psychiatry 2003;48:250–7.
2. Ramasubbu R. Minor strokes related to paroxetine discontinuation in elderly subjects: emergent adverse events [letter]. Can J Psychiatry 2003;48:281–2.
3. Rasmussen A, Lunde M, Poulsen DL, Sorensen K, Qvitzau S, Bech P. A double-blind placebo-controlled study of sertraline in the prevention of depression in stroke patients. Psychosomatics 2003;44:216–21.
4. Musselman DL, Tomer A, Manatunga AK, Knight BT, Porter MR, Kasey S, and others. Exaggerated platelet reactivity in major depression. Am J Psychiatry 1996;153:1313–7.
5. Dalton SO, Johansen C, Mellemkjaer L, Sorenson HT, Norgard Olsen JH. Use of selective serotonin reuptake inhibitors and risk of upper gastrointestinal tract bleeding, Arch Intern Med 2003;163:59–64.
6. Penninx BWJH, Beekman ATF, Honig A, Deeg DJH, Schoevers RA, van Eijk JTM, and others. Depression and cardiac mortality. Arch Gen Psychiatry 2001;58:221–7.
Dr SH McNevin, MD, FRCPC
Kingston, Ontario
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