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The documentation of a 20% prevalence of depression after stroke1 has important therapeutic implications for patients with significant ischaemic heart disease and/or cardiac arrhythmia coexisting, either coincidentally or in an aetiopathogenetic role, with stroke illness. In such patients therapeutic choices now need to be governed by the recognition that, despite comparable therapeutic benefit, adverse cardiac events such as sinus tachycardia, severe angina, and ventricular ectopy, are more likely to occur after tricyclic drugs such as nortryptiline, than after selective serotonin reuptake inhibitors such as paroxetine (p<0.03).2 Whereas nortryptiline causes a sustained increase in heart rate and a reduction in heart rate variability,2 the second being a marker of increased cardiac mortality risk,3 no such sequelae occur after paroxetine.2
We wholeheartedly agree with Jolobe’s comments on the need to treat depressive illness after stroke with appropriate antidepressant drugs that have a low risk of cardiovascular side effects. Other studies using trazodone1-1 and other selective seratonin reuptake inhibitors such as citalopram1-2 have shown that these are safe and effective in the treatment of this condition. Unfortunately, the problem remains that the vast majority of patients with depressive illness after stroke remain untreated. Despite clear evidence of negative effects on recovery in functional status and cognitive performance1-3 it has been shown that inadequate and insufficient efforts at treatment had not influenced the prevalence of depression up to 5 years after stroke.1-4 The first important step therefore seems to be to encourage clinicians to recognise and treat depression after stroke, the second being to educate them about which are the appropriate medications to prescribe.
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