A single low dose of escitalopram may trigger life-threatening severe bradycardia in patients with acute stroke, particularly those with insular cortex involvement.
May warrant heart-rate monitoring after low-dose escitalopram in acute stroke; hypothesis-generating case report requiring prospective confirmation.
ing any medication. ECG at admission was normal, i.e. it did not demonstrate QT prolongation ( fig. 1 a). MRI confirmed an acute ischemic infarction of the right temporo-insular cortex. Doppler ultrasonography and cerebral angiography revealed a 90% stenosis of the left internal carotid artery and complete occlusion of the right internal carotid artery. The patient was known for depression that had significantly worsened after her stroke. Therefore anti-depressive treatment with escitalopram 5 mg was started on the third day post-stroke. Forty-five minutes after the first administration of escitalopram, a severe bradycardia (20–30 beats/min) with loss of consciousness and respiratory failure occurred ( fig. 1 b). Because of continuous monitoring in the stroke unit, the patient could be successfully reanimated in time. As a consequence of severe bradycardia the pre-existing cerebral hypoperfusion was enhanced, thereby increasing the deficit of cerebral perfusion in the area of brain infarction (controlled by follow-up MRI scans). Retrospectively, the patient remembered an episode of ‘dizziness and fainting’ in association with a single citalopram dose of 20 mg some years ago. The exact cause of the life-threatening bradycardia in our patient remains obscure. It has been reported that involvement of the insular cortex in stroke may induce ECG abnormalities, increasing the risk for cardiac arrhythmia and death [8] . Not only lesions within the left insular reDear Sir, Selective serotonin reuptake inhibitors as treatment for post-stroke depression are considered the state of the art, even though there are no recommendations on the right time to start the therapy or which substance to choose [1] . Escitalopram, the Senantiomer of citalopram, is considered to be more effective in the treatment of depression than its racemic parent. Improvement of symptoms seems to start earlier than with citalopram [2] . Its tolerability profile is described as predictable, mild and transient. Main side effects are nausea, diarrhea, ejaculatory problems and insomnia [3] . Citalopram-associated bradycardia has been reported in overdose or long-term administration of therapeutic doses, especially in older patients [4–7] . To the best of our knowledge, severe bradycardia caused by a single small dose (5 mg) of escitalopram has not been described before.
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Beyenburg et al. (2006) studied this question.
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