Cardiac syncope due to pain
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an1 · S.A. Kocaman2, 3 · M.E. Durakoğlugil3 · E. Kaya4 · M.G. Şenol5 1 Department of Neurology, Bursa Military Hospital, Bursa 2 Department of Cardiology, Bursa Military Hospital, Bursa 3 Medical Faculty, Department of Cardiology, Rize University, Rize Education and Research Hospital, Rize 4 Department of Physical Medicine and Rehabilitation, Bursa Military Hospital, Bursa 5 Department of Neurology, GATA Haydarpaşa Education and Research Hospital, Istanbul
Cardiac syncope due to pain Report of a case responsive to duloxetine treatment
Neurocardiogenic syncope comprises situations triggered by neurological reflexes resulting in abnormal responses of the neurocardiovascular system that cause loss of consciousness. A vast number of clinical conditions may cause this disorder including pain, defecation, micturition, swallowing, cough, sudden fear or excitement, exercise, and long-time standing [1]. The pathophysiology of neurally mediated syncope is still not clarified. A series of reflex reactions that paradoxically result in decreased sympathetic activity, bradycardia, and hypotension remains the most accepted mechanism. Nevertheless, how these reflex mechanisms are triggered in certain conditions like pain is still not known [2]. Treatment options for syncope prevention are mostly not satisfactory. Several agents including β-blockers, disopyramide, ephedrine, etilefrine, clonidine, and serotonin re-uptake inhibitors were implicated for pharmacological treatment; however, without success [1]. Selective inhibitors of neuronal norepinephrine transporter (NET) like duloxetine may have a role in neurally mediated syncope by increasing synaptic norepinephrine levels. Therefore, we report the effect of duloxetine in a patient with pain induced syncope resistant to standard regimens.
Case report A 34-year-old female patient was admitted to our cardiology clinic complaining of syncope triggered by trauma-induced pain. A previous diagnosis of cardioinhibitory syncope by tilt-table testing had been made in another facility 2 years previously. The patient had 15 syncope episodes during a 2-year follow-up, initially under β-blocker treatment and then with sertraline therapy. Afterwards, duloxetine 30 mg/day was initiated and was increased to 60 mg/day after 1 month. A pain of 4–5 degrees according to the visual analogue scale (VAS) triggered syncope under treatment with β-blocker or sertraline, whereas a sharp pain with a scale of 9, due to a twisted ankle, during duloxetine treatment did not. The patient remained asymptomatic under duloxetine treatment during a 1-year follow-up period.
Discussion The pathophysiology of neurocardiogenic syncope is still not understood. Nonpharmacological interventions are the frontline of treatment that includes avoiding triggering factors, recognizing prodromal symptoms, and implementing physical counter-pressure maneuvers. Triggering causes should be controlled if possible, for example, curing a cough if it is the ini-
tiator or relieving pain if pain is the trigger, as in our case. Recentl
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