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A 74-year-old caucasian woman, with no history of ischemic heart disease, was admitted to our old-age psychiatric unit with severe depression.She had a diagnosis of recurrent major depressive disorder and had deteriorated despite high-dose antidepressant medications (venlafaxine and mirtazapine) in combination with lithium and aripiprazole, an antipsychotic medication.Five years prior to this presentation, she had required 3 months of hospitalization and eight sessions of ect for a severe depressive episode.No complications resulted from this course of ect.Her comorbid physical health conditions were chronic obstructive pulmonary disease and hypertension.For the latter, she was taking the oral adrenergic receptor blocking agent, bisoprolol, 2.5mg once daily and lisinopril, an oral ace inhibitor, 20mg once daily.She had stopped smoking 3 years previously and denied use of alcohol or illicit drugs.She had a strong family history of depression but otherwise had no significant family history.As recommended by the national institute for health and care excellence guidelines for refractory depression, the patient was consented for a further course of ect.2 her pre-ect physical health examination, bloods and ecg were unremarkable, with the latter showing sinus rhythm in the absence of ischemic changes.The patient remained on her oral bisoprolol prior to ect and did not receive additional intravenous blockers.A standard general an aesthetic protocol was employed, during which she was premedicated with propofol and succinyl choline, before receiving unilateral ect.Shortly after the first session of ect, while in the recovery suite, the patient developed acute epigastric discomfort, without radiation and dyspnea.A repeat physical examination was unchanged and her vital signs were as follows: blood pressure 120/70 mm hg; pulse rate 84/min; temperature 35.6°c; oxygen saturations 98% (breathing room air); respiratory rate 18/min.A repeat ecg showed new-onset st-segment depression and t-wave inversion in leads v5 and v6.A troponin-i level, taken 12h after the onset of symptoms, was elevated at 2847ng/l (normal range <40ng/l).Echocardiography demonstrated mild, mixed systolic and diastolic dysfunction of the left ventricle, with an ejection fraction of 52% (normal range 55¿70%).Right ventricular function was preserved and no valvular abnormalities were seen.A coronary angiogram was performed to further investigate a presumed acute coronary syndrome.This revealed no stenoses or occlusions of the coronary arteries.An angiogram of the left ventricle did, however, show mid-segment and apical hypokinesia in addition to apical ballooning, with preserved function in the basal segment.In a patient with acute-onset chest or epigastric pain, ecg changes and a troponin rise, an acute coronary syndrome should be strongly suspected.Atherosclerotic coronary artery disease is the most frequent underlying cause of an acute coronary syndrome, with other less common causes including coronary vasospasm, coronary emboli and vasculitis of the coronary arteries.Other differential diagnoses to consider include aortic dissection, acute pericarditis, myocarditis and pulmonary embolism.The combined clinical, biochemical and radiological findings in this case, however, favoured a diagnosis of takotsubo cardiomyopathy.While awaiting her angiogram, the patient was started on aspirin and clopidogrel for a presumed acute coronary syndrome and transferred to a cardiology ward for close monitoring.A repeat left ventricular angiogram, performed after discharge, demonstrated resolution of the apical dilation and hypokinesia.For additional information, please see (b)(6) md, (b)(6) cardiomyopathy following electroconvulsive therapy: an increasingly recognized phenomenon.Case reports 2014;2014: (b)(4).This article does not detail which device was used, nor does it detail pulse-width, hertz, mc, electrode placement, or which of the seven possible dosing methods used, or which of the 500+ possible doses the device can be configured to generate.(see thymatron system iv user manual, 2009 or mecta user manual.) the fda has not provided dosing consensus standards or any information which can be used to prevent permanent cardiac damage in the form of hypokinesia or death from happening in other ect patients."an alternative adequate and evidence-based dosing-strategy would be welcomed by the field." -pascal sienaert, anzjp correspondence 2018, 8;52:710¿1.The case report is submitted to the fda by a mandated reporter determined to prevent cardiomyopathy in other ect recipients.Not reporting and tracking serious adverse events makes it impossible to accurately track occurrence rates and provide patients, family members and the court with accurate information regarding ect risks to make legally informed treatment choices.
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