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      ECG changes after electroconvulsive therapy, cause or consequence?

      case-report
      1 , 2 ,
      Netherlands Heart Journal
      Bohn Stafleu van Loghum

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          Abstract

          Electroconvulsive therapy (ECT) is a commonly used treatment in psychiatric disease for severe depression. It is considered to be a relatively safe procedure, although several case reports have described cardiac complications. Significant ECG changes may occur after this treatment [1–3] and echocardiographic abnormalities have been described [4–6]. Noninvasive evaluation of several cases after ECT failed to demonstrate underlying cardiac abnormalities [1, 7]. Despite the lack of invasive studies, a generally accepted viewpoint is that ECG changes after ECT are the result of increased sympathetic activity due to massive release from the hypothalamus [2]. However, in the following two cases, we demonstrate by using invasive evaluation that the relation between ECT and subsequent ECG changes may not always be explained by this theory. Patient 1 A 67-year-old male was admitted to our cardiology department after ECT because of low oxygen saturation and persistent ECG abnormalities (Fig. 1). His medical history comprised hypertension, dilated abdominal aorta, diabetes and severe mental depression. MRI of his brain showed an old cerebral infarction. His ECG 6 months before ECT showed sinus rhythm with small biphasic T waves in leads V5-6. Fig. 1 ECG of patient 1 showing new negative T waves after ECT After ECT he did not express any symptoms. Physical examination revealed no abnormalities. Blood pressure was 140/80 mmHg. His ECG showed a normal sinus rhythm of 67 beats/min with a left axis deviation. Negative T waves were seen in leads V1-5, which were new compared with previous ECGs. Laboratory investments showed maximal troponin-T level of 0.06 μg/l (normal value <0.05 μg/l). All other parameters were normal except an increased d-dimer. Echocardiography showed a normal left ventricular function with mild concentric hypertrophy. Because of the combination of ECG changes, increased troponin level and low oxygen saturation at admission, coronary angiography was performed. In the proximal left anterior descending artery a significant stenosis was demonstrated at the division of the first diagonal branch. The other coronary arteries did not show stenoses. A few days later, the patient underwent elective PCI with stenting of the stenotic artery. The negative T waves on the ECG resolved. Afterwards he remained clinically stable. Patient 2 A 78-year-old female patient, temporarily admitted to the recovery department after ECT, developed atrial fibrillation and chest pain. Her medical history showed hypertension, severe depression and paroxysmal atrial fibrillation. Her ECG 3 months before ECT was completely normal. Immediately after ECT her blood pressure was 230/140 mmHg, but later decreased to 110/45 mmHg. Examination of heart and lungs revealed no abnormalities. The ECG showed atrial fibrillation with a ventricular rate of 140 beats/min and new negative T waves in leads I, II, aVL and V2-6. The second ECG showed sinus rhythm and persisting negative T-waves (Fig. 2). Troponin T level was 0.02 μg/l (normal) and no other laboratory abnormalities were found. A differential diagnosis was made and the following possible causes were taken into account: post ECT, post tachycardia due to atrial fibrillation, severe hypertension or myocardial ischaemia. Since the patient reported to have had previous anginal complaints, coronary angiography was performed. In the left anterior descending artery two significant stenoses were identified in the proximal and the mid section, respectively. Furthermore, a stenosis was found in the right coronary artery. Due to her psychiatric condition, PCI was not performed and she was treated with anti-anginal medication and warfarin. Fig. 2 Second ECG of patient 2, 8 h after ECT, showing persistent negative T waves Discussion External control of the heart by cerebral and neurohormonal factors is well established [8, 9]. Although ECT is a generally accepted, widely performed and safe therapy, cardiac complications may occur. The most frequently observed are arrhythmias and T-wave inversion on the surface ECG, but also transient wall motion abnormalities have been reported [4–6]. Transient cardiac abnormalities have been explained by the concept of adrenergic excess [10]. In this concept, however, coronary artery disease was not considered to play an important role, because intense sympathetic activity was thought to be the exclusive explanation. One case report supported this concept by showing development of acute myocardial infarction during a course of ECT without underlying coronary artery disease [11]. In the present report, we describe two patients with an initially recognised ‘classic’ pattern of newly developed ECG abnormalities after ECT. However, after invasive evaluation, both patients were shown to have severe coronary artery disease. To our knowledge, this is the first study reporting two consecutive patients who were invasively evaluated after ECT, demonstrating that coronary artery disease may be the primary cause of ECG abnormalities. This finding is important because ECG abnormalities due to coronary artery stenosis have significant prognostic impact. As a consequence, we think that T-wave abnormalities after ECT cannot be used to differentiate between ECT-induced ECG changes and actual myocardial ischaemia. Useful clues to differentiate may be increased troponin levels and previous anginal complaints. Finally we suggest that shortly before ECT, a 12-lead ECG should be performed.

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          Most cited references10

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          Electrocardiographic changes simulating myocardial ischemia and infarction associated with spontaneous intracranial hemorrhage.

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            Evaluation of importance of central effects of atenolol and metoprolol measured by heart rate variability during mental performance tasks, physical exercise, and daily life in stable postinfarct patients.

            Physical exercise and mental work cause alterations in cardiac autonomic control. beta-Blockers protect the heart against stress, and this effect may be in part centrally mediated. In this context, the lipophilicity of the drug would be clinically relevant. Thirty postinfarct patients were randomized to receive 100 mg atenolol or 200 mg metoprolol CR in a double-blind, crossover manner, each for a 6-week period. Heart rate (HR) variability was used to study autonomic effects during mental and physical stress and to study circadian variations. Mean 24-hour HR decreased from 77 +/- 7 to 60 +/- 6 beats per minute after atenolol and to 62 +/- 6 beats per minute after metoprolol (P = .046). At baseline, mental performance tasks did not affect HR, but decreased HR variability (SDNN index from 51 +/- 26 to 30 +/- 13 milliseconds [ms], P < .001; high-frequency power from 130 +/- 143 to 110 +/- 125 ms2, P = .046; and low-frequency power from 538 +/- 447 to 290 +/- 275 ms2, P < .001). Both beta-blockers decreased HR during mental performance tasks (P < .001) and increased SDNN index and high-frequency power. Before treatment, bicycle exercise decreased HR variability; root-mean-square of successive difference decreased from 21 +/- 8 to 15 +/- 10 ms (P = .004). beta-Blockade could not prevent this decrease. No differences between atenolol and metoprolol were observed for absolute high- and low-frequency power or after adjustment for HR. Vagal blockade with methylatropine during chronic beta-blocker treatment nearly abolished all components of spectral power. HR was found to be the parameter most strongly affected by beta-blockade but not by an influence on vagal tone. No differences were found between atenolol and metoprolol. In stable postinfarct patients, chronic treatment with metoprolol and atenolol attenuates the reduction in HR variability induced by mental performance tasks, but the effects during exercise are limited. beta-Blockers do not appear to increase vagal tone in this stable patient group. The point of action in these patients is mainly a reduction in HR, probably due to a reduction in stress-induced sympathetic activation. Clinically significant differences between atenolol and metoprolol were absent, indicating that the degree of lipophilicity does not distinguish among the beta-blockers what their salutary effects are on HR variability during the specific challenges used.
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              Acute coronary syndrome (Takotsubo cardiomyopathy) following electroconvulsive therapy in the absence of significant coronary artery disease: case report and review of the literature.

              We report a case of myocardial infarction occurring in a 45-year-old woman in the absence of coronary artery disease during a course of electroconvulsive therapy (ECT) for major depression. After the third ECT session, the patient reported substernal chest pain, and although the electrocardiogram was normal, cardiac enzymes were found to be elevated. Cardiac workup to determine etiology during hospital stay showed no evidence of coronary artery disease on catheterization. Cardiac echocardiograph and computed tomography findings were consistent with a diagnosis of Takotsubo cardiomyopathy. This cardiac syndrome is a stress-induced syndrome occurring in the absence of coronary artery stenosis and associated with surging of catecholamines. It is diagnosed on the basis of the shape of the apical ballooning observed on cardiac imaging, which resembles a "takotsubo" or octopus fishing pot in Japan, where this syndrome was first recognized. Coincidentally, after termination of her ECT course, this patient was also diagnosed with Loeys-Dietz syndrome, an inherited connective tissue disorder that can predispose sufferers to aortic dissection. This case illustrates the importance of careful workup of chest pain in the setting of ECT, even if electrocardiogram findings seem unremarkable initially.
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                Author and article information

                Contributors
                +31-570-535353 , y.s.tuininga@dz.nl
                Journal
                Neth Heart J
                Netherlands Heart Journal
                Bohn Stafleu van Loghum (Heidelberg )
                1568-5888
                1876-6250
                10 June 2011
                10 June 2011
                March 2012
                : 20
                : 3
                : 129-131
                Affiliations
                [1 ]Department of Cardiology, Deventer Hospital, Nico Bolkesteinlaan 75, 7416 SE Deventer, the Netherlands
                [2 ]PO Box 5001, 7400 GC Deventer, the Netherlands
                Article
                167
                10.1007/s12471-011-0167-4
                3286501
                21660671
                40d6ef09-6d1f-4008-a421-6bf417dba117
                © The Author(s) 2011
                History
                Categories
                Case Report
                Custom metadata
                © Springer Media / Bohn Stafleu van Loghum 2012

                Cardiovascular Medicine
                Cardiovascular Medicine

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