The use of electroconvulsive therapy (ECT) in patients with underlying cardiac disease like hypertrophic cardiomyopathy (HCM) remains without satisfactory clinical guidelines. We provide a case report of successful application of ECT in a 43-year-old patient with bipolar disorder and comorbid HCM, including detailed diagnostic information and outlining key clinical considerations

Baessler, Andrea

Kufner, Marco

Maier, Lars S.

Nothdurfter, Caroline

Qamar, Yasmin

Steffling, Dagmar

PubMed

The use of electroconvulsive therapy (ECT) in patients with underlying cardiac disease like hypertrophic cardiomyopathy (HCM) remains without satisfactory clinical guidelines. We provide a case report of successful application of ECT in a 43‐year‐old patient with bipolar disorder and comorbid HCM, including detailed diagnostic information and outlining key clinical considerations

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Electroconvulsive therapy in a patient with hypertrophic cardiomyopathy: A case report

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Clin Case Rep. 2022;10:e06286.    | 1 of 6https://doi.org/10.1002/ccr3.6286wileyonlinelibrary.com/journal/ccr31  |  INTRODUCTIONMental disorders often co- occur with cardiologic comor-bidities.1 Thus, it is important for mental health practi-tioners to have access to guidelines for patients underlying cardiologic comorbidities, as those lead to further mor-bidity. For treatment- resistant depressive episodes, elec-troconvulsive therapy (ECT) is among the most effective recommended treatment options. A comorbidity with hy-pertrophic cardiomyopathy (HCM) is considered a high- risk constellation for an ECT treatment and the decision pro or contra ECT remains an individual case decision without clear clinical guidelines. Also, case reports of ECT in HCM are rare2 within the literature on ECT treat-ment of depression or bipolar disorder with cardiologic comorbidities.In current clinical practice, ECT is used for the treat-ment of therapy- resistant depression, depression of psy-chotic subtype as well as in therapy- resistant depressive episodes of bipolar disorder. It is typically applied for 6 to 12 sessions with a frequency of 2 to 3 times per week in presence of a psychiatrist and an anesthesiologist. However, doubts about the evidence for ECT have been raised regarding critical side effects like neurocognitive deficits. This has triggered a critical review of ECT use.3 The cardiovascular side effects of ECT reflect those of a generalized seizure starting with a parasympathetic pre-dominance during the tonic phase and a subsequent sym-pathetic reaction during the clonic phase of the seizure.2 Cardiac arrhythmias are also considerable side effects of seizures: Temporal seizures are prone to show ictal asys-toles which might be caused by a central stimulation of Received: 11 May 2022 | Accepted: 30 July 2022DOI: 10.1002/ccr3.6286  C A S E  R E P O R TElectroconvulsive therapy in a patient with hypertrophic cardiomyopathy: A case reportMarco Kufner1  |   Caroline Nothdurfter1 |   Dagmar Steffling1 |   Andrea Baessler2 |   Lars S. Maier2 |   Yasmin Qamar2This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.© 2022 The Authors. Clinical Case Reports published by John Wiley & Sons Ltd.1Klinik und Poliklinik für Psychiatrie und Psychotherapie der Universität Regensburg am Bezirksklinikum Regensburg, Universitätsstr, Regensburg, Germany2Klinik und Poliklinik für Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, GermanyCorrespondenceMarco Kufner, Klinik und Poliklinik für Psychiatrie und Psychotherapie, der Universität Regensburg am Bezirksklinikum Regensburg, Universitätsstr, 84, Regensburg 93053, Germany.Email: marco.kufner@ukr.deAbstractThe use of electroconvulsive therapy (ECT) in patients with underlying cardiac disease like hypertrophic cardiomyopathy (HCM) remains without satisfactory clinical guidelines. We provide a case report of successful application of ECT in a 43- year- old patient with bipolar disorder and comorbid HCM, including detailed diagnostic information and outlining key clinical considerations.K E Y W O R D Sbipolar disorder, case report, electroconvulsive therapy, hypertrophic cardiomyopathy, major depressive disorder2 of 6 |   KUFNER et al.the autonomic nervous system as well as a vasovagal re-flex.4 In up to 80% of all seizures, sinustachycardia can be observed as the most common cardiac consequence and is evaluated as appropriate vegetative reaction to ECT in-dicating a satisfactory seizure quality. Especially when ob-struction is present, the tachycardic episode following an ECT session bears substantial risk of decreased left ven-tricular output.Hypertrophic cardiomyopathy has first been described in 1869 by Henri Liouville, and later in the 1950s in con-text with sudden cardiac death.5 It is the most common genetic cardiomyopathy and is known to be an important cause of cardiovascular morbidity and mortality across all ages. Its prevalence in the general population has been previously estimated to be about 1:500, and recent investigations showed that globally 20 million people are affected by this autosomal dominantly inherited disor-der. Meanwhile, a variety of mutations associated with modifications of cardiac myocytes have been described. Clinical diagnosis is usually made by echocardiography or cardiac magnetic resonance imaging (MRI), whereas for genetic testing a great diversity of mutations is known. The areas of myocardial fibrosis accompanying the dis-ease can serve as sources for arrhythmia.6 Therefore, a careful cardiologic examination is required for an ECT treatment.2  |  CASE EXAMINATIONThe 43- year- old caucasian male industrial worker with a history of a bipolar II disorder was admitted with a se-vere amotivational/anhedone depressive episode with psychotic symptoms, suicidal tendencies, and mood- congruent delusions of guilt. Up to this time, he had suffered several moderate to severe depressive episodes and a few hypomanic episodes which had been treated mainly ambulatory with a plethora of antidepressant medication including neuroleptics and mood stabiliz-ers. He also received repetitive transcranial magnetic stimulation over several months without any effect. In the current admission, he showed a persistent depressed mood, loss of interest in activities he formerly enjoyed, appetite loss, loss of hope, social withdrawal, and con-centration deficits. The patient reported that 16 years ago during a severe depressive episode, ECT was applied with a positive therapeutic effect lasting several months. Comorbidities were an essential stage 1 hypertension (ESC / ESH guidelines) and chronic kidney disease with a mildly decreased glomerular filtration rate. No fam-ily history of cardiac or psychiatric pathologies were reported by the patient. At the admission time, he had been treated with lamotrigine, a tricyclic antidepressant (imipramine) and lithium, of which the latter was dis-continued due to the renal impairment.3  |  DIFFERENTIAL DIAGNOSIS, INVESTIGATIONS, AND TREATMENTAt the time of hospital admission, the patient showed an athletic constitution without further abnormalities in the physical and neurologic examination. Upon admission, he scored 31 on the Beck depression inventory (BDI) indicating a severe depressive episode. A cranial MRI scan showed no intracranial pathologies. Neuropsychological tests showed cognitive, attentional, and memory functions within a lower normal to mildly impaired range.Shortly before the psychiatry admission, he was diag-nosed with hypertrophic cardiomyopathy, after repolar-ization abnormalities had been recognized in a routine electrocardiogram (ECG— see Figure  1). Subsequently, hypertrophic cardiomyopathy had been diagnosed using echocardiography and MRI, indicating concentric left ven-tricular hypertrophy particularly in the apex and medial third of the left ventricle (see Figures 2 and 3). Myocardial fibrosis has initially been considered by echocardiography but could not be detected by MRI. An obstruction of the LVOT was not evident, and no ventricular arrhythmias had been reported so far. However, on further inquiry, the patient reported two unexplained syncopes.Prior to treatment, coronary artery disease had been excluded by coronary angiography. We calculated an HCM risk- SCD score of 3.5% according to 2014 ESC guidelines, considering age, maximum LV wall thickness (16 mm), left atrial diameter (43 mm), maximum LV outflow gradi-ent (6 mmHg), and unexplained syncopes in the patient history.7 In patients with a 5- year risk of SCD <4%, an ICD is generally not indicated. In our case, we therefore de-cided against the implantation of an ICD for primary pre-vention. Late gadolinium enhancement (LGE) by cardiac MRI is also a known predictor of adverse cardiovascular outcome, such as malignant ventricular arrhythmias and fibrosis itself and should thus be included into the deci-sion pro or contra ICD. Taken into account that such ad-ditional risk factors are not sufficiently displayed within the SCD risk score, it has been shown that the present risk score is lacking sensitivity and leaves certain patient groups unprotected.6In our case, the decision for a medicinal treatment with bisoprolol had been made; further cardiologic drug treat-ment was not necessary. Due to the cardiological risk con-stellation, the psychiatric medication with lamotrigine and    | 3 of 6KUFNER et al.imipramine at admission time was discontinued and ECT treatment was started under a co- medication of sertraline (125 mg/d) and olanzapine (dose increase up to 30 mg/d). Twenty trains of ECT were performed without complications resulting in a substantial but short- lasting improvement in patients' symptomatology (see Figure  4). Right unilateral (d'Elia position) stimuli of 302.4– 352.8 mC strength, pulse width 0.5 ms, and a frequency of 50 Hz were applicated via a Thymatron System IV ECT device. Stimulation strength was determined using an age- adapted formula. General anesthesia during ECT was performed using ketamine and propofol. For muscle relaxation, mivacuronium was used. All sessions were performed under continuous readiness for defibrillation and reanimation.ECG monitoring of an ECT session showed a short sinus arrest followed by a sinustachycardia (see Figure 5). Repolarization after the ECT stimulus application showed no difference to pre- stimulation ECG. Holter ECGs showed F I G U R E  1  Electrocardiography. Negative T- waves and a positive Sokolov– Lyon Score indicate left ventricular hypertrophyF I G U R E  2  Magnetic resonance imaging, SSFP sequences. (A) diastole; (B) systole. RA denotes right atrium, RV right ventricle, LA left atrium, LV left ventricle and VS ventricular septum, indicating a concentric hypertrophic cardiomyopathy mostly stressed in the apex and medial third of the left ventricle4 of 6 |   KUFNER et al.a stable sinus rhythm with only occasional ventricular and supraventricular extrasystoles and irregular repolarization mostly comprehensible in the context of hypertrophy. No ventricular arrhythmias were observed. After the first train of ECT (14 sessions), the patient showed a substantial im-provement in subjective mood and motivation as in clinical appearance with no further delusional symptoms (BDI: 11).4  |  OUTCOME AND FOLLOW- UPAfter a 2- week period, he suffered a relapse of depres-sive symptoms and ECT was continued for another 6 ses-sions. Thereby, a significant improvement was reached where the patient could resume work receiving weekly ambulatory ECT sessions over 1 month. After 1 month of F I G U R E  3  Echocardiography examples. (A) parasternal long axis; (B) parasternal short axis; (C) apical view. Left ventricle (asterisk), ventricular septum (arrow) with left ventricular hypertrophyF I G U R E  4  Clinical time course during ECT. The area resembles the subjective ratings of the patient on a visual analogue scale (VAS) between “very bad” to “very good.” Red triangles indicate the ECT dates. A rise in scores during ECT therapy with an immediate setback after ECT discontinuation (after 2.5 months) is observable. At the end of the observation time (end of blue area), subjective VAS ratings reflected a good clinical state after a second setback at time of hospital discharge (after 3 months).F I G U R E  5  ECG monitoring during ECT. A sinus arrest of 8 s followed by a sinustachycardia of approximately 130 beats per minute is observable   | 5 of 6KUFNER et al.maintenance ECT, the patient ended the treatment re-maining stable under continued medication and outpa-tient psychotherapy.Follow- up cardiac diagnostics showed a stable situa-tion regarding the hypertrophic cardiomyopathy, still at an HCM- SCD- risk- score of 3.5%. No signs of progress of hypertrophy or obstruction could be found. Therefore, no modification of treatment had been made, and a cardio-logic re- evaluation is planned 12 months later.5  |  DISCUSSIONWe report the case of an ECT treatment without severe side effects in a bipolar patient with hypertrophic cardiomyopathy (HCM) and indicators of an intrinsic cardiac risk. Patients with HCM especially in advanced stages are prone to develop malign ventricular arrhythmias in the context of myocytal electric instability.However, a patient should not be deprived of a potent therapy, such as ECT, due to unjustified concerns regard-ing adverse effects. Current findings suggest that risk of sudden cardiac death due to hypertrophic cardiomyopa-thy is low (less than 1% per year), as long as treatment is performed in accordance with current guidelines.6This report adds further support to address the exist-ing uncertainty and controversy of ECT in patients with significant cardiac comorbidities. As the presented case of HCM shows only mild structural cardiac abnormal-ities, we decided to perform ECT considering the for-merly reported successful application in patient history, the patient's request and exhausted psychotherapeutic and pharmacological treatment options as well as the deteriorating clinical situation. The use of ECT had short- lasting positive effects on the psychiatric situation and allowed a transition to an outpatient care, and the patient was able to resume his employment and daily life activities.The sinus arrest observed in the ECG during ECT is also commonly observable in generalized seizures, caused by an initially strong vagal stimulus followed by a sympathetic response. In other disease patterns, asymp-tomatic electrocardiographic pauses over few seconds can be frequently observed; furthermore, intermittent pauses of several seconds described as self- limiting ictal asystoles have been reported in context of seizures.4 As a result, we resolved to continue ECT treatment in the presented case. In obstructive hypertrophic cardiomyop-athy, it is mentionable that the cardiovascular circum-stances of a generalized seizure during ECT including hypertension and therefore increasing intraventricular pressure as well as diminished ventricular output may potentially result in severe acute heart failure. In this context, Robinson et al.8 have shown that even in HCM with a mildly increased resting LVOT gradient no further increase of obstruction had been caused by ECT under pretreatment with beta- blocking medication (labetalol and esmolol). This report now additionally shows that ECT therapy in HCM may be feasible without complica-tions under strict safety conditions: low HCM risk- SCD score with absence of late gadolinium enhancement and LVOT obstruction, lack of arrhythmia in holter ECG as well as bedside defibrillation therapy during the ECT sessions. Considering the latest discussion on ECT safety, experiences as the presented case seem valuable to drive further research.9AUTHOR CONTRIBUTIONSKufner, Marco: Main Investigator psychiatric part— Patient admission and consent, diagnostic and clinical scoring, literature search, and manuscript preparation. Nothdurfter, Caroline: Psychiatric part— Diagnostic supervision and manuscript revision, ECT informed consent and conduction. Steffling, Dagmar: Anesthesiology: Pre- Treatment and narcosis conduction of ECT, intellectual input and revision of safety considerations, manuscript review. Baessler, Andrea: Cardiology part— Diagnostic supervision, therapeutic decision- making, and manuscript revision. Maier, Lars S.: Cardiology part— Diagnostic supervision and manuscript revision. Qamar, Yasmin: Main Investigator cardiology part— Cardiologic evaluation, diagnostics and clinical scoring, and manuscript preparation.ACKNOWLEDGMENTSWe would like to thank Patrycja Ganslmeier for her support in the discussion of cardiologic findings and theoretical input during manuscript creation. Open Access funding enabled and organized by Projekt DEAL. WOA Institution: UNIVERSITAET REGENSBURG Consortia Name : Projekt DEALFUNDING INFORMATIONNone.DATA AVAILABILITY STATEMENTData available on request due to privacy/ethical restrictions.CONSENTThe author has obtained written informed consent from the patient for this publication.ORCIDMarco Kufner   https://orcid.org/0000-0002-2177-3884 6 of 6 |   KUFNER et al.REFERENCES 1. Igoumenou A, Alevizopoulos G, Anastasakis A, Stavrakaki E, Toutouzas P, Stefanadis C. Depression in patients with hyper-trophic cardiomyopathy: is there any relation with the risk fac-tors for sudden death? Heart Asia. 2012;4(1):44- 48. doi:10.1136/heartasia- 2012- 010099 2. Adabag AS, Kim HG, al Aloul B. Arrhythmias associated with electroconvulsive therapy in hypertrophic cardio-myopathy. Pacing Clin Electrophysiol. 2008;31(2):253- 255. doi:10.1111/j.1540- 8159.2007.00979.x 3. Read J, Kirsch I, Mcgrath L. Electroconvulsive therapy for depression: a review of the quality of ECT versus sham ECT trials and meta- analyses. Ethical Hum Psychol Psychiatry. 2019;21(2):64- 103. 4. Van Der Lende M, Surges R, Sander JW, Thijs RD. Cardiac ar-rhythmias during or after epileptic seizures. J Neurol Neurosurg Psychiatry. 2016;87(1):69- 74. doi:10.1136/jnnp- 2015- 310559 5. Braunwald E. Hypertrophic cardiomyopathy: the first century 1869– 1969. Glob Cardiol Sci Pract. 2012;2012(1):5. doi:10.5339/gcsp.2012.5 6. Maron MS, Rowin EJ, Wessler BS, et al. Enhanced American College of Cardiology/American Heart Association strat-egy for prevention of sudden cardiac death in high- risk patients with hypertrophic cardiomyopathy supplemental content. JAMA Cardiol. 2019;4(7):644- 657. doi:10.1001/jamacardio.2019.1391 7. O'Mahony C, Jichi F, Pavlou M, et al. A novel clinical risk pre-diction model for sudden cardiac death in hypertrophic cardio-myopathy (HCM risk- SCD). Eur Heart J. 2014;35(30):2010- 2020. doi:10.1093/eurheartj/eht439 8. Robinson AR, Holbert R, Modell JH, Gravenstein N. Continuous transthoracic echocardiography in a 93- year- old patient with hy-pertrophic cardiomyopathy during electroconvulsive therapy. J ECT. 2011;27(3):224- 226. doi:10.1097/YCT.0b013e318223821b 9. Cristancho MA, Satterthwaite TD, O'Reardon JP. Cardiac com-plications of ECT: myocardial stunning syndrome and takot-subo cardiomyopathy after ECT different names for the same phenomenon. J ECT. 2010;26(2):146- 147.How to cite this article: Kufner M, Nothdurfter C, Steffling D, Baessler A, Maier LS, Qamar Y. Electroconvulsive therapy in a patient with hypertrophic cardiomyopathy: A case report. Clin Case Rep. 2022;10:e06286. doi: 10.1002/ccr3.6286

Electroconvulsive therapy in a patient with hypertrophic cardiomyopathy: A case report

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