Psychosomatics 49:341-344, July-August
doi: 10.1176/appi.psy.49.4.341
© 2008 Academy of Psychosomatic Medicine
Electroconvulsive Therapy in a Candidate for Heart Transplant With an Implantable Cardiovertor Defibrillator and Cardiac Contractility Modulator
Alison M. Lynch, M.B., B.Ch,
Ananda K. Pandurangi, M.D., and
James L. Levenson, M.D.
Received January 4, 2007; revised June 5, 2007; accepted June 18, 2007. From the Department of Psychiatry, Virginia Commonwealth University, Medical College of Virginia. Send correspondence and reprint requests to Dr. A.M. Lynch, Dept. of Psychiatry, VCU/MCV Campus, P.O. Box 980701, Richmond, VA 23298–0710. e-mail: alynch2{at}mcvh-vcu.edu
© 2008 The Academy of Psychosomatic Medicine
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ABSTRACT
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BACKGROUND: Electroconvulsive therapy (ECT) can be life-saving in treating depression, even for high-risk cardiac patients. A 56-year-old man with type 2 diabetes and dilated cardiomyopathy, using both a defibrillator and an experimental cardiac contractility modulator, had had episodes of severe depression superimposed on dysthymia for 27 years, with a current exacerbation over the past 2 years, and little response to antidepressant treatment. METHOD: He received a course of 12 ECTs (6 right-unilateral and 6 left-anterior/right-temporal electrode placements). RESULTS: After these, he was judged moderately but not dramatically improved. DISCUSSION: Serious adverse events, such as myocardial infarction, lethal arrhythmias, and cardiac rupture are possible in these high-risk patients, especially those with ejection fractions <50%, previous myocardial infarction, or significant arrhythmias. This case illustrates the complex decision-making involved and the need for close interdisciplinary collaboration entailed in preparing a high-risk patient with an implanted device for ECT.
Key Words: ECT • Heart Transplant • Arrhythmia
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INTRODUCTION
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Depression associated with cardiovascular disease can increase morbidity and mortality.1 Electroconvulsive therapy (ECT) can be life-saving, even in high-risk cardiac patients. Major adverse events during the ECT-induced hyperdynamic state are rare.2 ECT has been administered to patients with cardiac pacemakers, implantable cardioverter defibrillators,3 and those with congestive cardiac failure.4 To the best of our knowledge, this is the first report of the use of ECT in a depression patient with chronic heart failure who had both a defibrillator and an experimental cardiac contractility modulator (an experimental device that delivers electric currents during the cardiac cycle refractory period).5
Case Report
"Mr. C," a 56-year-old severely depressed white man with dilated cardiomyopathy, stable hypertension, and type 2 diabetes mellitus was referred for ECT. He had had six episodes of major depression superimposed on almost continuous dysthymia and feelings of inadequacy for 27 years. The current episode of 2 years was triggered by his developing heart failure. His symptoms included passive suicidal thoughts, psychomotor retardation, significant anxiety, low energy, lack of interest, social isolation, low self-esteem, guilt, difficulty remembering, poor appetite, and a 50-pound weight loss (from 275 to 225 pounds). He was barely able to perform on his job and had not cleaned his home in 2 years. He had a poor response to adequate trials with multiple combinations of medications: tricyclics (nortriptyline, desipramine), at least four SSRIs (paroxetine, sertraline, citalopram, escitalopram), two SNRIs (venlafaxine, duloxetine), bupropion, a stimulant (methylphenidate), a mood stabilizer (lithium), anxiolytics (alprazolam, clonazepam), and an atypical antipsychotic (risperidone). He had been in insight-oriented psychotherapy for 4 years in the 1980s and, more recently, in cognitive-behavioral therapy, with limited benefit.
The sudden onset of acute heart failure was precipitated by the administration of routine preoperative intravenous fluids. He was diagnosed with idiopathic dilated cardiomyopathy and refractory congestive heart failure (CHF) and was considered for a heart transplant. An implantable cardioverter defibrillator (ICD) had been placed, and an experimental cardiac contractility modulator (CCM) inserted 6 months before the ECT.
ECT was recommended for his unrelenting depression, even though we recognized that some of his anergy and cognitive slowing could be related to cardiac failure. There was concern that ECT 3 times per week might further compromise his cardiac functioning and adversely affect the CCM. In view of these risks, it was decided that he be admitted as a 23-hour observation patient. Pre-ECT physical examination; laboratory tests, including CBC and comprehensive metabolic panel; and ECG were normal, except for a fasting glucose of 187 mg/dL, and the ECG was consistent with cardiomyopathy. His 2-D echocardiogram ejection fraction was 10%–15%.
Planning for ECT was made in conjunction with the cardiology and anesthesiology teams. His cardiologist assessed his risk for ECT-related cardiac complications to be low in the absence of coronary artery disease as long as no intravenous fluids were given. The preoperative anesthesiology consultation initially rated him as a moderate risk at an ASA (American Society of Anesthesiologists) level of 3. This was changed to ASA 4 at the second ECT. The consultants felt that the ECT could be safely performed in the ECT suite with routine monitoring by the anesthesia team.
Three expert technicians were present for the first ECT: an EP (electrophysiology) technician from Cardiology, a technician for the ICD, and a technician for the CCM, from their respective manufacturers. The CCM was programmed "Off" for the duration of the ECT series. To ensure that neither the ECT stimulus nor the skeletal muscle potentials during the seizure would trigger the ICD to fire erroneously, a Medtronic Smart Magnet was placed over the ICD during each procedure. This causes temporary suspension of ventricular arrhythmia detection. If an arrhythmia were to develop, the magnet was to be removed to allow the ICD to detect and treat it. The ICD was interrogated after the first and last ECT.
Mr. C had a course of 12 ECTs (six right-unilateral treatments and six left-anterior/right-temporal electrode placements), using a Thymatron DGx device (Somatics, Inc., Lake Bluff, IL). The electrode placement was changed after six treatments to improve efficacy. No anticholinergic premedication was given, but he took his routine cardiac medications several hours before each ECT. Noninvasive peripheral monitors were placed to monitor blood pressure, heart rate, oxygen level, and ECG. A magnet was taped over the ICD before electrical stimulation and removed as soon as the seizure stopped. He was thoroughly pre-oxygenated before induction of anesthesia using methohexital 100 mg–150 mg and succinylcholine 100 mg–120 mg intravenously. A nerve stimulator was used to determine the optimal time to stimulate because of his low ejection fraction and slow circulation time. The stimulus dose titration method was used to determine the seizure threshold at the first treatment. The initial charge of 15% (75.6 millicoulombs [mC]) produced a poor-quality EEG seizure lasting 40 seconds. The charge was increased as necessary during the remaining treatments on the basis of the seizure response. By the 12th ECT, the charge was 100% (502 mC), producing an EEG seizure of 39 seconds, good postictal suppression of >94%, and a "Seizure Energy Index" of 820.
After the end of each seizure, Mr. C developed extreme hypertension, with blood pressures recorded as high as 213/165. This was managed by initially administering esmolol prestimulation and labetolol as needed postseizure. Upon the advice of the cardiologist, during the last four treatments, beta-blockers were avoided, and Mr. C was treated with the vasodilators nitroglycerin and hydralazine. The hyperdynamic cardiovascular changes were associated with profuse sweating, but he had no pathological ECG changes, and the hypertension responded to treatment within a few minutes. He did not develop symptoms of acute heart failure or myocardial ischemia. He had partial airway obstruction with snoring while waking up, suggestive of obstructive sleep apnea, and he was referred for a sleep study. See Table 1 for details of each treatment and management.
Medications were continued throughout the course of ECT, including duloxetine 120 mg/day, lithium carbonate 900 mg/day, and clonazepam 1 mg/day; enalapril 30 mg/day, digoxin 0.25 mg/day, bumetanide 2 mg/day, esomeprazole 15 mg/day, simvastatin 40 mg/day, repaglinide 3 mg/day, tamsulosin 0.4 mg/day, aspirin 325 mg /day, multivitamins, vitamin C, and folate.
Mr. C’s depression responded minimally and variably to the first six treatments. More significant improvement was noted after 10 treatments. He had mild memory deficits by the last ECT, but planned to go to work the next day. After 12 treatments, he was judged moderately but not dramatically improved. Whereas energy and affect were visibly improved, and he returned to work, he continued to have low self-esteem and much self-doubt.
Discussion
This case illustrates the complex decision-making involved and the need for close interdisciplinary collaboration entailed in preparing a high-risk patient with an implanted experimental device for ECT. Everyone agreed that the presence of the electrophysiologists was essential at the first treatment. Since the CCM was part of an experimental protocol, it was deactivated to protect the device from unknown harm and the research from a protocol violation. The lack of ECT-related complications such as worsening of congestive heart failure or cerebrovascular events in this patient, in spite of the extreme increases in blood pressure, was reassuring. The fact that he had no coronary-artery disease reduced the risk. His ICD had never fired in the past, so it is not surprising that he had no malignant arrhythmias during ECT while it was deactivated by the magnet.
The modest improvement in Mr. C’s depressive symptoms was disappointing. However, it is not always possible to attribute symptoms such as fatigue and discouragement purely to depression in the presence of chronically low cardiac output.
ECT can be a life-saving treatment for refractory depression. The risk is higher in patients with significant coronary-artery disease. Myocardial workload can increase sevenfold and cardiac output by more than 80%. Transient, nonspecific, and/or serious ECG changes and transient left-ventricular systolic dysfunction can occur.2,6,7 Serious adverse events, such as myocardial infarction, lethal arrhythmias, and cardiac rupture have been reported.8,9 These are more likely to occur in patients with ejection fractions <50%, previous myocardial infarction, or significant arrhythmias.10 Careful interdisciplinary pre-ECT assessment and proper risk-reduction strategies are essential in order to minimize complications.2
ECT has been performed with mixed results in patients with CHF. There are reports of ECT being used in over 20 CHF patients with ejection fractions varying from 20% to 47%. Two deaths occurred, one from myocardial infarction and one from progressive heart failure. Three others had major complications, including one nonfatal myocardial infarct, prolonged ischemic changes, or dysrhythmias that resolved.4,8,10,11
ECT has been used in patients with cardiac pacemakers for over 35 years.3 Since the introduction of ICDs in 1980 for patients at high risk for sudden death by ventricular arrhythmias, few patients with these devices have received ECT.3,11–13 In the seven patients with ICDs reported in the literature, the only death was due to progressive heart failure and unrelated to the ICD.3 When patients with pacemakers or ICDs are given ECT, cardiac monitoring and grounding of the equipment is essential. Older pacemakers should be converted from a demand mode to fixed mode, and transesophageal pacing is advised if there is a risk of asystole.14 It has also been recommended for patients with ICDs that a ring magnet be available to inactivate the unit. Gloves should be worn by doctors and nurses being exposed to them, in order to limit the risk of electric shock. If external defibrillation is needed, the external paddles should be oriented perpendicularly to the line joining the two implanted electrodes.15
Consultation with a cardiac electrophysiologist is needed in each individual case to identify the type of device and obtain recommendations regarding whether or not to deactivate it during ECT. The presence of a pacemaker or ICD should not be a contraindication to receiving ECT.13
In summary, this is the first reported case of a full course of ECT provided to a man with low-ejection cardiomyopathy and two implanted cardiac devices, a defibrillator and a cardiac contractility modulator. Despite extreme hypertensive and tachycardic responses immediately after ECT, there were no untoward complications. Although this patient derived only modest benefit from ECT, Mr. C’s case illustrates that ECT can be performed safely in patients with severe cardiac disease and implanted cardiac devices as long as appropriate precautions are taken and careful monitoring with expert management of hemodynamic changes is provided.16,17
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REFERENCES
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- Carney RM, Freedland KE, Veith RC: Depression, the autonomic nervous system, and coronary heart disease. Psychosom Med 2005; 67(suppl 1):S29-33
- Rasmussen KG, Rummans TA, Tsang SM, et al: Electroconvulsive therapy, in Textbook of Psychosomatic Medicine. Edited by Levenson JL. Washington DC; American Psychiatric Publishing, Inc., 2005, pp 957-977
- Dolenc TJ, Barnes RD, Hayes DL, et al: Electroconvulsive therapy in patients with cardiac pacemakers and implantable cardioverter defibrillators. Pacing Clin Electrophysiol 2004; 27:1257–1263[CrossRef][Medline]
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- Gerring JP, Shields HM: The identification and management of patients with a high risk for cardiac arrhythmias during modified ECT. J Clin Psychiatry 1982; 43:140–143[Medline]
- Ali PB, Tidmarsh MD: Cardiac rupture during electroconvulsive therapy. Anaesthesia 1997; 52:884–886[CrossRef][Medline]
- Zielinski RJ, Roose SP, Devanand DP, et al: Cardiovascular complications of ECT in depressed patients with cardiac disease. Am J Psychiatry 1993; 150:904–909[Abstract/Free Full Text]
- Goldberg RJ, Badger JM: Major depressive disorder in patients with the implantable cardioverter defibrillator: two cases treated with ECT. Psychosomatics 1993; 34:273–277[Free Full Text]
- Pornnoppadol C, Isenberg K: ECT with implantable cardioverter defibrillator. J ECT 1998; 14:124–126[Medline]
- Lapid MI, Rummans TA, Hofmann VE, et al: ECT and automatic internal cardioverter-defibrillator. J ECT 2001; 17:146–148[CrossRef][Medline]
- Rasmussen KG, Rummans TA, Richardson JW: Electroconvulsive therapy in the medically ill. Psychiatr Clin North Am 2002; 25:177–193[CrossRef][Medline]
- Stojeba N, Steib A, Fournier S, et al: [Anesthesia and implantable automatic defibrillator]. Ann Fr Anesth Reanim 1996; 15:295–303[Medline]
- American Psychiatric Association, Committee on Electroconvulsive Therapy: The Practice of Electroconvulsive Therapy. Washington, DC, American Psychiatric Association, 2001
- Saito S: Anesthesia management for electroconvulsive therapy: hemodynamic and respiratory management. J Anesth 2005; 19:142–149[CrossRef][Medline]
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ABSTRACT
INTRODUCTION
