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Takotsubo Cardiomyopathy After Electroconvulsive Therapy
Case Reports Takotsubo Cardiomyopathy After Electroconvulsive Therapy Scott R. Beach, M.D. Christina L. Wichman, D.O. R. J. Canterbury, M.D.
Background: Takotsubo cardiomyopathy is a novel acute cardiac syndrome characterized by transient regional systolic dysfunction of the left-ventricular apex and mid-ventricle, with hyperkinesis of the basal left ventricular segments, which has been associated with severe emotional or physical stress. Method: This is the second published case report of takotsubo cardiomyopathy occurring in the setting of electroconvulsive therapy (ECT). Results: The patient, a 52-year-old woman, experienced chest pain and discomfort shortly after ECT treatment. She was shown to have moderate left-ventricular dysfunction, with mid-cavity left-ventricular hypo- to akinesis, and hyperkinesis in the basilar region, consistent with a diagnosis of takotsubo cardiomyopathy. There was full resolution of her symptoms within 48 hours of the initial event. Discussion: This report highlights a previously undocumented complication of ECT and adds to the growing list of stressors responsible for cases of takotsubo cardiomyopathy. The prognosis is favorable, and recovery is generally complete, especially with early recognition of the syndrome and proper supportive treatment. (Psychosomatics 2010; 51:432– 436)
T
akotsubo cardiomyopathy, alternatively known as transient left-ventricular apical ballooning syndrome, broken heart syndrome, or ampulla cardiomyopathy, is a novel acute cardiac syndrome first described in the Japanese population in 1990.1 The syndrome takes its name from the shape of the patient’s heart as seen on left ventriculography, which is said to resemble the pot with a narrow neck and round bottom used by Japanese fisherman to catch octopus (tako-tsubo). The phenomenon is characterized by transient regional systolic dysfunction of the left-ventricular apex and mid-ventricle, with concomitant hyperkinesis of the basal left-ventricular segments.
Received January 23, 2009; revised April 3, 2009; accepted April 7, 2009. From the Dept. of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, VA, and the Dept. of Psychiatry and Psychology, Mayo Clinic, Rochester, MN. Send correspondence and reprint requests to Scott R. Beach, M.D., Massachusetts General Hospital, 55 Fruit St., Warren 605, Boston, MA 02114. e-mail: [email protected] © 2010 The Academy of Psychosomatic Medicine
432
http://psy.psychiatryonline.org
The incidence of Takotsubo cardiomyopathy is relatively low and has been estimated in various case series to account for 1%–2% of all patients hospitalized for apparent acute coronary syndrome.2 Takotsubo cardiomyopathy appears predominantly to affect postmenopausal women; the mean age of patients presenting is 62 to 75 years.3 Factors proposed to account for the striking demographic predisposition include influences of female hormones on sympathetic neuromodulation and coronary vasoreactivity, as well as postmenopausal alteration of endothelial function.2 The vast majority of patients also appear to have experienced a recent significant psychological or physiological stressor, such as the death of a loved one, surgery, grand mal seizure, blunt trauma, cocaine use, or opiate withdrawal.4 –6 For many years before the advent of selective serotonin-reuptake inhibitor (SSRI) antidepressants, electroconvulsive therapy (ECT) was cited as the antidepressant treatment of choice for patients with a history of cardiac Psychosomatics 51:5, September-October 2010
Beach et al. problems because older medications had well-described cardiotoxic effects. Nonetheless, ECT has been associated with cardiac complications, including arrhythmias, ischemic events, and myocardial stunning. Asymptomatic transient, left-ventricular dysfunction has also been demonstrated on echocardiogram after ECT.7 Although the mortality for ECT is estimated to be quite low, at 2 to 4 deaths per 100,000 treatments, a rate comparable to that of anesthesia alone, the morbidity rate is somewhat higher, and cardiovascular events are responsible for the majority of complications.3 The effects of ECT on the cardiovascular system are well-described. The electrical stimulus of ECT leads to an increase in vagal activity regardless of whether a seizure is induced. In the absence of seizure activity, as in the case of a subconvulsive stimulus, the parasympathetic discharge is unopposed and can lead to bradycardia or asystole. The risk of asystole increases with the use of betablockers, although this risk can be mediated to some extent by premedicating with an anticholinergic agent. If a seizure is induced, the initial response is a massive sympathetic discharge, with a resultant surge of catecholamines and subsequent tachycardia. This is accompanied by shortlived increases in cerebral blood flow and intracranial pressure. At the end of the seizure, reflex bradycardia may occur. To our knowledge, this is the second reported case of takotsubo cardiomyopathy after ECT.9
Case Report
“Mrs. A,” a 52-year-old white woman with a long history of treatment-resistant depression, was admitted to the hospital for ECT by her outpatient psychiatrist. Mrs. A had noted gradually worsening mood over the past several months, associated with several major psychosocial stressors in her life. She had a positive neurovegetative profile and endorsed occasional passive suicidal ideation. Mrs. A denied all symptoms of psychosis. Mrs. A’s medical history was significant for migraine headaches and a laparoscopic cholecystectomy 2 months earlier for biliary dyskinesia. She had no known cardiac history. She had a family history of hypertension on both sides, as well as diabetes and coronary artery disease affecting her father. She acknowledged rare alcohol use, but had no history of tobacco use or illicit drug use. At the time of admission, she was taking fluoxetine 80 mg daily, olanzapine 5 mg daily, and topirimate 200 mg Psychosomatics 51:5, September-October 2010
daily, the last of which primarily was to treat her migraine headaches. She also took gabapentin 800 mg at bedtime for restless leg syndrome. An ECG at the time of admission was normal. Blood pressure on admission was 128/84 mmHg, and heart rate was 90 bpm. A chest radiograph demonstrated a minimal opacity in the left lung base, most likely consistent with atelectasis. Brain CT, EEG, and spine films were normal. Just before being transported to the procedure room, Mrs. A’s blood pressure was noted to have increased to 150/102 mmHg, and her heart rate had increased slightly, to 100 bpm, suggesting some anxiety. Anesthesia was induced using methohexital 50 mg, and muscle relaxation achieved with succinylchoine 60 mg. ECT was initiated with a Thymatron System IV (Somatics, Inc.; Lake Bluff, IL), at 50% energy, with bifrontal electrode placement. A generalized tonic– clonic seizure was induced that lasted 33 sec by clinical indications and 50 sec by EEG. Heart rate increased to 130 bpm during the treatment. Upon arrival to the post-anesthesia recovery unit after the treatment, Mrs. A’s blood pressure was noted to be 155/82 mmHg, with a heart rate of 95 bpm. She initially reported feeling well and was observed to be resting comfortably on the stretcher. She was given oxycodone/acetaminophen 5/325 mg for headache prophylaxis before being transferred back to her room. Approximately 2 hours after her treatment, Mrs. A reported to her nurse that her chest felt “like it is bursting.” She described her chest pain as tightness and also reported nausea as well as slight jaw pain. At this time, her blood pressure had dropped to 90/62 mmHg. An ECG was performed and demonstrated normal sinus rhythm, with a rate of 70 bpm, a QTc of 416 msec, a 1-mm ST-segment elevation in leads V1–V3, and T-wave inversions of ⬍1 mm in leads I and AVL. Initial troponin-T was elevated, at 0.25 ng/ml (reference range: 0.00 – 0.10 ng/ml). Because of concern about anginal pain, Mrs. A was given aspirin 325 mg in addition to 3 doses of sublingual nitroglycerin, spaced 5 minutes apart, with no improvement in her symptoms. She also received morphine 10 mg IV, given in 5 divided doses, as well as two doses of IV metoprolol 5 mg, with minimal relief. A cardiology consultation was arranged, and Mrs. A was ultimately transferred to the Coronary Care Unit (CCU) for further monitoring and treatment. Before being admitted to the CCU, Mrs. A underwent a transthoracic echocardiogram, which demonstrated moderate left-ventricular dysfunction involving anteroapical, lateral, and inferior hypokinesis, with most of the hypokihttp://psy.psychiatryonline.org
433
Case Reports nesis in the midportion of the left ventricle, and sparing of the basal anterior wall. Her left-ventricular ejection fraction (EF) was estimated to be 30%– 40%. Upon admission to the CCU, 7 hours after her ECT treatment, Mrs. A had an ECG performed, demonstrating normal sinus rhythm with a rate of 79 bpm, a QTc of 437 msec, resolution of ST-segment changes, deepened T-wave inversions of ⬎1 mm in leads I and AVL, and new T-wave inversions of ⬍1 mm in leads V5 and V6. Blood pressure was 87/58 mmHg. Her troponin-T peaked at 0.86 ng/ml shortly after admission. A repeat chest radiograph revealed no acute cardiopulmonary disease. The next day, Mrs. A underwent cardiac catheterization, which revealed normal coronary arteries, but was notable for mid-cavity left-ventricular hypo- to akinesis, with hyperkinesis in the basilar region (Figure 1), consistent with a diagnosis of takotsubo cardiomyopathy. The wall-motion abnormalities seen in this study and the estimated EF were consistent with the echocardiogram findings. Mrs. A did well over the next few days, reporting full resolution of her symptoms within 48 hours of the initial event. Before her discharge, a repeat ECG demonstrated a normal sinus rhythm, with a rate of 77 bpm, an increased QTc of 493, and continued presence of T-wave inversions. Mrs. A did not experience any long-term complications or recurrence of her cardiomyopathy. An ECG performed 1 month after her hospitalization demonstrated a return to her baseline, with resolution of her T-wave inversions. A trans-thoracic echocardiogram performed 5 months later showed normal left-ventricular functioning. FIGURE 1.
A decision was made to not pursue any further courses of ECT. Mrs. A ultimately received a vagal nerve stimulator for treatment of her ongoing depression, and she responded well, with no medical or surgical complications noted.
Discussion
This case highlights a unique complication of ECT, adding to the growing literature regarding the effects of ECT on the cardiac system as well as the mechanisms underlying takotsubo cardiomyopathy. As was the case with Mrs. A, the classic clinical presentation of takotsubo cardiomyopathy mimics an acute myocardial infarction. The most common abnormality seen on ECG at the time of presentation is ST-segment elevation, especially in leads V3–V6.5 New left and right bundle-branch blocks on the presenting ECG have also been reported, and, in some series, the presenting QTc has been prolonged.3,4 Most patients progress to develop T-wave inversions over time, usually present in all leads, and pathologic Q waves have also been described in a significant percentage of patients. Cardiac biomarkers, such as troponin and CK-MB generally are elevated, although usually only slightly so. On echocardiography, patients typically have reduced leftventricular ejection fraction, sometimes as low as 10%, which tends to resolve over a period of days to weeks. Patients demonstrate moderate-to-severe mid-ventricular
Left Ventriculogram
Mrs. A’s heart appears normal on diastole (left). During systole (right), the apex of the heart appears hypokinetic, while the base is hyperkinetic.
434
http://psy.psychiatryonline.org
Psychosomatics 51:5, September-October 2010
Beach et al. dysfunction and apical akinesis or dyskinesis. The basal function is either preserved or hyperkinetic. Angiography demonstrates either no detectable or nonobstructive coronary disease. The diagnosis of takotsubo cardiomyopathy is generally based on the echocardiographic, angiographic, and ECG findings described above, all of which must occur in the absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, myocarditis, hypertrophic cardiomyopathy, or obstructive epicardial coronary-artery disease.3 The prognosis for takotsubo cardiomyopathy is generally favorable, with total in-hospital mortality estimated at 1.1%, and the most common complication being heart failure, occurring in 17.7% of patients.2 Although many patients experience a transient prolongation of the QTc interval, the risk of torsades de pointes remains low, and there is no definitive evidence to suggest a causal link between a long QTc interval at baseline and development of takotsubo cardiomyopathy. Recurrence of the syndrome appears to be an uncommon phenomenon, estimated to occur in up to 8% of patients.3 Treatment is largely supportive and typically includes aspirin, beta-blockers, angiotensin-converting enzyme inhibitors, diuretics, and calcium channel blockers. Mrs. A, a postmenopausal woman, met all four proposed diagnostic criteria for the phenomenon. Her course was typical of the syndrome, with resolution observed over the ensuing days. We believe that her symptoms occurred as a direct result of the procedure. Although she certainly experienced emotional stress related to her depression, her illness had been relatively unchanged in severity for some time before the episode, and there were no additional acute stressors at the time of the procedure. There has been at least one reported case of takotsubo cardiomyopathy associated with the induction of general anesthesia.10 In contrast to our patient, however, this patient received fentanyl, propofol, and cisatracurium. Furthermore, our patient had undergone a laparoscopic cholecystecomy 2 months earlier, during which she received general anesthesia and had no complications. She again received general anesthesia 2 months after her episode of
cardiomyopathy for implantation of a vagal nerve stimulator and again experienced no cardiac side effects. It therefore seems unlikely that the induction of general anesthesia alone would have caused her left-ventricular dysfunction in this isolated incident. Several studies have posited that increased levels of catecholamines may be a causative factor in left-ventricular apical ballooning syndrome, either via catecholaminemediated spasm or through direct myocyte injury. Prospective data are lacking, however, regarding plasma catecholamine levels before the onset of the syndrome, and it is therefore impossible to demonstrate a causal relationship. This case appears to lend credibility to the theory that takotsubo cardiomyopathy is mediated by a catecholamine surge. ECT is known to result in a massive sympathetic discharge after seizure induction, leading to a surge in catecholamine levels. Given that our patient experienced an adequate seizure, evidenced by both clinical and EEG data, her cardiac system was certainly subjected to significant transient increases in sympathetic stimuli. Given that postmenopausal women make up a substantial portion of the population referred for ECT, psychiatrists should be aware of this potentially life-threatening adverse event. Although currently there are no screening measures to detect patients at risk for the syndrome, immediate recognition of the phenomenon frequently leads to positive outcomes. The case raises again the question of relative and absolute contraindications to ECT. Although we chose not to rechallenge our patient with ECT, given the availability of newer alternative treatment modalities, the recurrence rate of the phenomenon, even with repeat exposure to precipitating stimuli, is low, and it is unclear whether previous episodes of the syndrome should constitute grounds for avoiding ECT. Further experience involving ECT in the setting of a previously documented episode of takotsubo cardiomyopathy is necessary to answer this question.
The authors do not have any financial support or conflicts of interest to disclose.
References 1. Dote K, Sato H, Tateishi H, et al: Myocardial stunning due to simultaneous multivessel coronary spasms: a review of five cases. J Cardiol 1991; 21:203–214 2. Gianni M, Dentali F, Grandi AM, et al: Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J 2006; 27:1523–1529
Psychosomatics 51:5, September-October 2010
3. Bybee KA, Kara T, Prasad A, et al: Systematic review: transient left-ventricular apical ballooning: a syndrome that mimics STsegment elevation myocardial infarction. Ann Intern Med 2004; 141:858 – 865 4. Bybee KA, Prasad A, Barsness GW, et al: Clinical characteristics and thrombolysis in myocardial infarction frame counts in
http://psy.psychiatryonline.org
435
Case Reports women with transient left-ventricular apical ballooning syndrome. Am J Cardiol 2004; 94:343–346 5. Arora S, Alfayoumi F, Srinivasan V: Transient left-ventricular apical ballooning after cocaine use: is catecholamine cardiotoxicity the pathologic link? Mayo Clin Proc 2006; 81:829 – 832 6. Rivera JM, Locketz AJ, Fritz KD, et al: “Broken heart syndrome” after separation (from Oxycontin). Mayo Clin Proc 2006; 81:825– 828 7. McCully RB, Karon BL, Rummans TA, et al: Frequency of
436
http://psy.psychiatryonline.org
left-ventricular dysfunction after electroconvulsive therapy. Am J Cardiol 2003; 91:1147–1150 8. Abrams R: The mortality rate with ECT. Convuls Ther 1990; 6:85–120 9. Wichman, CL: Broken Heart Syndrome Secondary to Electroconvulsive Therapy. Washington, DC, American Psychiatric Association, May 2008 10. Consales G, Campiglia L, Michelagnoli G, et al: Acute left-ventricular dysfunction due to tako-tsubo syndrome after induction of general anesthesia. Minerva Anestesiol 2007; 73:655– 658
Psychosomatics 51:5, September-October 2010
Background: Takotsubo cardiomyopathy is a novel acute cardiac syndrome characterized by transient regional systolic dysfunction of the left-ventricular apex and mid-ventricle, with hyperkinesis of the basal left ventricular segments, which has been associated with severe emotional or physical stress. Method: This is the second published case report of takotsubo cardiomyopathy occurring in the setting of electroconvulsive therapy (ECT). Results: The patient, a 52-year-old woman, experienced chest pain and discomfort shortly after ECT treatment. She was shown to have moderate left-ventricular dysfunction, with mid-cavity left-ventricular hypo- to akinesis, and hyperkinesis in the basilar region, consistent with a diagnosis of takotsubo cardiomyopathy. There was full resolution of her symptoms within 48 hours of the initial event. Discussion: This report highlights a previously undocumented complication of ECT and adds to the growing list of stressors responsible for cases of takotsubo cardiomyopathy. The prognosis is favorable, and recovery is generally complete, especially with early recognition of the syndrome and proper supportive treatment. (Psychosomatics 2010; 51:432– 436)
T
akotsubo cardiomyopathy, alternatively known as transient left-ventricular apical ballooning syndrome, broken heart syndrome, or ampulla cardiomyopathy, is a novel acute cardiac syndrome first described in the Japanese population in 1990.1 The syndrome takes its name from the shape of the patient’s heart as seen on left ventriculography, which is said to resemble the pot with a narrow neck and round bottom used by Japanese fisherman to catch octopus (tako-tsubo). The phenomenon is characterized by transient regional systolic dysfunction of the left-ventricular apex and mid-ventricle, with concomitant hyperkinesis of the basal left-ventricular segments.
Received January 23, 2009; revised April 3, 2009; accepted April 7, 2009. From the Dept. of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, VA, and the Dept. of Psychiatry and Psychology, Mayo Clinic, Rochester, MN. Send correspondence and reprint requests to Scott R. Beach, M.D., Massachusetts General Hospital, 55 Fruit St., Warren 605, Boston, MA 02114. e-mail: [email protected] © 2010 The Academy of Psychosomatic Medicine
432
http://psy.psychiatryonline.org
The incidence of Takotsubo cardiomyopathy is relatively low and has been estimated in various case series to account for 1%–2% of all patients hospitalized for apparent acute coronary syndrome.2 Takotsubo cardiomyopathy appears predominantly to affect postmenopausal women; the mean age of patients presenting is 62 to 75 years.3 Factors proposed to account for the striking demographic predisposition include influences of female hormones on sympathetic neuromodulation and coronary vasoreactivity, as well as postmenopausal alteration of endothelial function.2 The vast majority of patients also appear to have experienced a recent significant psychological or physiological stressor, such as the death of a loved one, surgery, grand mal seizure, blunt trauma, cocaine use, or opiate withdrawal.4 –6 For many years before the advent of selective serotonin-reuptake inhibitor (SSRI) antidepressants, electroconvulsive therapy (ECT) was cited as the antidepressant treatment of choice for patients with a history of cardiac Psychosomatics 51:5, September-October 2010
Beach et al. problems because older medications had well-described cardiotoxic effects. Nonetheless, ECT has been associated with cardiac complications, including arrhythmias, ischemic events, and myocardial stunning. Asymptomatic transient, left-ventricular dysfunction has also been demonstrated on echocardiogram after ECT.7 Although the mortality for ECT is estimated to be quite low, at 2 to 4 deaths per 100,000 treatments, a rate comparable to that of anesthesia alone, the morbidity rate is somewhat higher, and cardiovascular events are responsible for the majority of complications.3 The effects of ECT on the cardiovascular system are well-described. The electrical stimulus of ECT leads to an increase in vagal activity regardless of whether a seizure is induced. In the absence of seizure activity, as in the case of a subconvulsive stimulus, the parasympathetic discharge is unopposed and can lead to bradycardia or asystole. The risk of asystole increases with the use of betablockers, although this risk can be mediated to some extent by premedicating with an anticholinergic agent. If a seizure is induced, the initial response is a massive sympathetic discharge, with a resultant surge of catecholamines and subsequent tachycardia. This is accompanied by shortlived increases in cerebral blood flow and intracranial pressure. At the end of the seizure, reflex bradycardia may occur. To our knowledge, this is the second reported case of takotsubo cardiomyopathy after ECT.9
Case Report
“Mrs. A,” a 52-year-old white woman with a long history of treatment-resistant depression, was admitted to the hospital for ECT by her outpatient psychiatrist. Mrs. A had noted gradually worsening mood over the past several months, associated with several major psychosocial stressors in her life. She had a positive neurovegetative profile and endorsed occasional passive suicidal ideation. Mrs. A denied all symptoms of psychosis. Mrs. A’s medical history was significant for migraine headaches and a laparoscopic cholecystectomy 2 months earlier for biliary dyskinesia. She had no known cardiac history. She had a family history of hypertension on both sides, as well as diabetes and coronary artery disease affecting her father. She acknowledged rare alcohol use, but had no history of tobacco use or illicit drug use. At the time of admission, she was taking fluoxetine 80 mg daily, olanzapine 5 mg daily, and topirimate 200 mg Psychosomatics 51:5, September-October 2010
daily, the last of which primarily was to treat her migraine headaches. She also took gabapentin 800 mg at bedtime for restless leg syndrome. An ECG at the time of admission was normal. Blood pressure on admission was 128/84 mmHg, and heart rate was 90 bpm. A chest radiograph demonstrated a minimal opacity in the left lung base, most likely consistent with atelectasis. Brain CT, EEG, and spine films were normal. Just before being transported to the procedure room, Mrs. A’s blood pressure was noted to have increased to 150/102 mmHg, and her heart rate had increased slightly, to 100 bpm, suggesting some anxiety. Anesthesia was induced using methohexital 50 mg, and muscle relaxation achieved with succinylchoine 60 mg. ECT was initiated with a Thymatron System IV (Somatics, Inc.; Lake Bluff, IL), at 50% energy, with bifrontal electrode placement. A generalized tonic– clonic seizure was induced that lasted 33 sec by clinical indications and 50 sec by EEG. Heart rate increased to 130 bpm during the treatment. Upon arrival to the post-anesthesia recovery unit after the treatment, Mrs. A’s blood pressure was noted to be 155/82 mmHg, with a heart rate of 95 bpm. She initially reported feeling well and was observed to be resting comfortably on the stretcher. She was given oxycodone/acetaminophen 5/325 mg for headache prophylaxis before being transferred back to her room. Approximately 2 hours after her treatment, Mrs. A reported to her nurse that her chest felt “like it is bursting.” She described her chest pain as tightness and also reported nausea as well as slight jaw pain. At this time, her blood pressure had dropped to 90/62 mmHg. An ECG was performed and demonstrated normal sinus rhythm, with a rate of 70 bpm, a QTc of 416 msec, a 1-mm ST-segment elevation in leads V1–V3, and T-wave inversions of ⬍1 mm in leads I and AVL. Initial troponin-T was elevated, at 0.25 ng/ml (reference range: 0.00 – 0.10 ng/ml). Because of concern about anginal pain, Mrs. A was given aspirin 325 mg in addition to 3 doses of sublingual nitroglycerin, spaced 5 minutes apart, with no improvement in her symptoms. She also received morphine 10 mg IV, given in 5 divided doses, as well as two doses of IV metoprolol 5 mg, with minimal relief. A cardiology consultation was arranged, and Mrs. A was ultimately transferred to the Coronary Care Unit (CCU) for further monitoring and treatment. Before being admitted to the CCU, Mrs. A underwent a transthoracic echocardiogram, which demonstrated moderate left-ventricular dysfunction involving anteroapical, lateral, and inferior hypokinesis, with most of the hypokihttp://psy.psychiatryonline.org
433
Case Reports nesis in the midportion of the left ventricle, and sparing of the basal anterior wall. Her left-ventricular ejection fraction (EF) was estimated to be 30%– 40%. Upon admission to the CCU, 7 hours after her ECT treatment, Mrs. A had an ECG performed, demonstrating normal sinus rhythm with a rate of 79 bpm, a QTc of 437 msec, resolution of ST-segment changes, deepened T-wave inversions of ⬎1 mm in leads I and AVL, and new T-wave inversions of ⬍1 mm in leads V5 and V6. Blood pressure was 87/58 mmHg. Her troponin-T peaked at 0.86 ng/ml shortly after admission. A repeat chest radiograph revealed no acute cardiopulmonary disease. The next day, Mrs. A underwent cardiac catheterization, which revealed normal coronary arteries, but was notable for mid-cavity left-ventricular hypo- to akinesis, with hyperkinesis in the basilar region (Figure 1), consistent with a diagnosis of takotsubo cardiomyopathy. The wall-motion abnormalities seen in this study and the estimated EF were consistent with the echocardiogram findings. Mrs. A did well over the next few days, reporting full resolution of her symptoms within 48 hours of the initial event. Before her discharge, a repeat ECG demonstrated a normal sinus rhythm, with a rate of 77 bpm, an increased QTc of 493, and continued presence of T-wave inversions. Mrs. A did not experience any long-term complications or recurrence of her cardiomyopathy. An ECG performed 1 month after her hospitalization demonstrated a return to her baseline, with resolution of her T-wave inversions. A trans-thoracic echocardiogram performed 5 months later showed normal left-ventricular functioning. FIGURE 1.
A decision was made to not pursue any further courses of ECT. Mrs. A ultimately received a vagal nerve stimulator for treatment of her ongoing depression, and she responded well, with no medical or surgical complications noted.
Discussion
This case highlights a unique complication of ECT, adding to the growing literature regarding the effects of ECT on the cardiac system as well as the mechanisms underlying takotsubo cardiomyopathy. As was the case with Mrs. A, the classic clinical presentation of takotsubo cardiomyopathy mimics an acute myocardial infarction. The most common abnormality seen on ECG at the time of presentation is ST-segment elevation, especially in leads V3–V6.5 New left and right bundle-branch blocks on the presenting ECG have also been reported, and, in some series, the presenting QTc has been prolonged.3,4 Most patients progress to develop T-wave inversions over time, usually present in all leads, and pathologic Q waves have also been described in a significant percentage of patients. Cardiac biomarkers, such as troponin and CK-MB generally are elevated, although usually only slightly so. On echocardiography, patients typically have reduced leftventricular ejection fraction, sometimes as low as 10%, which tends to resolve over a period of days to weeks. Patients demonstrate moderate-to-severe mid-ventricular
Left Ventriculogram
Mrs. A’s heart appears normal on diastole (left). During systole (right), the apex of the heart appears hypokinetic, while the base is hyperkinetic.
434
http://psy.psychiatryonline.org
Psychosomatics 51:5, September-October 2010
Beach et al. dysfunction and apical akinesis or dyskinesis. The basal function is either preserved or hyperkinetic. Angiography demonstrates either no detectable or nonobstructive coronary disease. The diagnosis of takotsubo cardiomyopathy is generally based on the echocardiographic, angiographic, and ECG findings described above, all of which must occur in the absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, myocarditis, hypertrophic cardiomyopathy, or obstructive epicardial coronary-artery disease.3 The prognosis for takotsubo cardiomyopathy is generally favorable, with total in-hospital mortality estimated at 1.1%, and the most common complication being heart failure, occurring in 17.7% of patients.2 Although many patients experience a transient prolongation of the QTc interval, the risk of torsades de pointes remains low, and there is no definitive evidence to suggest a causal link between a long QTc interval at baseline and development of takotsubo cardiomyopathy. Recurrence of the syndrome appears to be an uncommon phenomenon, estimated to occur in up to 8% of patients.3 Treatment is largely supportive and typically includes aspirin, beta-blockers, angiotensin-converting enzyme inhibitors, diuretics, and calcium channel blockers. Mrs. A, a postmenopausal woman, met all four proposed diagnostic criteria for the phenomenon. Her course was typical of the syndrome, with resolution observed over the ensuing days. We believe that her symptoms occurred as a direct result of the procedure. Although she certainly experienced emotional stress related to her depression, her illness had been relatively unchanged in severity for some time before the episode, and there were no additional acute stressors at the time of the procedure. There has been at least one reported case of takotsubo cardiomyopathy associated with the induction of general anesthesia.10 In contrast to our patient, however, this patient received fentanyl, propofol, and cisatracurium. Furthermore, our patient had undergone a laparoscopic cholecystecomy 2 months earlier, during which she received general anesthesia and had no complications. She again received general anesthesia 2 months after her episode of
cardiomyopathy for implantation of a vagal nerve stimulator and again experienced no cardiac side effects. It therefore seems unlikely that the induction of general anesthesia alone would have caused her left-ventricular dysfunction in this isolated incident. Several studies have posited that increased levels of catecholamines may be a causative factor in left-ventricular apical ballooning syndrome, either via catecholaminemediated spasm or through direct myocyte injury. Prospective data are lacking, however, regarding plasma catecholamine levels before the onset of the syndrome, and it is therefore impossible to demonstrate a causal relationship. This case appears to lend credibility to the theory that takotsubo cardiomyopathy is mediated by a catecholamine surge. ECT is known to result in a massive sympathetic discharge after seizure induction, leading to a surge in catecholamine levels. Given that our patient experienced an adequate seizure, evidenced by both clinical and EEG data, her cardiac system was certainly subjected to significant transient increases in sympathetic stimuli. Given that postmenopausal women make up a substantial portion of the population referred for ECT, psychiatrists should be aware of this potentially life-threatening adverse event. Although currently there are no screening measures to detect patients at risk for the syndrome, immediate recognition of the phenomenon frequently leads to positive outcomes. The case raises again the question of relative and absolute contraindications to ECT. Although we chose not to rechallenge our patient with ECT, given the availability of newer alternative treatment modalities, the recurrence rate of the phenomenon, even with repeat exposure to precipitating stimuli, is low, and it is unclear whether previous episodes of the syndrome should constitute grounds for avoiding ECT. Further experience involving ECT in the setting of a previously documented episode of takotsubo cardiomyopathy is necessary to answer this question.
The authors do not have any financial support or conflicts of interest to disclose.
References 1. Dote K, Sato H, Tateishi H, et al: Myocardial stunning due to simultaneous multivessel coronary spasms: a review of five cases. J Cardiol 1991; 21:203–214 2. Gianni M, Dentali F, Grandi AM, et al: Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J 2006; 27:1523–1529
Psychosomatics 51:5, September-October 2010
3. Bybee KA, Kara T, Prasad A, et al: Systematic review: transient left-ventricular apical ballooning: a syndrome that mimics STsegment elevation myocardial infarction. Ann Intern Med 2004; 141:858 – 865 4. Bybee KA, Prasad A, Barsness GW, et al: Clinical characteristics and thrombolysis in myocardial infarction frame counts in
http://psy.psychiatryonline.org
435
Case Reports women with transient left-ventricular apical ballooning syndrome. Am J Cardiol 2004; 94:343–346 5. Arora S, Alfayoumi F, Srinivasan V: Transient left-ventricular apical ballooning after cocaine use: is catecholamine cardiotoxicity the pathologic link? Mayo Clin Proc 2006; 81:829 – 832 6. Rivera JM, Locketz AJ, Fritz KD, et al: “Broken heart syndrome” after separation (from Oxycontin). Mayo Clin Proc 2006; 81:825– 828 7. McCully RB, Karon BL, Rummans TA, et al: Frequency of
436
http://psy.psychiatryonline.org
left-ventricular dysfunction after electroconvulsive therapy. Am J Cardiol 2003; 91:1147–1150 8. Abrams R: The mortality rate with ECT. Convuls Ther 1990; 6:85–120 9. Wichman, CL: Broken Heart Syndrome Secondary to Electroconvulsive Therapy. Washington, DC, American Psychiatric Association, May 2008 10. Consales G, Campiglia L, Michelagnoli G, et al: Acute left-ventricular dysfunction due to tako-tsubo syndrome after induction of general anesthesia. Minerva Anestesiol 2007; 73:655– 658
Psychosomatics 51:5, September-October 2010