Myocardial Stunning after Electroconvulsive Therapy Wei-Xi Zhu, MD; David E. Olson, MD; Barry L. Karon, MD; and A. Jamil Tajik, MD Annals of Internal Medicine. 1992;117:914-915.

Myocardial stunning (1, 2), a prolonged but reversible myocardial contractile dysfunction, has not been reported after electroconvulsive therapy (ECT). We describe a patient with myocardial stunning after ECT and the apparent prevention of this complication by combined alpha- and beta-blockade. Case Report A 77-year-old woman was admitted for major depression. She had no history of cardiac disease. Physical examination, routine laboratory tests, and a chest radiograph were negative. An electrocardiogram was normal (Figure 1A). After antidepressant therapy failed, ECT was begun. The patient was premedicated with glycopyrrolate. Anesthesia was induced with thiopental, 100 mg, and succinylcholine, 40 mg. Baseline blood pressure was 140/80 mm Hg and heart rate was 90 beats/min. Electroconvulsive therapy was initiated with1 a Thymatron (Somatic, Inc., Lake Bluff, Illinois) at 80% with unilateral, nondominant-hemisphere electrode placement. A generalized tonic-clonic seizure was induced and lasted about 60 seconds. Blood pressure increased to 170/80 mm Hg, and heart rate increased to 160 beats/min during the seizure activity and gradually subsided. The patient awakened and denied any chest pain. However, an electrocardiogram revealed 1- to 2-mm ST-segment elevation in leads I, II, III, AVF, and V 5 to V 6 (Figure IB). Silent myocardial ischemia was suspected. An immediate echocardiogram showed a moderately enlarged left ventricle with an ejection fraction of 35%. There was akinesis of the inferior wall and severe hypokinesis of the anteroseptal and anterior walls. Coronary angiography showed only 50% stenotic lesions in the proximal and middle portions of the left anterior descending coronary artery and multiple 20% stenotic lesions in the dominant right coronary artery. Clinically, the left ventricular dysfunction seemed disproportionate to the mild coronary artery disease. During the next 48 hours, electrocardiographic changes evolved into giant T-wave inversions (Figure IC). Cardiac enzyme levels remained normal. No evidence was found of a stroke or pericarditis. The electrocardiographic and echocardiographic changes completely resolved 4 days later (Figure ID). The ejection fraction increased to 65%. A dobutamine stress echocardiogram done 6 weeks later gave negative results when the patient's peak blood pressure was 156/58 mm Hg and heart rate was 87 beats/min. From the Mayo Clinic, Rochester, Minnesota. For current author addresses, see end of text.

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The patient was readmitted 6 months later for recurrent major depression. A repeat course of ECT was considered. Preventive therapy with nitrates and diltiazem was given in the event that coronary artery spasm was the mechanism of ischemia associated with the previous ECT. During the repeat ECT, systolic blood pressure increased to 180 mm Hg and heart rate increased to 120 beats/min. The patient had no immediate complications. An electrocardiogram done 24 hours later, however, showed diffuse T-wave inversions (Figure IE). Echocardiographic evaluation showed depressed left ventricular systolic function (ejection fraction, 45%) with hypokinesis of the inferior and anteroseptal walls. These changes resolved during the next 3 days. At the next ECT session, labetalol hydrochloride (Normodyne, Schering Corporation, Kenilworth, New Jersey), 15 mg, was given intravenously to block the effects of sympathetic surge. The hemodynamic alterations during ECT were attenuated. No immediate or delayed electrocardiographic or echocardiographic changes occurred. The patient underwent five more sessions of ECT while receiving labetalol and experienced no complications.

Discussion Many cardiovascular complications have been associated with ECT: acute myocardial infarction; circulatory collapse; exaggerated hypertensive responses; and arrhythmias. In addition, transient electrocardiographic repolarization abnormalities in the setting of normal cardiac enzyme levels have been reported (3-5). However, coronary artery anatomy and left ventricular function were not assessed. In our patient, we showed repeatedly that ECT-induced repolarization abnormalities were temporally related to global and regional left ventricular dysfunction, whereas resolution of electrocardiographic changes was associated with normalization of myocardial function. Hence, transient repolarization abnormalities after ECT may represent myocardial stunning. Central nervous system events can affect the electrocardiogram. Many "neurogenic" electrocardiographic changes have been reported. A recent study showed that echocardiographic evidence of regional left ventricular dysfunction was present in most patients with subarachnoid hemorrhage whose electrocardiogram showed repolarization abnormalities (6). The mechanism underlying myocardial dysfunction after electrically induced grand mal seizures is not clear. The failure of nitrates and a calcium-channel blocker to prevent myocardial stunning argues against coronary artery spasm as the mechanism. The seizure induced by ECT leads to a two-phase response of the autonomic nervous system (7). Initial marked parasympathetic discharge with resultant bradycardia is followed by a sympathetic surge, which can produce a marked increase in norepinephrine and epinephrine levels (8). The subsequent hemodynamic and inotropic changes produce a marked increase in myocardial oxy-

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Figure 1. Twelve-lead electrocardiograms. Panel A. Normal electrocardiogram at admission. Panel B. Electrocardiogram immediately after the first electroconvulsive therapy (ECT) session shows ST-segment elevation in leads I, II, III, AVF, and V5 to V6. Panel C. Electrocardiogram 24 hours after the first ECT session shows global, deep T-wave inversions. Panel D. Electrocardiogram 4 days after the first ECT therapy session shows complete resolution of previous changes. Panel E. Electrocardiogram 24 hours after the second ECT session shows T-wave inversions in leads I, II, III, AVF, AVL, and V5 to V6. gen demand that may result in prolonged myocardial ischemia or even infarction in patients with compromised coronary arteries. Beta-adrenergic blockade has been used to reverse sympathetically mediated cardiovascular complications. However, severe hypertension may occasionally occur with beta-adrenergic blocker therapy alone as a result of an unopposed alpha-stimulating effect of the circulatory catecholamines. In addition, cardiac asystole during ECT modified by beta-adrenergic blockade has been reported (9). Labetalol is an alpha- and beta-adrenergic blocking agent that blunts exercise-induced increases in blood pressure and heart rate in dose-related fashion and only minimally affects the resting heart rate. Thus, labetalol may be a useful addition to the premedication for ECT, especially in patients with ischemic heart disease. Requests for Reprints: A. Jamil Tajik, MD, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. Current Author Addresses: Drs. Zhu, Karon, and Tajik: Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, 200 First Street SW, Rochester, MN 55905.

Dr. Olson: Department of Psychiatry, Mayo Clinic and Mayo Foundation, 200 First Street SW, Rochester, MN 55905. References 1. Braunwald E, Kloner RA. The stunned myocardium: prolonged, posti s h e m i c ventricular dysfunction. Circulation. 1982;66:1146-9. 2. Bolli R. Mechanism of myocardial "stunning." Circulation. 1990;82: 723-38. 3. Green R, Woods A. Effects of modified ECT on the electrocardiogram. Br Med J. 1955;1:1503-5. 4. Gould L, Copalaswamy C, Chandy F, Kim B. Electroconvulsive therapy-induced ECG changes simulating a myocardial infarction. Arch Intern Med. 1983;143:1786-7. 5. Dec GW, Stern TA, Welch C. The effects of electroconvulsive therapy on serial electrocardiograms and serum cardiac enzyme values: a prospective study of depressed hospitalized inpatients. JAMA. 1985;253:2525-9. 6. Fine DG, Oh JK, Edwards WD, Sandok BA, Meloy TD, Marsh R, et al. Electrocardiographic, echocardiographic, and pathological correlation in patients with subarachnoid hemorrhage [Abstract]. J Am Coll Cardiol. 1990;15:215A. 7. Selvin BL. Electroconvulsive therapy—1987. Anesthesiology. 1987; 67:367-85. 8. Jones RM, Knight PR. Cardiovascular and hormonal responses to electroconvulsive therapy. Anaesthesia. 1981;36:795-9. 9. Decina P, Malitz S, Sackeim HA, Holzer J, Yudofsky S. Cardiac arrest during ECT modified by /3-adrenergic blockade. Am J Psychiatry. 1984;141:298-300. © 1992 American College of Physicians

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Myocardial stunning after electroconvulsive therapy.

Myocardial Stunning after Electroconvulsive Therapy Wei-Xi Zhu, MD; David E. Olson, MD; Barry L. Karon, MD; and A. Jamil Tajik, MD Annals of Internal...
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