Electroconvulsive therapy-associated acute coronary syndrome in the absence of coronary artery disease.

To the Editor: Electroconvulsive therapy (ECT)-related cardiac complications have been documented extensively in the literature and include circulatory collapse, arrhythmias, hypertensive responses, transient left ventricular dysfunction, and transient ST abnormalities. The rate of ECT-induced cardiac complications has been estimated to be as high as 28%; (1) however, many reports either do not delineate the degree of preexisting cardiac disease or include patients with known cardiac disease. Furthermore, no case report has demonstrated an elevation in cardiac-specific enzymes after ECT. I present a case in which a patient undergoing her 91st ECT session developed chest pain, elevated troponin levels, and transient T-wave inversion in the absence of angiographic coronary artery disease.

A 42-year-old woman presented for elective ECT. The patient's medical history included depression, gastroesophageal reflux disease, and obesity. She had no cardiac history and did not use alcohol or tobacco. Her family history included a paternal myocardial infarction (MI) at age 40.

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The patient was premedicated, and anesthesia was induced with penthathol (175 mg) and succinylcholine (50 mg). The electrocardiogram (ECG) immediately before the initiation of treatment failed to demonstrate any significant abnormalities and was unchanged from previous ECGs (Fig. 1A). ECT was initiated with a Thymatron (Somatic, Inc., Lake Bluff, IL) at 60% with modified bifrontal electrode placement. A generalized tonicoclonic seizure was induced and lasted approximately 30 seconds. The patient awakened and complained of headache but denied chest pain. An ECG obtained after treatment failed to reveal any changes.

Approximately 30 minutes later, the patient complained of mild, nonradiating, substernal chest pain. The patient was notably anxious and diaphoretic with increased pain intensity and was subsequently transferred to the emergency department (ED). The ECG obtained in the ED did not demonstrate ST elevations or depressions and was comparable to the patient's prior ECG. Troponin studies initiated in the ED revealed an initial value of 0.29 ng/ml (normal, <0.04 ng/ml) approximately 4 hours after ECT.

The next day the patient attempted to ambulate and developed severe pressure-type chest pain. The ECG obtained at that time demonstrated ST depression in leads V1 and V2, which were not present on prior ECGs (Fig. 1B). Thirty minutes later an additional ECG confirmed the ST depressions in V1 and V2. The patient was transferred to the cardiac intensive care unit (CCU) and became chest pain-free after intravenous nitroglycerin was administered. An ECG obtained in the CCU demonstrated resolution of ST depressions in leads V1 and V2 approximately 2 hours after the initial ST changes and 24 hours after ECT. During the hospital course, three additional troponin levels were elevated (0.08 ng/ml, 0.06 ng/ml, and 0.19 ng/ml). Coronary angiography failed to demonstrate any evidence of coronary artery disease or left ventricular dysfunction, and the patient's ejection fraction was reported to be greater than 50%. The patient was discharged to home the next day.

Although cardiac complications are relatively common, case reports and prospective studies have failed to show elevations in CK-MB after ECT. (2) These studies were limited by the sensitivity of the CK-MB assay. In contrast, the troponin assay possesses unparalleled specificity and sensitivity as a marker of myocyte damage and has facilitated the diagnosis of ACS, microinfarction, and non-ST elevation MI (NSTEMI).

In this patient, the presence of chest pain and elevated troponin levels resulted in a diagnosis of ACS. Approximately 94% of all myocardial infractions are due to acute occlusion of a coronary vessel associated with plaque rupture; (3) however, this patient's sex and age, as well as the absence of coronary artery disease, suggest that vasospasm may have resulted in transient ischemia. Furthermore, the ECT-induced seizure results in a profound alteration of the systemic autonomic nervous system. (4) This autonomic alteration is thought to be the etiologic mechanism of coronary artery vasospasm. Therefore, I hypothesize that the ECT-induced seizure that this patient experienced resulted in significant autonomic dysfunction, producing coronary artery vasospasm and subsequent myocardial ischemia.

Vasospasm-induced myocardial ischemia may be a complication of ECT and should be suspected in young individuals who present with signs and symptoms of MI after ECT, regardless of cardiac history or cardiac risk factors. This may become increasingly evident with the nearly universal use of troponin markers to detect microinfarction, ACS, and NSTEMI and may indicate that cardiac complications of ECT are more frequent and more severe than previously reported.

I have no financial support or proprietary interests to disclose in connection with this letter.

References

(1.) 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.

(2.) Dec GW Jr, 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;253:2525-2529.

(3.) Betriu A, Pare JC, Sanz GA, et al. Myocardial infraction with normal coronary arteries: A prospective clinical-angiographic study. Am J Cardiol 1981;48:28-32.

(4.) Jones RM, Knight PR. Cardiovascular and hormonal responses to electroconvulsive therapy: Modification of an exaggerated response in an hypertensive patient by [beta]-receptor blockade. Anaesthesia 1981;36:795-799.

Stephen M. Selkirk, MD, PHD

Department of Neurology

University Hospital of Cleveland

Cleveland, OH