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Dmitriy Kireyev and Kian-Keong Poh
American Heart Hospital Journal Volume 8 No.1

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Baclofen withdrawal syndrome is a rare and potentially life-threatening condition manifesting with autonomic dysreflexia, high fevers, spasticity, seizures, and multiorgan failure. Reversible cardiomyopathy due to this condition is extremely rare. A high level of suspicion is needed to recognize this condition and start an early intervention to improve patient outcome. Electrocardiographic ST-segment elevation in lead aVR was previously described in association with left main, left anterior descending, and triple-vessel coronary artery disease as well as Takotsubo cardiomyopathy. In this article we present a rare case of reversible cardiomyopathy due to baclofen withdrawal syndrome associated with diffuse ST-segment depressions and ST-segment elevation in lead aVR.

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Baclofen intrathecal infusion is frequently used to treat muscle spasticity of spinal or cerebral origin. Hyperthermia, hemodynamic instability, rebound spasticity, and multiorgan failure are some of the manifestations of abrupt discontinuation of therapy.^1,2 Due to the heterogeneity of symptoms at presentation it is often hard to elicit a correct diagnosis, as baclofen withdrawal syndrome may be mistaken for a severe infectious process. Very few cases of reversible cardiomyopathy associated with this condition have been described. We present a challenging case of a young man presenting with ischemic-looking electrocardiogram (ECG) changes, fever, hypotension, and global left ventricular hypokinesis.

Case Report
A 23-year-old man with a history of quadriplegia and muscular spasticity secondary to a previous motor vehicle accident presented to the emergency department for refill of his baclofen pump. He had no known cardiovascular risk factors and no history of drug (cocaine) abuse. He had missed an earlier appointment to refill his baclofen pump, which ran out. He had a low-grade fever for a few days. One to two hours after refill, he spiked a fever of 40.8°C. The patient's heart rate was noted to be 105 beats per minute (bpm). His blood pressure was fluctuating widely. On physical examination, he appeared diffusely spastic. Cardiovascular examination revealed regular tachycardia at 120bpm, absence of cardiac murmurs, and lack of jugular venous distension. The lungs were clear to auscultation bilaterally. His abdomen was non-distended and not tender. There was no lower-extremity edema. The patient's skin was dry and hot. Serum for investigations and blood cultures were obtained. Within five minutes of blood drawing, the patient suddenly became bradycardic. Telemetry monitoring showed sinus bradycardia at 38bpm. The patient started complaining of shortness of breath. Despite increasing his oxygen to 8l/minute via a nasal cannula, oxygen saturation dropped to 86% (measured by pulse oxymetry). He started looking ashen and his responsiveness rapidly declined. A code blue was called.

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