Abstract

A 73-year-old Caucasian woman admitted to the neurology ward with Guillain–Barre syndrome (GBS) developed acute breathlessness 7 days after the onset of symptoms. Initial presentation was with symmetrical lower limb weakness, patchy sensory loss, absent tendon reflexes, normocellular cerebrospinal fluid (CSF) with raised protein (1.05 gm/l) and absent of waves on electromyography. There were no other associated cardiac symptoms, no neuromuscular respiratory weakness, normal neck muscle power, stable vital capacity and no hypercapnia on arterial blood gas analysis. She was a smoker. No arrhythmias were detected with continuous electrocardiogram (ECG) monitoring that is initiated on admission in the view of the well-recognized risk of autonomic dysfunction with GBS.1 On examination, she was apyrexial, well perfused, in sinus rhythm at a rate of about 70 beats/min and normotensive. There was congestive cardiac failure with elevated jugular venous pressure, bibasal crepitations and a fourth heart sound. Her ECG (Figure 1b) demonstrated downsloping ST segments, T-wave inversion in inferior and precordial leads and a prolonged corrected QT interval at 490 ms. A portable transthoracic echocardiogram revealed apical and antero-septal hypokinesia with impairment of left ventricular function. Troponin was mildly elevated (0.06 ng/ml, normal range <0.04 ng/ml). The differential diagnoses were Acute Coronary Syndrome (ACS) and stress cardiomyopathy. Atherothrombotic disease was a concern considering the prothrombotic risk with intravenous immunoglobulin. She was transferred to …

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