Cardiac conduction and rhythm disturbances in a patient with postinfectious polyradiculoneuritis and unilateral diaphragmatic paralysis

Abstract

Introduction: Autonomic dysfunction, ranging from labile blood pressure to life-threatening cardiac conduction and rhythm disturbances, can result as a consequence of postinfectious polyradiculoneuritis. Case report description: We report the case of a 57-year-old male admitted to our hospital for intense dyspnoea and chest pain when changing to supine position. The symptoms installed four months previously, following an episode of acute pneumopathy. At that moment he was diagnosed with left diaphragmatic paralysis, the native cranian and cervico-thoracic CT scan was normal and any chronic autoimmune disease was ruled out. In the supine position, we found an intensely dyspnoeic patient, the ECG showing progressive bradycardia, sinus arrest and episodes of accelerated idioventricular rhythm. With any change in body position the symptoms and the conduction abnormalities disappeared and the heart rate stabilized at 120 beats/min. The neurologic examination showed signs of C7-T11 left and T6-T8 right polyradiculitis, associated with left brachial plexitis and a secondary myasthenic syndrome. Although the patient presented months after the onset of symptoms, treatment with dexamethasone was initiated and continued for a month with significant symptomatic and electromyographic improvement. Following therapy, the Holter ECG control monitoring showed no further cardiac conduction or rhythm disturbances, as a result the electrophysiology team deciding there was no need for the insertion of a permanent cardiac pacemaker. The patient had several episodes of symptomatic exacerbations over the following year that responded each time to cortisonic treatment. Discussion: Autonomic dysfunction represents a severe, but usually transient complication of postinfectious polyradiculoneuritis. Serious bradyarrhythmias result from either an under activity of the sympathetic pathways or an excessive activity of the parasympathetic ones. The peculiarity of the case reported consists in the presence of the cardiac conduction and rhythm disturbances only in relation to the supine position. The anomaly can be explained as a consequence of the left diaphragmatic paralysis and may be caused by two mechanisms: the compression of the vegetative cardiac plexuses at the base of the heart and the upward traction of the celiac plexus by the elevated diaphragm, leading to parasympathetic stimulation. Conclusion: Cardiac autonomic impairment can be a complicating factor in postinfectious polyradiculoneuritis. Careful monitoring of these patients by a team formed by cardiology, electrophysiology and neurology specialists is mandatory.