Reversible left ventricular dysfunction associated with Guillain-Barré syndrome--an expression of catecholamine cardiotoxicity?

The patient was a 76-year-old female who had a history of Guillain-Barré syndrome 3 years previously; ST-segment elevation was noted in association with reversible left ventricular dysfunction. Left ventrioculogram and coronary angiograms were normal and ergonovine test was negative during the chronic period of Guillain-Barré syndrome. She was hospitalized again due to the recurrence of Guillain-Barré syndrome. Two days later, ST-segment elevation in leads V2 through V5 prompted us to perform cardiac catheterization, although she did not complain of any chest symptoms. A large akinetic area was found mainly around the apex on left ventriculography, despite the lack of coronary stenoses. Peak creatine kinase and C-reactive protein were 400 IU/ml and 3.5 mg/dl, respectively. Left ventricular dysfunction was normalized within one week. During the acute phase of the cardiac episode, plasma norepinephrine and epinephrine were 1340 pg/ml and 112 pg/ml, respectively. I123 metaiodobenzyl-guanidine myocardial scintigram 3 weeks after the episode showed an extensive apical defect which was improved markedly 3 months later. We think that this reversible left ventricular dysfunction was due to the synergistic toxic effect of mildly increased catecholamine and transiently damaged sympathetic nerve endings in the myocardium, presumably due to Guillain-Barré syndrome.