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A Journal on Cardiac, Vascular and Thoracic Surgery

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The Journal of Cardiovascular Surgery 2009 October;50(5):665-8

language: English

The role of procalcitonin as predictor for neurological deficits after carotid endarterectomy

Mommertz G. 1, Langer S. 1, Koeppel T. 1, Schiefer J. 2, Mess W. H. 3, Jacobs M. J. 1, Das M. 4

1 European Vascular Center Aachen-Maastricht, Germany-The Netherlands
2 Department of Neurology, RWTH Aachen University Hospital, Germany
3 Department of Neurophysiology University Hospital Maastricht, The Netherlands
4 Department of Diagnostic Radiology, RWTH Aachen, University Hospital, Germany


Aim. Outcome of carotid endarterectomy (CEA) is defined by mortality rate as well as the neurological outcome due to cerebral ischemia. Thus the aim of this study was to evaluate the role of the acute phase protein procalcitonin (PCT) as a predictor for neurological deficits after carotid endarterectomy.
Methods. Fifty-five patients with high grade stenosis of the internal carotid artery and interdisciplinary consensus for endarterectomy were followed. Neurological examination was performed before and after the procedure to analyze perioperative neurological deficits. Blood samples were obtained before and after CEA and procalcitonin was analyzed in 55 consecutive patients (65.5% symptomatic/34.5% asymptomatic).
Results. No perioperative or in-hospital death was observed. Major complications did not occur, two patients suffered from bleeding requiring surgical intervention and one patient had a temporary peripheral facial nerve lesion. Postoperative neurological examination revealed no new deficit, there was no significant change of PCT (level pre- and post-CEA (the mean preoperative PCT was 0.25 ng/mL [SD 0.78, min 0.1, max 4.3]; the mean postoperative PCT was 0.11 ng/mL [SD 0.06, min 0.1, max 0.5]). There was no association found between perioperative neurological deficit and PCT.
Conclusion. The present study demonstrates that there is still not sufficient evidence to recommend PCT measurement as a predictor for perioperative neurological deficit during CEA.

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