Release of neuron-specific enolase and S100 after implantation of cardioverters/defibrillators.
OBJECTIVE
Repeated induction of ventricular fibrillation with ensuing alterations in electroencephalogram and jugular venous oxygen saturation is common practice during insertion of transvenous implantable cardioverters/defibrillators. We investigated whether these functional changes are also associated with cerebral injury.


METHODS
Prospective study.


METHODS
University hospital.


METHODS
We studied 45 patients undergoing implantable cardioverter/defibrillator insertion. Eleven patients with cardiac pacemaker implantation, which was performed in the same manner yet without the necessity to induce ventricular fibrillation, served as controls.


RESULTS
Serum neuron-specific enolase and S100 were determined before, immediately postoperatively, and 2 hrs postoperatively. In a randomly composed subgroup, neuron-specific enolase was also determined 6 and 24 hrs after surgery. Implantable cardioverter/defibrillator patients only showed an increase of both markers postoperatively. Median neuron-specific enolase values climbed from a preoperative 9.9 to 12.3 and 14.4 microg/L at 2 and 24 hrs after surgery, respectively. This increase was associated with the number of shocks and the cumulative time in circulatory arrest. The highest median S100 level (0.075 microg/L) was reached 2 hrs after the procedure. Neuron-specific enolase and S100 were extremely elevated (13.7 and 0.970 microg/L, respectively) in one patient after an extended episode of ventricular fibrillation. Plasma hemoglobin levels were in the normal range in implantable cardioverter/defibrillator patients throughout the observation period.


CONCLUSIONS
Apparently, even brief successive periods of global cerebral ischemia cause neuronal damage without obvious severe neurologic deficits. However, they may be related to subtle postoperative neurologic or cognitive dysfunctions that a number of implantable cardioverter/defibrillator patients exhibit after implantation.
Dworschak
Martin
M
Division of Cardiothoracic Anesthesia and Intensive Care, University Hospital, Vienna, Austria. matin.dworschak@univie.ac.at
Franz
Maximilian
M
Czerny
Martin
M
Gorlitzer
Michael
M
Blaschek
Marieluise
M
Grubhofer
Georg
G
Haider
Wolfram
W
D000368:Aged; D002545:Brain Ischemia / Q000097:blood / Q000209:etiology*; D002560:Cerebrovascular Circulation; D017147:Defibrillators, Implantable / Q000009:adverse effects*; D005260:Female; D006324:Heart Arrest, Induced / Q000009:adverse effects*; D006801:Humans; D008297:Male; D016343:Monitoring, Intraoperative; D010751:Phosphopyruvate Hydratase / Q000097:blood*; D011184:Postoperative Period; D011446:Prospective Studies; D009418:S100 Proteins / Q000097:blood*; D017180:Tachycardia, Ventricular / Q000628:therapy
D009418:S100 Proteins; D010751:Phosphopyruvate Hydratase