T. Hirotani et al., Aortic arch repair using hypothermic circulatory arrest technique associated with pharmacological brain protection, EUR J CAR-T, 18(5), 2000, pp. 545-549
Objective: Hypothermic circulatory arrest is a standard procedure for the t
reatment of aortic arch. However, there is a time limit for this procedure.
There is now an urgent need to develop prophylactic measures to extend the
time Limit. We have used a pharmacological mixture of thiopental, nicardip
ine and mannitol for all patients undergoing circulatory arrest since 1991
to extend the safe limit. The purpose of this study was to analyze the neur
ological complications demonstrated by these patients and to evaluate the b
rain-protective effects of our measure. Methods: The clinical records of 75
consecutive patients undergoing an aortic arch repair using a hypothermic
circulatory arrest technique during thr past 8 years were retrospectively r
eviewed. Systemic cooling was continued until a total disappearance of EEG
activity. Prior to circulatory arrest, 15 or 30 mg/kg of thiopental, 20 mg
of nicardipine and 300 mi of mannitol were infused into the venous reservoi
r of a cardiopulmonary bypass circuit. Graft replacement was performed in a
ll patients and the extent of replacement was a total aortic arch in 43 pat
ients, a distal aortic arch in 17, a hemiarch in 13 and a distal aortic arc
h and a total descending aorta in two. Results: The duration of circulatory
arrest ranged from 16 to 80 min (mean 41.5 min), and it exceeded 45 min in
37 patients. Operative mortality was 10.7% and two patients died of stroke
. Three patients had permanent and three other patients had transient neura
l deficits. The incidence of stroke was 8.0% as a whole, and no correlation
between the incidence of neurological complications and the duration of ci
rculatory arrest was found. A multivariate analysis showed that the duratio
n of circulatory arrest was determined as a predictor of neither operative
mortality nor postoperative stroke. Conclusions: The findings of the presen
t study suggest that our pharmacological brain protection appears to be eff
ective for safely extending hypothermic circulatory arrest. (C) 2000 Elsevi
er Science B.V. All rights reserved.