Background: Neurological injuries are frequent following Acute Type A Aortic Dissection (ATAAD) repair occurring in 4-30% of all patients. Our objective was to study whether S100B can predict neurological injury following ATAAD repair.
Methods: This was a single-center, retrospective, observational study. The study included all patients that underwent ATAAD repair at our institution between Jan 1998 and Dec 2021 and had recorded S100B-values. The primary outcome measure was neurological injury, defined as focal neurological deficit or coma diagnosed by clinical assessment with or without radiological confirmation and with a symptom duration of more than 24 hours. Secondary outcome measures were 30-day mortality and postoperative complications.
Results: 538 patients underwent surgery during the study period and 393 patients, had recorded S100B-values. The patients had a mean age of 64.4 ± 11.1 years and 34% were female. Receiver operating characteristic (ROC) curve for S100B 24 hours postoperatively yielded area under the curve (AUC) 0.687 (95% CI 0.615-0.759) and best Youden’s index corresponded to S100B 0.225 which gave a sensitivity of 60% and specificity of 75%. Multivariable logistic regression identified S100B ³ 0.23 mg/l at 24 hours as an independent predictor for neurological injury (OR 4.71, 95% CI 2.59-8.57; p<0.01) along with preoperative cerebral malperfusion (OR 4.23, 95% CI 2.03-8.84; p<0.01) as well as an independent predictor for 30-day mortality (OR 4.57, 95% CI 1.18-11.70; p<0.01).
Conclusions: We demonstrated that S100B, 24 hours after surgery is a strong independent predictor for neurological injury and 30-day mortality after ATAAD repair.
Trial registration: As this was a retrospective observational study it was not registered.