Background: Acute Stanford Type A aortic dissection (ATAAD) is a devastating disease requiring immediate surgery. A life-threatening complication hereby represents organ malperfusion. Lactate is a product of anaerobic glycolysis indicating organ malperfusion. The current study analyzes preoperative lactate acidosis as a surrogate marker for patients' outcome after surgery for ATAAD over a 15-year period. Methods: In a single-center setting, 306 consecutive patients, who underwent surgery for ATAAD between 2000 and 2016, were analyzed retrospectively. Serum lactate measurements were taken before surgery. To define a simple cut-point of the predictor lactate, the maximally selected rank statistics method was used. Results: Median survival was 9.3 ± 0.5 and CI 95% [8.3-10.2] years. Mean lactate levels were 1.95 mmol/L ± 2.19 mmol/L (range: 0.15-19.27 mmol/L). Patients with a lactate level > 3.71 mmol/L had a higher 30-day mortality compared to patients with lactate levels ≤ 3.71 mmol/L (51.5% versus 18.7%). In a logistic regression model adjusted for clinical baseline characteristics at index procedure, lactate levels > 3.71 mmol/L reached the highest Odd for 30-day mortality of all tested risk factors (OR = 7.292; CI95% [3.029-17.555]; p < 0.0001). Analyzing the overall mortality, the early effect of lactate level > 3.71 mmol/L persists. The HRs for overall mortality, however, revealed substantially lower effects (HR = 2.772; (CI95% [1.689-4.550]; p < 0.0001). In patients who survived the first 30 days postoperatively, no clinical parameter other than age had a significant impact on survival, including lactate > 3.71 mmol/L (p = 0.494). Conclusions: In patients with ATAAD, preoperative lactate represents an easily obtainable surrogate marker for organ malperfusion. A preoperative lactate level > 3.71 mmol/L depicts the strongest marker for early mortality after surgery.