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Published on: March 28, 2025
Hyperlactemia Predicts Surgical Mortality in Patients Presenting With Acute Stanford Type-A Aortic Dissection
Jeremy M Bennett1, Eric S Wise2, Kyle M Hocking3
1Division of Cardiovascular Anesthesiology, Vanderbilt University Medical Center, Nashville, TN.
Objective:
Inspired by the limited facility of the Penn classification, the authors aimed to determine a rapid and optimal preoperative assessment tool to predict surgical mortality after acute Stanford type-A aortic dissection (AAAD) repair.
Design:
Patients who underwent an attempted surgical repair of AAAD were determined using a de-identified single institution database. The charts of 144 patients were reviewed retrospectively for preoperative demographics and surrogates for disease severity and malperfusion. Bivariate analysis was used to determine significant (p≤0.05) predictors of in-hospital and 1-year mortality, the primary endpoints. Receiver operating characteristic curve generation was used to define optimal cut-off values for continuous predictors.
Setting:
Single center, level 1 trauma, university teaching hospital.
Participants:
The study included 144 cardiac surgical patients with acute type-A aortic dissection presenting for surgical correction.
Interventions:
Surgical repair of aortic dissection with preoperative laboratory samples drawn before patient transfer to the operating room or immediately after arterial catheter placement intraoperatively.
Measurements And Main Results:
The study cohort comprised 144 patients. In-hospital mortality was 9%, and the 1-year mortality rate was 17%. Variables that demonstrated a correlation with in-hospital mortality included an elevated serum lactic acid level (odds ratio [OR] 1.5 [1.3-1.9], p<0.001), a depressed ejection fraction (OR 0.91 [0.86-0.96], p = .001), effusion (OR 4.8 [1.02-22.5], p = 0.04), neurologic change (OR 5.3 [1.6-17.4], p = 0.006), severe aortic regurgitation (OR 8.2 [2.0-33.9], p = 0.006), and cardiopulmonary resuscitation (OR 6.8 [1.7-26.9], p = 0.01). Only an increased serum lactic acid level demonstrated a trend with 1-year mortality using univariate Cox regression (hazard ratio 1.1 [1.0-1.1], p = 0.006). Receiver operating characteristic analysis revealed optimal cut-off lactic acid levels of 6.0 mmol/L and 6.9 mmol/L for in-hospital and 1-year mortality, respectively.
Conclusion:
Lactic acidosis, ostensibly as a surrogate for systemic malperfusion, represents a novel, accurate, and easily obtainable preoperative predictor of short-term mortality after attempted AAAD repair. These data may improve identification of patients who would not benefit from surgery.
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