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Glycated Hemoglobin is Associated with Glycemic Control and 6-Month Neurologic Outcome in Cardiac Arrest Survivors
Byung Kook Lee1, Dong Hun Lee1, Kyung Woon Jeung1
1Department of Emergency Medicine, Chonnam National University Hospital, 42 Jebong-ro, Dong-gu, Gwangju, Republic of Korea.
Insights
Higher glycated hemoglobin (HbA1c) levels in cardiac arrest survivors undergoing therapeutic hypothermia are linked to worse neurologic outcomes. Glycemic control during hypothermia also differed based on chronic glycemic status.
Area of Science:
- Cardiology
- Neurology
- Endocrinology
Background:
- Chronic glycemic status and its impact on cardiac arrest outcomes are not well understood.
- Investigating the role of glycated hemoglobin (HbA1c) in post-cardiac arrest recovery is crucial.
Purpose of the Study:
- To examine the association between HbA1c and 6-month neurologic outcomes in cardiac arrest survivors treated with therapeutic hypothermia (TH).
- To compare glucose control parameters (mean glucose, AUC) and neuron-specific enolase (NSE) levels between normal and high HbA1c groups during TH.
Main Methods:
- Retrospective analysis of 384 adult comatose cardiac arrest survivors who underwent TH.
- HbA1c levels were used to categorize patients into normal (<6.4%) and high (≥6.4%) groups.
- Neurologic outcome was assessed at 6 months; glucose levels and NSE were measured during TH.
Main Results:
- A high HbA1c level (≥6.4%) was independently associated with unfavorable neurologic outcomes (OR 1.414).
- Patients with high HbA1c experienced more hyperglycemia during TH compared to the normal HbA1c group.
- NSE demonstrated good prognostic performance, but glucose parameters were not independent predictors of outcome after adjustment.
Conclusions:
- Elevated HbA1c is an independent predictor of poor neurologic outcomes in cardiac arrest survivors treated with TH.
- Glycemic control and outcomes during TH are significantly influenced by patients' chronic glycemic status (HbA1c levels).
Background:
Glucose control status after cardiac arrest depending on chronic glycemic status and the association between chronic glycemic status and outcome in cardiac arrest survivors are not well known. We investigated the association between glycated hemoglobin (HbA1c) and 6-month neurologic outcome in cardiac arrest survivors undergoing therapeutic hypothermia (TH) and whether mean glucose, area under curve (AUC) of glucose during TH, and neuron-specific enolase (NSE) are different between normal and high HbA1c groups.
Methods:
This retrospective single-center study included adult comatose cardiac arrest survivors who underwent TH from September 2011 to December 2017. HbA1c and glucose were measured after return of spontaneous circulation (ROSC), and normal or high HbA1c was defined using cutoff value of 6.4% of HbA1c. Blood glucose was measured at least every 4 h and treated with a written protocol to maintain the range of 80-200 mg/dL. Hypoglycemia and hyperglycemia were defined with glucose < 70 or > 180 mg/dL. Mean glucose during induction and rewarming phase and AUC of glucose during every 6 h of maintenance were calculated, and NSE at 48 h after cardiac arrest was recorded. The primary outcome was unfavorable neurologic outcome, defined as Glasgow Pittsburgh Cerebral Performance Category scale 3-5 at 6 months after cardiac arrest.
Results:
Of 384 included patients, 81 (21.1%) had high HbA1c and 247 (64.3%) had an unfavorable neurologic outcome. Patients with high HbA1c were more common in the unfavorable group than in favorable group (27.5% vs 9.5%, p < 0.001), and the unfavorable group had significantly higher HbA1c level (5.8% [5.4-6.8%] vs 5.6% [5.3-6.0%], p = 0.007). HbA1c level was independently associated with worse neurologic outcome (odds ratio 1.414; 95% confidence interval 1.051-1.903). High HbA1c group had higher glucose after ROSC, glucose AUC during maintenance, and rewarming phase than normal HbA1c group. High HbA1c group had significantly higher incidence of hyperglycemia throughout the TH, while normal HbA1c group had significantly higher incidence of normoglycemia. However, no glucose parameter remained as an independent predictor of neurologic outcome after adjustment, irrespective of HbA1c level. NSE showed good prognostic performance (area under curve 0.892; cutoff value 26.3 ng/mL). Although NSE level was not different between HbA1c groups, high HbA1c group had higher proportion of patient having NSE over cutoff.
Conclusions:
Higher HbA1c was independently associated with unfavorable neurologic outcome. Glycemic status during TH was different between normal and high HbA1c groups.
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