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Updated: Jun 1, 2025

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
Published on: November 29, 2024
The impact of diabetes on Sepsis-induced cardiomyopathy
Weiwei Lai1, Li Liu1, Shuhang Wang1
1Department of Emergency Medicine, Tianjin Medical University General Hospital, Tianjin, China.
Purpose:
This study investigated the association between diabetes and Sepsis-induced cardiomyopathy (SIC), focusing on how changes in inflammatory response and cardiac function influence SIC prognosis. The aim is to provide clinicians with more accurate treatment and management strategies, ultimately enhancing patient outcomes and quality of life.
Methods:
This retrospective cohort study analyzed 258 Sepsis-induced cardiomyopathy (SIC) patients, stratified by diabetes status and HbA1C levels. Data were collected from electronic medical records. Statistical tests included the Kolmogorov-Smirnov, t-test, Mann-Whitney U, Kruskal-Wallis, chi-square, and Spearman correlation. Univariate and multivariate logistic regression assessed diabetes' impact on SIC severity. Model fit was evaluated with the Hosmer-Lemeshow and negative log-likelihood ratio tests. A nomogram was constructed and validated using ROC curves, calibration curves, and decision curve analysis. Subgroup and interaction analyses were performed (P < 0.05).
Results:
Diabetes worsened inflammation and immune responses in SIC, significantly affecting markers like LVEF, TnI, CK-MB, BNP, NLR, IL-6, PCT, CRP, APACHE II, and SOFA scores (P < 0.05). Grouping by HbA1C levels revealed no significant differences in LVEF (P = 0.078), Alb (P = 0.105), or L/A (P = 0.211), but differences were found for TnI, CK-MB, BNP, NLR, IL-6, PCT, CRP, APACHE II, and SOFA (P < 0.05). HbA1C strongly correlated with CRP (rs = 0.8664). BNP (OR 1.001) and HbA1C (OR 1.302) were significant risk factors for SIC, with the nomogram showing good predictive performance (AUC 0.693). No significant interaction between HbA1C and BNP on SIC severity was observed (P = 0.791).
Conclusion:
Diabetes exacerbates inflammatory and immune responses in Sepsis-induced cardiomyopathy patients, leading to worsened cardiac function.
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