Key result
HbA1c, triglycerides, and urea predict cardiac autonomic neuropathy severity in T2D, affecting ~83% of patients.
Why the study?
Cardiac autonomic neuropathy carries heightened cardiovascular risk and early mortality in T2DM, but its metabolic determinants remain incompletely elucidated.
Are glycemic, lipid, and renal markers associated with the presence and severity of cardiac autonomic neuropathy in patients with type 2 diabetes?
Case-Control (n=200)
No
Are glycemic, lipid, and renal markers associated with the presence and severity of cardiac autonomic neuropathy in patients with type 2 diabetes?
p-value: p=<0.0001
Poor glycemic control, dyslipidemia, and subtle renal dysfunction are strong independent predictors of cardiac autonomic neuropathy in patients with type 2 diabetes.
Metabolic markers associated with CAN severity in T2D; hypothesis-generating and leaves open whether targeting them alters progression.
Background: Cardiac autonomic neuropathy (CAN) represents one of the most overlooked yet clinically consequential complications of type 2 diabetes mellitus (T2DM), as it predisposes patients to heightened cardiovascular risk and contributes substantially to early mortality. While cardiovascular autonomic reflex tests (CARTs) provide standardized diagnostic tools, the metabolic determinants of CAN remain incompletely elucidated. Objective: This study aimed to identify glycemic, lipid, and renal predictors of CAN and to determine their associations with CART-derived indices in Iraqi patients with T2DM. Methods: A case–control study was conducted in Mosul, Iraq, between October 2024 and January 2025, enrolling 100 patients with T2DM (≥5 years duration) and 100 age- and sex-matched controls. Clinical data, anthropometry, glycemic markers (HbA1c, fasting plasma glucose), lipid profile (TC, TG, HDL-C, LDL-C, VLDL-C), and renal function (urea, creatinine, proteinuria) were measured using standardized laboratory methods. Autonomic function was assessed via CARTs (Valsalva, E/I, and 30:15 ratios). Associations were analyzed using correlations, multivariable regression, and mediation analysis. Results: CAN was detected in 82.5% of participants, with 40.0% classified as early and 42.5% as definite. HbA1c, TC, TG, LDL-C, VLDL-C, creatinine and serum urea increased progressively with CAN severity (p < 0.0001). CART indices (E/I and 30:15 ratios) declined stepwise across severity groups. Multivariable analysis identified HbA1c, TG, and urea as independent predictors of CAN severity, and mediation modeling suggested that lipid fractions partially mediated the effect of hyperglycemia on autonomic impairment. Receiver operating characteristic (ROC) analysis revealed acceptable discriminatory ability of HbA1c, triglycerides, and urea for definite CAN, with combined models outperforming individual predictors. Conclusion: CAN is highly prevalent among Iraqi patients with T2DM and is strongly associated with poor glycemic control, dyslipidemia, and subtle renal dysfunction. Integrating these metabolic indices may provide an early biochemical signature of CAN risk, underscoring the need for targeted screening and preventive strategies.
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Sondos Amer Abdulraheem1*, Afraa Mohammed Alameen2, Zayd Kays Omer3 (2026) conducted a case-control in Type 2 diabetes mellitus and cardiac autonomic neuropathy (n=200). Type 2 diabetes mellitus and metabolic dysregulation vs. Non-diabetic controls / Normal metabolic parameters was evaluated on Cardiac autonomic neuropathy (CAN) severity (p=<0.0001). HbA1c, triglycerides, and serum urea were identified as independent predictors of cardiac autonomic neuropathy severity, progressively increasing with disease stage (p < 0.0001).
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