Effect of glycemic control and disease duration on cardiac autonomic function and oxidative stress in type 2 diabetes mellitus.

Abstract

Cardiac autonomic neuropathy (CAN) is a commonly overlooked complication of type 2 diabetes mellitus (T2DM), with a complex pathogenesis involving hyperglycemia-induced oxidative stress which results in neuronal ischemia and cellular death. The level of hyperglycemia as well as disease duration might be significant determinants of the prognosis of T2DM, but limited studies have explored their relationship with these diabetic complications. Therefore, the purpose of this study was to examine the effect of glycemic control and disease duration on cardiac autonomic function and oxidative stress in patients with T2DM. 60 T2DM patients along with 63 healthy controls were recruited for the study. Diabetic patients were further classified based on glycemic control (HbA1c levels <8% vs. ≥8%) and disease duration (<5 vs. 5-10 vs. >10years). All participants were assessed for cardiac autonomic function (HRR: heart rate recovery; HRV: heart rate variability), levels of antioxidant enzymes (CAT: catalase; SOD: superoxide dismutase), serum nitric oxide (NO) and other cardiometabolic risk factors (resting blood pressure, glycemic and lipid profile). T2DM patients showed a significant reduction in HRR, HRV, CAT, SOD and an increase in LFnu, LF: HF ratio and NO. These impairments were significantly greater for the group with poor glycemic control (p < 0.05). However, no difference for these parameters was observed with respect to different disease durations. Cardiac autonomic regulation and endogenous antioxidant defense were compromised and levels of nitric oxide found to be raised in patients with Type 2 diabetes. These findings were more pronounced in subjects with poor glycemic control.