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Introduction: Glycaemic control in diabetic patients is directly related to the severity of Coronary Artery Disease (CAD) and increased morbidity and mortality rates. Inflammation plays an important role in the pathogenesis of disease and inflammatory markers such as High sensitive C-Reactive Protein (hsCRP), and inflammatory cytokines such as Interleukin-6 (IL-6), and Tumour Necrosis Factor-alpha (TNF-α) have been found to be implicated in the initiation and progression of CAD. Literature suggests that inflammation is a key feature for atherogenesis in Type 2 Diabetes Mellitus (T2DM). Aim: To compare the severity of CAD and assess the level of glycaemic control and inflammatory mediators in CAD patients with and without T2DM. Materials and Methods: The present prospective study was conducted on 80 angiographically diagnosed CAD patients (aged >30 years) with (40) and without (40) T2DM. The metabolic risk factors including levels of blood sugar fasting and postprandial were assessed by Glucose Oxidase Peroxidase (GODPOD) method, and glycated haemoglobin (HbA1c) level by “Nycocard” reader. Serum Total Cholesterol (TC) was estimated by CHOD-POD method, Triglyceride (TG) by GPO-PAP method, and High density lipoprotein-cholesterol (HDL-C) by Immunoinhibition method. Low-density lipoprotein cholesterol (LDL-C) and Very low-density lipoprotein (VLDL-C) was calculated by Friedewald formula. Serum insulin, hsCRP, IL-6, TNF-α levels was assessed by sandwich Enzyme linked Immunosorbent Assay (ELISA), and Homeostasis Model was used for assessment of insulin Resistance (HOMA-IR). Chi-square test, Independent t-test and ANOVA were used for statistical analysis, and p-value <0.05 considered as significant. Results: The level of hsCRP, IL-6, TNF-α, and HbA1c was significantly increased due to cytokines released by monocytes/ macrophages mediated β-cell damaging process. Diabetic patients with poor glycaemic control, i.e., HbA1c >8.5%, had higher incidence of triple/multivessel disease suggesting involvement of higher number of coronary vessels with higher severity of the stenosis. Among lipid profile, significantly raised TG and LDL-C levels (p<0.005) and significantly decreased HDL-C in CAD patients with T2DM and its severity (p<0.005) was observed. Significantly elevated inflammatory markers, hsCRP, IL-6 and TNF-α were found to be associated with severity of CAD. Conclusion: Combinatorial analysis of glycaemic control (HbA1c) and serum cytokines (IL-6, TNF-α, and hsCRP) with clinical risk factors (Triglyceride and LDL-C) may contribute to the assessment of the severity of CAD, and thereby help in the risk stratification of T2DM and CAD.