P200Biochemical markers in patients with coronary artery disease and diabetes mellitus: prospective observational study

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The role of chronic inflammation in development of cardiovascular complications in patients with coronary artery disease (CAD) and diabetes mellitus (DM) has been widely discussed in recent decades.

Purpose: To perform a prospective comparative analysis of lipid profiles and markers of inflammation and endothelial dysfunction in groups of CAD patients with and without DM.

Methods: 86 patients aged 60.3±9.8 years with CAD and stable angina were divided into two groups: I group included patients with CAD (n=33) and II group – CAD patients with type 2 DM (n=53). Selective coronary angiography showed no signs of significant coronary stenosis in all patients.

Results: Serum laboratory tests were performed during the course of standard therapy at baseline and in 12±2.4 months of observation. At baseline, patients of II group had significantly increased atherogenic indices of the lipid profile (total cholesterol, LDL, apolipoprotein B) and inflammation markers (high-sensitivity C-reactive protein, homocysteine, interleukin-1β) compared to I group. Group I had higher levels of soluble CD40 ligand (CD40L). In II group patients with CAD and DM had more numerous and highly significant interrelations between atherogenic lipid fractions (lipoprotein (a), LDL), inflammatory markers (high-sensitivity C-reactive protein, homocysteine, interleukins, tumor necrosis factor-α), endothelial functional activity indices (endothelin-1), thrombogenic factors (soluble CD40L), and glycated hemoglobin. A prospective observational study showed the absence of significant positive changes in the lipid profile and the preserved prolonged inflammation response as indicated by interleukin-1β, high-sensitivity C-reactive protein, homocysteine, matrix metalloproteinases and the presence of disorders in the endothelin system in both groups of patients.

Conclusion: The study showed that prolonged endothelial inflammatory process is an initiating factor of atherosclerotic process destabilization in patients with CAD and DM.

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