Platelet-endothelial cell adhesion molecule-1 (PECAM-1) has role in atherosclerotic plaque development as well as in thrombosis leading to myocardial infarction (MI). Present study was aimed to analyse the association of PECAM-1 Leu125Val gene polymorphism with MI in Indian population. Subjects included healthy individuals as control (N = 116) and MI patients (N = 100) divided into two groups; MI patients at presentation of the acute event (MI-Group-1, N = 46) and patients with recent event of MI stabilized with treatment 4.5 days from their symptoms (MI-Group-2, N = 54). The difference in the distribution of Leu125Val genotype frequencies of controls and patients did not reach statistical significance. However Leu allele frequency (0.57) was more associated with MI patients as compared to control (0.504). sPECAM-1 levels were significantly elevated in patients at acute event of MI (MIGroup-1) by 44.1% (P = 0.009) as compared to controls and by 95.2% (P = 0.001) as compared to stabilized MI patients (MI-Group-2).
A B S T R A C TAims/objective: Over expression of matrix degrading enzymes have been implicated in plaque destabilisation and rupture. Cathepsins associated with extracellular matrix breakdown make them intriguing suspects. The aim of the study was to analyse peripheral levels of cathepsin B and cathepsin K and their inhibitor cystatin C during acute myocardial infarction (AMI).
Materials and methods:Study population included AMI patients at acute event (AMI group, n = 48), stable angina patients (stable angina group n = 17), and healthy individuals (Control group, n = 31).Cathepsin B, cathepsin K, cystatin C, and matrix metalloproteinases (MMP)-9 were analysed by enzyme-linked immunosorbent assay (ELISA) method.Results: Cathepsin B (45.9%) and cathepsin K (92.31%) at acute event of myocardial infarction (AMI group) increased (P = 0.001) while cystatin C decreased marginally (12.5%) as compared to controls. Stable angina group, demonstrated only marginal reduction in all the parameters studied as compared to controls.
Hyperinsulinemia was observed in our non-diabetic hypertensive patients, but no association was found between IMT and insulin resistance. That IMT of hypertensives was associated with triglyceride levels suggests that high levels of insulin may be related to the development of ATH indirectly through its effects on lipid metabolism in our population.
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