ABSTRACT
Background: Few studies have assessed the relation of uric acid level with the severity of coronary artery disease (CAD). This study investigated the association between high uric acid levels with the presence and severity of CAD. Materials and Methods: This study was designed as an observational cohort study. The study was composed of 180 patients admitted at our institution due to symptoms related to CAD. Patients having angiographic evidence of stenosis in coronary artery were as case group and without stenosis control group. Patients with high uric acid (hyperuricemia) were defined as serum uric acid concentration >7.0mg/dl or >420 μmol/L in men and >6mg/dl or >360 μ mol/L in women. The presence of CAD has been defined as the Gensini score being >1. Results: There was a statistically significant difference between the mean uric acid levels of patients with and without CAD (358.23±71.11 μmol/l vs251.32±54.92 μmol/l respectively, p<0.001). There was a statistically significant difference between ejection fraction of patients with and without CAD (54.50±9.25 vs. 63.16±6.56 respectively, p<0.001). Spearman correlation analysis demonstrated a positive correlation between the serum uric acid level and the severity of CAD (p=<0.001, r=0.39). When patients were classified into four groups according to their Gensini score, mean serum uric acid level was found to be significantly increased across the tertiles, and a statistically significant difference was detected between the tertiles (p= <0.001). Conclusion: In conclusion, a significant association has been found between serum uric acid level and the presence and severity of CAD. In addition to the evaluation of conventional risk factors in daily clinical practice, the measurement of uric acid level might provide significant prognostic benefits in terms of global cardiovascular risk and management of the patients.
ABSTRACT
Type 2 Diabetes Mellitus (T2DM) is a complex disease with the co-existence of several pathophysiological abnormalities. Both microvascular and macrovascular complications are the main causes of morbidity and mortality, which develops due to endothelial dysfunction. Upregulation of reactive oxygen species, chronic inflammatory and hypercoagulable states are the pathologic basis of vascular dysfunctions in T2DM. To overcome all these abnormalities, different classes of antihyperglycaemic agents have developed. Unfortunately none is able to show satisfactory glycaemic control and to modulate vascular dysfunction. Incretin hormones are secreted from intestine during meal, which enhance insulin secretion and inhibit glucagon secretion from the pancreas. The incretin effect is severely reduced or absent in T2DM. Incretin-based new antidiabetics, both Dipeptidyl Peptidase-4 (DPP-4) inhibitors (Saxagliptin, Sitagliptin, Vildagliptin) and Glucagon Like Peptide-1 (GLP-1) analogs (Exenatide) are now being used globally. They are almost equally effective as conventional antidiabetics like Sulphonylureas (SU), Metformin (MET), Thiazolidinediones (TZD) and insulin when given as monotherapy or combined with SU, MET or TZD as second line agent. Incretin-based agents do not cause hypoglycaemia, produce weight loss in spite of weight gain and do not retain salt or water and almost no gastrointestinal (GIT) symptoms. The agents correct vascular dysfunctions and dyslipidaemia and can be given in elderly and renal impaired patients.