ABSTRACT
The aim of the present work was to study the possible relationships between each of plasma adiponectin level, myeloperoxidase [MPO] activity, serum nitric oxide [NO] metabolites and the occurrence and the severity of coronary atherosclerosis. It also aimed to detect potential interaction among these factors and to find if there is relationship between these factors and some of the traditional CAD risk factors. In order to achieve this goal, 48 male subjects were evaluated and divided into 4 groups who had coronary angiography to evaluate the severity of coronary atherosclerosis if present; group I consisted of 12 CAD patients with single vessel disease, group II consisted of 12 CAD patients with double vessel disease, group III consisted of 12 CAD patients with multivessel disease, and group IV [control group] consisted of 12 individuals of matched age and sex presented with chest pain with normal coronary angiography. Following proper selection of patients and control subjects, the following laboratory tests were performed for all of them: determination of plasma adiponectin concentration, estimation of MPO activity, determination of serum NO metabolites concentrations [nitrite / nitrate] and determination of serum lipids concentration [total cholesterol, triglycerides [TG], high density lipoprotein-cholesterol [HDL-ch], and low density lipoprotein-cholesterol [LDL-ch]]. The result of the present study showed significant association between the occurrence of CAD and each of low adiponectin level, high MPO activity, low nitrite level, low nitrate level, high total cholesterol level, high TG level, high LDL-ch level, low HDL-ch level and high LDL/HDL-ch ratio. They may all be regarded as predictors or risk factors for CAD. Furthermore, adiponectin, MPO activity, nitrite, total cholesterol, LDL-ch and LDLJHDL-ch ratio were the factors that affected the severity of coronary atherosclerosis. Significant correlation was found between low adiponectin level and atherogenic lipid profile. Moreover, the present study showed significant decrease in adiponectin level in hypertensive and cigarette smoking CAD patients compared to normotensive and non cigarette smoking CAD patients suggesting that low adiponectin level might interact with these traditional risk factors to induce oxidative stress and endothelial dysfunction, thereby promoting atherosclerosis. Furthermore, significant correlation was found between high MPO activity and each of cigarette smoking and atherogenic lipid profile in CAD patients suggesting a possible interaction between MPO and these risk factors to induce and promote oxidative stress and vascular inflammatory process in coronary atherosclerosis. However, there was no significant correlation between MPO activity and hypertension. Another point of interest in the results of the present study was the significant correlation of both low adiponectin level and high MPO activity with NO metabolites [nitrite / nitrate] level. Such correlation suggests that NO could be a link parameter and a common mediator for the action of adiponectin and MPO activity. The latter result highlights the importance of NO as both diagnostic tool and therapeutic target in atherosclerosis. The present study supports the hypothesis that endothelial dysfunction, vascular inflammation, and oxidative stress are primary interacting mediators in the pathogenesis of coronary atherosclerosis. It also highlights the importance of adiponectin as a marker for the presence and extent of CAD. MPO might serve as a marker of a general capacity for oxidative damage to the vasculature rather than functioning solely through direct consumption of NO. Furthermore, NO can act as a predictor of CAD severity, a mediator of coronary atherosclerosis and a common mediator of the action of adeponectin and MPO