Oxidative stress and inflammatory marker: possible pathogenic role in acute coronary syndrome

Acute coronary syndrome [ACS], which comprise unstable angina [UA] and acute myocardial infarction [AMI] are multifactor diseases involving both thrombotic and inflammatory processes. C-reactive protein [CRP] has emerged as independent risk indicator of active atherosclerosis. Reactive oxygen species [ROS] are key mediators of signaling pathways that underlie vascular inflammation in atherogenesis starting from the initiation of fatty streak development through lesion progression to ultimate plaque rupture. CRP directly up-regulate AND[P]H oxidase p22 [phox] and enhance ROS generation. Recently it has been shown that 8-iso-prostaglandin F2 alpha [8-iso-PGF2_] is a specific, chemically stable and quantitative marker of oxidative stress in vivo. It is formed in situ in cell membranes following free radical attack on the arachidonic acid. To counteract the effect of ROS, cells are endowed with a complex antioxidant network that operates to prevent or limit oxidant damage. The present study was designed to investigate the changes of 8-iso-PGF2_, total antioxidant capacity [TAC] and CRP levels in patients with acute coronary syndrome in order to evaluate the role of oxidative stress as well as inflammation in pathogenesis and consequence of the disease. The present study included 30 patients with ACS and 15 healthy, age and sex-matched controls. The patients were divided into two groups; 15 patients with UA and 15 patients with AMI. Serum leuel of 8-iso-PGF2-_ was measured using an ELISA kit Serum CRP and TAC levels was measured by turbidimetric immunoassay and colorimetric methods respectively. Serum levels of both 8-iso-PGF2- _, and CRP were significantly increased in patients compared with control [p<0.05]. TAG showed significant decrease in patients with AMI when compared to controls [p<0.05]. It could be concluded that elevated levels of 8-iso-PGF2-_ and CRP together with decreased TAC level contribute directly and actively to the pathogenesis of ACS. The oxidative stress is likely to either induce or intensify the inflammatory action, and may co-affect with inflammatory factors to accelerate plaque rupture. The evaluation of oxidative stress would enable formulation of specific antioxidant therapy as promising strategy against atherogenesis for an early intervention and better management of the disease

study of autonomic functions in patients with mitral valve prolapse

This work was performed to evaluate autonomic functions by cardiovascular reflexes among patients with mitral valve prolapse [MVP]. It comprised 45 patients [16 males and 29 females] with MVP diagnosed on clinical and echocardiographic basis. Twenty-three normal individuals [7 males and 16 females] with matched sex, age, weight, height and body mass index were taken as a control group. Abnormal autonomic functions had been observed in the MVP patients in the form of parasympathetic dysfunction and inappropriate [imbalance] sympathetic response to different stress in the form of hyperactive early response and hypoactive response on sustained stress and this autonomic imbalance was not related to age or sex but could be related to the severity of MVP. The degree of autonomic affection [quantitative defect] was related to the presence of symptoms among the studied MVP patients. The symptomatology of MVP was not related to sex, severity of MVP, but it was related to the younger age group