Cardiovascular diseases among Egyptian patients with rheumatoid arthritis and its relation to traditional risk factors

Rheumatoid arthritis [RA] is associated with increased mortality which is due to accelerated coronary artery and cerebrovascular atherosclerosis and researchers have not been able to clearly identify specific aspects of RA or its treatment that might higher the risk for cardiovascular [CV] disease. Prevalence of CV events in patients with rheumatoid arthritis. Effects of rheumatoid arthritis as a risk factor in developing CV diseases as well as influence of early and proper treatment on such risk. Association between RA as a risk factor and other traditional risk factors on CV diseases. 300 patients with RA and 150 controls matched with age and sex were subjected to full clinical assessment, laboratory investigations especially for rheumatoid factor [RF], erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], electrocardiography [ECG], conventional radiographs of both hands and feet to detect joint erosions and Doppler echocardiography. 13.5% of patients with RA has CV events, 7% for myocardial infarction and 2% for stroke. RA-related risk factors [extra articular disease, joints erosions and presence of RF were associated with CV events, the use of disease modifying antirheumatic drugs [DMARDs] were associated with lower risk for CV events. Our study confirm the role of traditional risk factors and their interplay with RA-retated risk factors in development of CV events. It also supports the beneficial effects of some DMARDs in lowering such risks

Subclinical atherosclerosis in patients with early rheumatoid arthritis

Rheumatoid arthritis [RA] patients have increased mortality and morbidity as a result of cardiovascular [CV] and cerebrovascular diseases. Surprisingly the extent of atherosclerosis [AS] in RA is not known, nor have standard CVD risk factors have been fully evaluated. Study of these changes in early RA and early diagnosis of AS in this population might trigger more aggressive prophylaxis. To demonstrate subclinical atherosclerosis in early RA and possible underlying mechanism. 60 patients with early RA and 40 controls matched for age, sex and traditional risk factors for AS were selected. All patients and controls were subjected to a complete history and full clinical examination, laboratory assessment and carotid ultrasonography. Patients with early RA had average greater cIMT than controls and an increased prevalence of atherosclerotic plaques. Positive association between cIMT and age, joint count, disease activity score [DAS], smoking, serum cholesterol and c-reactive protein [CRP] were observed. Age and CRP were independently associated with atherosclerosis. Patients with early RA developed accelerated atherosclerosis compared with controls. Age and CRP are strong predictors for occurrence of CV disease before onset of symptoms

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