ABSTRACT
BACKGROUND AND AIMS: There is evidence demonstrating the influence of oxidative stress on atherosclerosis progression and cardiovascular diseases (CVD). However, different from dyslipidemia and inflammation, nonoxidative biomarkers have been applied to analyze the primary or secondary prevention treatment of these patients. Many factors can explain this paradox: the higher complexity of the methods applied to quantify oxidative markers, the high variability observed among the studies, lack of reference values and weak correlation with clinical endpoints. METHODS: In this review, data from 116 treatments in 55 studies that evaluated oxidative stress markers under the atherosclerotic context were included RESULTS: showed that antioxidant capacity measured as Ferric Reducing Antioxidant Power (FRAP), Superoxide Dismutase (SOD), Glutathione (GSH), Malondialdehyde (MDA), oxidized LDL (oxLDL) and Isoprostanes (F2-IsoP) were the oxidative markers more present. From them, MDA, IsoPs and oxLDL are directly formed from lipid oxidation, while FRAP, SOD and GSH have their values associated to general oxidative conditions. Among the lipid oxidative markers, MDA had the highest proportion among the treatments. A higher concentration of MDA (p»0.041) in patients with CVD (17.05 ± 37.24 mmol/L, n»51) was found than in healthy individuals (5.07 ± 7.54 mmol/L, n»21), despite the high general variability (235.85%). CONCLUSIONS: Multivariate analysis suggested that MDA was an independent factor compared with traditional markers used in the algorithms to stratify the patient's risk. Thus, it is necessary to achieve a reference value for patients under prevention, and correlate MDA increase according to the disease's progression before including it in the algorithms applied to estimate CVD risk.
