Introduction: Reactive oxygen species (ROS) are responsible for generalized oxidation which results in cell dysfunction, necrosis or apoptosis. Assessment of oxidative stress markers could modify course of treatment of patients with coronary artery disease (CAD).
The aim of this study was to evaluate association of markers of oxidative stress, stress glycaemia and glycated hemoglobin (HgbA1c) with CAD.
Methods: Crosssectional observational study. Variables: demographics, risk factors and comorbidities,
lipoprotein and glycemic profile, oxidative stress biomarkers: malondialdehyde (MDA) and hydro peroxide
(HP), and antioxidant enzymes: superoxide dismutase (SOD), CATALASE and glutathione peroxidase (GPS).
Comparison was performed between CAD patients and healthy controls, patients with acute coronary syndrome (ACS) versus chronic CAD, and between PCI revascularised and stable post MI patients.
Results: 300 patients, (64.7% m/36.3% f), mean age 62±11 y. (p=ns between genders). 187 (62.3%) were ACS and 113 (37.7%) chronic CAD patients. There was no statistical significant difference in the risk profile
between the CAD groups. Patients with CAD had significantly higher prooxidative and significantly lower antioxidative levels of biomarkers (Table 1), as compared with healthy volunteers. Statistically significant differences were observed for HP and SOD between ACS and HCAD group. In HCAD group, revascularized patients
demonstrated higher oxidative stress as compared to stable post MI patients. In ACS patients statistical
significant intergroup difference was registered, but not pointing to the single type of ACS. ACS patients had
also higher levels of stress glycaemia and HgbA1c. Significant positive correlation were found for HgbA1c and stress glycaemia with MDA (r=,154**, p=0,008; r=,254**, p=0,024 respectively).
Conclusion: CAD patients demonstrated pronounced oxidative stress when compared to healthy controls, ACS
patients had higher oxidative stress as compared with chronic CAD patients, PCI subgroup performed worse
that stable post MI patients. Higher oxidative stress activity was linked to worse glycemic control as measured
threw stress glycaemia and HbA1c
