Metabolic syndrome (MS) is not a homogeneous entity, but this term refers to the coexistence of factors that increase the risk for the development of type 2 diabetes and cardiovascular disease. There are different versions of the criteria for the diagnosis of MS, which makes the population of patients diagnosed with MS heterogeneous. Research to date shows that MS is associated with oxidative stress (OS), but it is unclear which MS component is most strongly associated with OS. The purpose of the study was to investigate the relationship between the parameters of OS and the presence of individual elements of MS in young adults, as well as to identify the components of MS by means of principal components analysis (PCA) and to investigate how the parameters of OS correlate with the presence of individual components. The study included 724 young adults with or without a family history of coronary heart disease (population of the MAGNETIC study). Blood samples were taken from the participants of the study to determine peripheral blood counts, biochemical parameters, and selected parameters of OS. In addition, blood pressure and anthropometric parameters were measured. In subjects with MS, significantly lower activity of superoxide dismutase (SOD), copper- and zinc-containing SOD (CuZnSOD), and manganese-containing SOD (MnSOD) were found, along with significantly higher total antioxidant capacity (TAC) and significantly lower concentration of thiol groups per gram of protein (PSH). We identified three components of MS by means of PCA: “Obesity and insulin resistance”, “Dyslipidemia”, and “Blood pressure”, and showed the component “Obesity and insulin resistance” to have the strongest relationship with OS. In conclusion, we documented significant differences in some parameters of OS between young adults with and without MS. We showed that “Obesity and insulin resistance” is the most important component of MS in terms of relationship with OS.

Introduction. Obesity is one of the most important public health problems in the world. Among obese people, there are those who, apart from excessive body weight, do not exhibit other metabolic dysfunctions, have a lower risk of developing cardiovascular diseases (CVDs), and show lower mortality. According to the theory, they are referred as metabolically healthy obese (MHO), in contrast to metabolically unhealthy obese (MUO). Metabolic disturbances occurring with obesity have been well established to be associated with oxidative stress. Aim. The purpose of this study was to analyse the association between selected anthropometric and biochemical parameters with oxidative stress in MHO, MUO, and normal weight young adults. Material and Methods. Individuals with age between 18 and 36 years with no history of chronic diseases and use of medicaments, with or without obesity, participated in the study. Complete blood counts, biochemical measurements, and parameters of oxidative stress such as total antioxidant capacity (TAC), total oxidative status (TOS), oxidative stress index (OSI), serum concentration of malondialdehyde (MDA), ceruloplasmin, thiol groups and lipid hydroperoxides (LPH), concentration of lipofuscin (LPS) in erythrocytes, and the activity of superoxide dismutase (SOD) were measured. Results. 422 patients who met the inclusion criteria were enrolled in the study. Among the study participants, 208 people (49.29%) were offspring of patients with angiographically confirmed coronary artery disease. Among the participants, 16 patients have been included in the group of metabolically healthy obese (MHO) people and 61 patients in the group of metabolically unhealthy obese (MUO) people and 345 patients had normal body weight. Significant differences between metabolically unhealthy obese and normal weight patients, as well as between women and men, have been found. Conclusions. We showed significant differences in the selected parameters of oxidative stress between metabolically unhealthy obese (MUO) individuals and young volunteers with normal body weight as well as without significant medical history.

Red blood cell distribution width (RDW) is a measure of red blood cell volume variations (anisocytosis) and is reported as part of a standard complete blood count. In recent years, numerous studies have noted the importance of RDW as a predictor of poor clinical outcomes in the settings of various diseases, including coronary artery disease (CAD). In this paper, we discuss the prognostic value of RDW in CAD and describe the pathophysiological connection between RDW and acute coronary syndrome. In our opinion, the negative prognostic effects of elevated RDW levels may be attributed to the adverse effects of independent risk factors such as inflammation, oxidative stress, and vitamin D₃and iron deficiency on bone marrow function (erythropoiesis). Elevated RDW values may reflect the intensity of these phenomena and their unfavorable impacts on bone marrow erythropoiesis. Furthermore, decreased red blood cell deformability among patients with higher RDW values impairs blood flow through the microcirculation, resulting in the diminution of oxygen supply at the tissue level, particularly among patients suffering from myocardial infarction treated with urgent revascularization.

Data regarding the association between red cell distribution width (RDW) values and mortality in patients with stable coronary artery disease are scarce. We aimed to investigate the link between mortality and RDW in patients with stable coronary artery disease undergoing percutaneous coronary intervention (PCI).

Background: We aimed to compare statin monotherapy and upfront combination therapy of statin and ezetimibe in patients with acute coronary syndromes (ACSs). Methods and Results: The study included consecutive patients with ACS included in the PL‐ACS (Polish Registry of Acute Coronary Syndromes), which is a national, multicenter, ongoing, prospective observational registry that is mandatory for patients with ACS hospitalized in Poland. Data were matched using the Mahalanobis distance within propensity score matching calipers. Multivariable stepwise logistic regression analysis, including all variables, was next used in propensity score matching analysis. Finally, 38 023 consecutive patients with ACS who were discharged alive were included in the analysis. After propensity score matching, 2 groups were analyzed: statin monotherapy (atorvastatin or rosuvastatin; n=768) and upfront combination therapy of statin and ezetimibe (n=768 patients). The difference in mortality between groups was significant during the follow‐up and was present at 1 (5.9% versus 3.5%; P =0.041), 2 (7.8% versus 4.3%; P =0.019), and 3 (10.2% versus 5.5%; P =0.024) years of follow‐up in favor of the upfront combination therapy, as well as for the overall period. For the treatment, rosuvastatin significantly improved prognosis compared with atorvastatin (odds ratio [OR], 0.790 [95% CI, 0.732–0.853]). Upfront combination therapy was associated with a significant reduction of all‐cause mortality in comparison with statin monotherapy (OR, 0.526 [95% CI, 0.378–0.733]), with absolute risk reduction of 4.7% after 3 years (number needed to treat=21). Conclusions: The upfront combination lipid‐lowering therapy is superior to statin monotherapy for all‐cause mortality in patients with ACS. These results suggest that in high‐risk patients, such an approach, rather than a stepwise therapy approach, should be recommended.