RESUMO
Patients with systemic lupus erythematosus (SLE) are 2-10 times more likely to develop cardiovascular disease (CVD) than the general population. The assessment of the risk of developing CVD is an important direction for further clinical management. The study was conducted retrospectively and included patients with SLE. The aim of the study was to assess the measurements of pulse wave velocity (PWV), carotid intima-media thickness (CIMT), ankle-brachial index (ABI) and biochemical parameters. Subclinical atherosclerosis was also assessed. The study included 98 patients with SLE with an age- and sex-matched control group of 68 healthy adults. Statistical significance was found in the SLE group and the controls for N-terminal fragment of pro-B-type natriuretic peptide (NT proBNP) (144.87 vs. 36.41 pg/mL, p = 0.0018), high-sensitivity cardiac troponin (hs-cTn) (25.43 vs. 6.38 ng/L, p = 0.0303) and D-Dimer levels (0.73 vs. 0.36 µg/mL, p = 0.0088), left CIMT (1.03 vs. 0.62 mm, p < 0.0001), right CIMT (0.93 vs. 0.63 mm, p < 0.0001) and PWV CF (9.74 vs. 7.98 m/s, p = 0.0294). A positive correlation was found between NT proBNP and PWV CF (r = 0.6880, p = 0.0498) and hs-cTn and PVW carotid-femoral (CF) (r = 0.8862, p = 0.0499) in SLE. A positive correlation was reported between PWV CF and systolic blood pressure (r = 0.5025, p = 0.0487). The measurement of carotid-femoral PWV is a simple, non-invasive, and reproducible method and may independently predict future CVD events and their cause. Further studies are warranted to establish the prognostic value of PWV in patients with SLE, as it may be superior to CIMT measurements in the early stages of vascular disorders.
RESUMO
Heart failure (HF) is a multifactorial clinical syndrome involving many complex processes. The causes may be related to abnormal heart structure and/or function. Changes in the renin-angiotensin-aldosterone system, the sympathetic nervous system, and the natriuretic peptide system are important in the pathophysiology of HF. Dysregulation or overexpression of these processes leads to changes in cardiac preload and afterload, changes in the vascular system, peripheral vascular dysfunction and remodeling, and endothelial dysfunction. One of the important factors responsible for the development of heart failure at the cellular level is oxidative stress. This condition leads to deleterious cellular effects as increased levels of free radicals gradually disrupt the state of equilibrium, and, as a consequence, the internal antioxidant defense system is damaged. This review focuses on pharmacotherapy for chronic heart failure with regard to oxidation-reduction metabolism, with special attention paid to the latest group of drugs, SGLT2 inhibitors-an integral part of HF treatment. These drugs have been shown to have beneficial effects by protecting the antioxidant system at the cellular level.