One of the greatest burdens on the healthcare systems of modern civilization is cardiovascular diseases (CVDs). Therefore, the medical community is looking for ways to reduce the incidence of CVDs. Simple lifestyle changes from an unhealthy to a healthy lifestyle are the cornerstone of prevention, but other risk factors for cardiovascular disease are also being currently targeted, most notably dyslipidaemia. It is well known that lowering serum lipid levels, and in particular lowering elevated LDL-cholesterol, leads to a reduction in major cardiovascular events. Although the focus to date has been on LDL-cholesterol levels and lowering them with statin therapy, this is often not enough because of increased concentrations of other lipoprotein particles in the serum and residual cardiovascular risk. Since lowering LDL-cholesterol levels is successful in most cases, there has been a recent focus on lowering residual cardiovascular risk. In recent years, new therapeutic options have emerged that target triglyceride-rich lipoproteins, lipoprotein (a) and apolipoproteins C and B. The effects of these drugs on serious adverse cardiovascular events are not yet known, but recent studies with some of these drugs have shown significant results in lowering total lipid levels. The aim of this review is to present the current therapeutic options for the treatment of dyslipidaemia and to describe the newly approved drugs as well as the drugs that are still in development. Although at this stage we cannot say with certainty whether these agents will be approved and widely used, it is safe to say that our views on the treatment of dyslipidaemia are certainly changing.

Background: Carotid-femoral pulse wave velocity (cfPWV), acknowledged as a reliable proxy of arterial stiffness, is an independent predictor of cardiovascular (CV) events. Carotid-femoral PWV is considered the gold standard for the estimation of arterial stiffness. cfPWV is a demanding, time consuming and expensive method, and an estimated PWV (ePWV) has been suggested as an alternative method when cfPWV is not available. Our aim was to analyze the predictive role of ePWV for CV and all-cause mortality in the general population. Methods: In a stratified random sample of 1086 subjects from the general Croatian adult population (EH-UH study) (men 42.4%, average age 53 ± 16), subjects were followed for 17 years. ePWV was calculated using the following formula: ePWV = 9.587 − 0.402 × age + 4.560 × 10⁻³ × age2 − 2.621 × 10⁻⁵ × age2 × MBP + 3.176 × 10⁻³ × age × MBP − 1.832 × 10⁻² × MBP. MBP= (DBP) + 0.4(SBP − DBP). Results: At the end of the follow-up period, there were 228 deaths (CV, stroke, cancer, dementia and degenerative diseases, COLD, and others 43.4%, 10.5%, 28.5%, 5.2%, 3.1%, 9.3%, respectively). In the third ePWV tercile, we observed more deaths due to CV disease than to cancer (20.5% vs. 51.04%). In a Cox regression analysis, for each increase in ePWV of 1 m/s, there was a 14% increase risk for CV death. In the subgroup of subjects with higher CV risk, we found ePWV to be a significant predictor of CV deaths (ePWV (m/s) CI 1.108; p < 0.029; HR 3.03, 95% CI 1.118–8.211). Conclusions: In subjects with high CV risk, ePWV was a significant and independent predictor of CV mortality.

Type 2 diabetes mellitus (T2DM) is a common metabolic disease characterised by insulin resistance and elevated blood glucose levels, affecting millions of people worldwide. T2DM individuals with dyslipidaemia have an increased risk of cardiovascular disease (CVD). A complex interplay of risk factors such as hyperglycaemia, dyslipidaemia, hypertension, obesity, inflammation, and oxidative stress favour the development of atherosclerosis, a central mechanism in the pathogenesis of cardiovascular disease. Dyslipidaemia, a hallmark of T2DM, is characterised by elevated triglycerides, decreased high-density lipoprotein (HDL) cholesterol and the presence of small, dense low-density lipoprotein (LDL) particles, all of which promote atherosclerosis. In this article, we have attempted to present various treatment strategies that include pharmacological interventions such as statins, ezetimibe, PCSK9 inhibitors, fibrates, and omega-3 fatty acids. We have also tried to highlight the pivotal role of lifestyle modifications, including physical activity and dietary changes, in improving lipid profiles and overall cardiovascular health in T2DM individuals. We have also tried to present the latest clinical guidelines for the management of dyslipidaemia in T2DM individuals. In conclusion, the treatment of dyslipidaemia in T2DM individuals is of great importance as it lowers lipid particle levels, slows the progression of atherosclerosis, and ultimately reduces susceptibility to cardiovascular disease.

Dyslipidaemia is one of the main causes of atherosclerotic cardiovascular disease (ASCVD) worldwide. Although statins remain the cornerstone of lipid-lowering therapy, many patients do not achieve optimal target levels of low-density lipoprotein cholesterol (LDL-C) due to intolerance or inadequate response. Bempedoic acid, an oral ATP citrate lyase inhibitor, provides a liver-specific mechanism that lowers LDL-C levels while minimising muscle-related side effects. Recent clinical trials, including the CLEAR Outcomes Study, have shown that bempedoic acid was able to reduce LDL-C by approximately 29 mg/dL and major adverse cardiovascular events (MACEs) by 13% in patients intolerant to statins. Combination therapy with ezetimibe further enhances this effect. However, adverse effects such as increased uric acid and gout have been reported, requiring careful patient selection and continuous monitoring. This review provides a comparative synthesis of the latest evidence on bempedoic acid, including its pharmacological profile, its efficacy in different patient groups, and its place within current treatment strategies for dyslipidaemia. It also identifies research gaps and directions for future studies.

Background/Objectives: Fabry disease (FD) is a genetic lysosomal storage disease caused by a pathogenic variant in GLA gene coding for a functional alpha-galactosidase A enzyme whose disfunction leads to globotriaosylceramide (Gb3) accumulation in cells, which results in multiple organ disorders. The aim of this study was to identify mutations associated with Fabry disease among 829 kidney transplant recipients and to investigate the correlation between the factors such as age, dialysis vintage, eGFR, proteinuria and corticosteroid dose and the deviations in alpha-galactosidase A and lyso-Gb3 levels. Methods: Dry blood spot samples were collected for genetic analysis. The GLA genetic variants were analysed by an amplicon-based next-generation sequencing approach in all female patients and in male patients with reduced alpha-galactosidase A levels. Alpha-galactosidase A and Lyso-Gb3 were not determined in female patients. Pearson’s correlation coefficient was used to assess the relationship between the above-mentioned factors with the activity of alpha-galactosidase A and Lyso-Gb3. Results: Genetic testing was performed in 476 patients, all female patients (334), 69 male patients with decreased level of alpha-galactosidase A activity, one male patient with alpha-galactosidase A levels above the quantification limit and 72 male patients with no interpretable results of alpha-galactosidase A activity due to preanalytical error. In 3 (0.4%) male patients, hemizygous mutations associated with Fabry disease were found, and those were c.427G>A p.(Ala143Thr), c.1181T>C p.(Leu394Pro), and c.352C>T p.(Arg118Cys). The dose of corticosteroid therapy seemed to be positively correlated to alpha-galactosidase A activity and negatively to Lyso-Gb3 levels in blood. Conclusions: Genetic testing of individuals with chronic kidney disease and reporting of genetic variants associated with the Fabry phenotype are important to improve the overall knowledge of the disease. Further research is needed to define factors influencing levels of alpha-galactosidase A and Lyso-Gb3.