Despite the enormous progress in the treatment of atrial fibrillation, mainly with the use of invasive techniques, many questions remain unanswered regarding the pathomechanism of the arrhythmia and its prevention methods. The development of atrial fibrillation requires functional changes in the myocardium that result from disturbed ionic fluxes and altered electrophysiology of the cardiomyocyte. Electrical instability and electrical remodeling underlying the arrhythmia may result from a cellular energy deficit and oxidative stress, which are caused by mitochondrial dysfunction. The significance of mitochondrial dysfunction in the pathogenesis of atrial fibrillation remains not fully elucidated; however, it is emphasized by the reduction of atrial fibrillation burden after therapeutic interventions improving the mitochondrial welfare. This review summarizes the mechanisms of mitochondrial dysfunction related to atrial fibrillation and current pharmacological treatment options targeting mitochondria to prevent or improve the outcome of atrial fibrillation.

In the aging society, the issue of coronary chronic total occlusion (CTO) has become a challenge for invasive cardiologists. Despite the lack of clear indications in European and American guidelines, the rates of percutaneous coronary interventions (PCI) for CTO increased over the last years. Well-conducted randomized clinical trials (RCT) and large observational studies brought significant and substantial progress in many CTO blind spots. However, the results regarding the rationale behind revascularization and the long-term benefit of CTO are inconclusive. Knowing the uncertainties regarding PCI CTO, our work sought to sum up and provide a comprehensive review of the latest evidence on percutaneous recanalization of coronary artery chronic total occlusion.

Hypertension remains a global threat to public health, affecting the worldwide population. It is one of the most common risk factors for cardiovascular disease. Today’s treatments focus on creating a hypotensive effect. However, there is a constant search for additional factors to reduce the potential of developing hypertension complications. These factors may act as a parallel treatment target with a beneficial effect in specific populations. Some studies suggest that uric acid may be considered such a factor. This study investigated the potential effect of uric acid concentrations over 5 mg/dL on the incidence of hypertension complications among patients with very high cardiovascular risk. A total of 705 patients with hypertension and very high cardiovascular risk were selected and included in the analysis. The patients were divided and compared according to serum uric acid levels. The study showed a higher occurrence of heart failure (OR = 1.7898; CI: 1.2738–2.5147; p = 0.0008), atrial fibrillation (OR = 3.4452; CI: 1.5414–7.7002; p = 0.0026) and chronic kidney disease (OR = 2.4470; CI: 1.3746–4.3558; p = 0.0024) among individuals with serum uric acid levels over 5 mg/dL, males and those with a BMI > 25 kg/m². These findings suggest that even serum uric acid concentrations over 5 mg/dL may affect the prevalence of hypertension-related complications among patients with very high cardiovascular risk.

Atrial fibrillation (AF) is the most common arrhythmia worldwide, and is associated with a significant risk of thromboembolic events. Left atrial appendage occlusion (LAAO) has emerged as a promising alternative for patients with contraindications or intolerance to anticoagulant therapy. This review summarises the current evidence, indications, and technical advancements in surgical and percutaneous LAAO. Preprocedural planning relies on various imaging techniques, each with unique advantages and limitations. The existing randomised clinical trials and meta-analyses demonstrate favourable results for both percutaneous and surgical LAAO. Postprocedural management emphasises personalised anticoagulation strategies and comprehensive imaging surveillance to ensure device stability and detect complications. Future focus should be put on antithrombotic regimens, investigating predictors of device-related complications, and simplifying procedural aspects to enhance patient outcomes. In summary, LAAO is presented as a valuable therapeutic option for preventing AF-related thromboembolic events, with ongoing research aimed at refining techniques and improving patient care.

(1) Background: Coronary artery disease (CAD) remains the leading cause of death in both sexes. The male sex is considered a classical atherosclerosis risk factor, whereas females should be protected by hormonal effects until menopause. Although there are known differences in the development, type, and prognosis of chronic coronary syndrome (CCS) between both sexes, there are no differences in approach in the guidelines. (2) Methods: The sex-related differences in CAD risk factors, treatment, echocardiographic, and angiographic results were assessed among 3291 patients with CCS. (3) Results: Women were older and had a higher prevalence of hypertension, dyslipidaemia, and diabetes mellitus than men. Women were more often treated conservatively than men. There was no difference in the use of beta-blockers and statins among the sexes. The LDL cholesterol goal was less frequently reached by women. Women were treated less often with aspirin than men, but they were treated more often with angiotensin receptor blockers than men. The left ventricle ejection fraction was higher among females. The number of obstructed vessels was higher in men. (4) Conclusions: Women may be more exposed to the risk factors of CAD than men. Men are diagnosed with CAD earlier, and their prevention and therapy are more efficient.

Atrial fibrillation (AF) is associated with energetic deficiency and oxidative stress due to mitochondrial dysfunction, resulting in electric remodeling. Long-term treatment was found to ameliorate mitochondrial function and decrease inducibility in animal models. No studies examine the short-term effect of SGLT-2 inhibitors administration in AF. In the present study, the samples of the right atrial appendage collected from 10 patients subjected to elective cardiac surgery were sliced and incubated in a control buffer (EMPA 0), 0.2 µmol/L empagliflozin (EMPA 0.2), or 1.0 µmol/L (EMPA 1). The expression of mitochondrial biogenesis, fission, and fusion proteins was measured by Western blot after 30 min of electrical stimulation (control—1 Hz or tachypacing—5 Hz). The PGC-1α protein expression was increased after 30 min of stimulation with 1 Hz when incubated under a higher concentration of empagliflozin. After tachypacing, EMPA 0.2 increased PGC-1α, while EMPA 1.0 upregulated NRF-1. Both concentrations increased NRF-2 during control stimulation. The oxygen consumption was higher in AF, and was decreased by SGLT-2i. Empagliflozin exerts dynamic effects on the expression of PGC-1α and other proteins involved in mitochondrial function and oxidative stress in cardiomyocytes and may modulate cellular response to tachycardia.