Chronic alcohol exposure induces complex pathophysiological changes in the central nervous system (CNS), contributing to the onset and progression of neurodegenerative disorders. This review integrates recent findings on ethanol-induced neurotoxicity, focusing on key mechanisms including oxidative stress, protein misfolding, mitochondrial dysfunction, calcium dysregulation, neuroinflammation, and epigenetic alterations. We further discuss the detrimental impact of ethanol metabolism particularly its neurotoxic intermediates such as acetaldehyde and salsolinol on neuronal integrity. Special emphasis is placed on glial cell activation, blood–brain barrier disruption, and dysregulation of survival pathways such as PI3K/Akt/mTOR. Finally, we highlight promising therapeutic strategies targeting these molecular and cellular disruptions. A comprehensive understanding of these processes is critical for the development of neuroprotective interventions aimed at mitigating alcohol-related cognitive and functional decline.

Atherosclerosis is a chronic inflammatory disease that causes degenerative and productive changes in the arteries. The resulting atherosclerotic plaques restrict the vessel lumen, causing blood flow disturbances. Plaques are formed mainly in large- and medium-sized arteries, usually at bends and forks where there is turbulence in blood flow. Depending on their location, they can lead to various disease states such as myocardial infarction, stroke, renal failure, peripheral vascular diseases, or sudden cardiac death. In this work, we reviewed the literature on the early detection of atherosclerosis markers in the application of photodynamic therapy to atherosclerosis-related diseases. Herein, we described the roles of C-reactive protein, insulin, osteopontin, osteoprotegerin, copeptin, the TGF-β cytokine family, and the amino acid homocysteine. Also, we discuss the role of microelements such as iron, copper, zinc, and Vitamin D in promoting the formation of atherosclerotic plaque. Dysregulation of the administered compounds is associated with an increased risk of atherosclerosis. Additionally, taking into account the pathophysiology of atherosclerotic plaque formation, we believe that maintaining homeostasis in the range of biomarkers mentioned in this article is crucial for slowing down the process of atherosclerotic plaque development and the stability of plaque that is already formed.

Background: Thyroid dysfunction is a prevalent endocrine disorder with significant cardiovascular consequences, particularly through its effects on cardiac electrophysiology. Electrocardiography (ECG), as a widely available and cost-effective diagnostic tool, provides valuable insight into these alterations. This systematic review and meta-analysis aimed to evaluate the relationship between thyroid hormone imbalance and ECG parameters. Methods: A comprehensive search of PubMed, ScienceDirect, and Google Scholar identified 1099 studies, of which 121 underwent full-text analysis. Ultimately, 37 studies with complete datasets were included in the quantitative synthesis, encompassing 167,074 participants across overt hyperthyroidism, subclinical and overt hypothyroidism, and euthyroid control groups. Results: Meta-analysis revealed significant alterations in key electrophysiological markers. Overt hyperthyroidism was associated with QTc and Tp-e prolongation, consistent with increased repolarization heterogeneity and arrhythmic risk. In overt hypothyroidism, QTc and Tp-e intervals were also prolonged, accompanied by reduced heart rate variability, reflecting autonomic imbalance. Subclinical forms demonstrated more variable results, though trends toward conduction and repolarization disturbances were observed. Importantly, several studies indicated that levothyroxine therapy or surgical treatment normalized abnormal ECG findings, underscoring their reversible nature. Conclusions: These results highlight the strong association between thyroid hormone abnormalities and ECG alterations, which may serve as early markers of arrhythmic risk and sudden cardiac death. Incorporating ECG screening into thyroid disease management could improve early detection, risk stratification, and cardiovascular prevention strategies.

The origins of photodynamic therapy (PDT) date back to 1904. Since then, the amount of research proving PDT and, consequently, its applicability to various disease states has steadily increased. Currently, PDT is mainly used in oncology to destroy cancer cells. It is being worked on for possible use in other medical fields as well, including cardiology. It can be used in the prevention of restenosis, often occurring after vascular surgical interventions, for destroying atherosclerotic plaques and as a new ablative method of ectopic centers in the treatment of atrial fibrillation. The purpose of this review is to summarize the knowledge to date regarding the therapeutic potential of using PDT for various pathological conditions in cardiology. The review also focuses on the current limitations associated with the use of PDT and identifies areas where more research is needed to develop better drug regimens. Materials and methods: The study analyzed 189 medical articles. The articles came from PubMed, Frontiers, Google Scholar, Science Direct and Web of Science databases. Through the excitation of light, a photosensitizer (PS) introduced into the body, the destruction of pathological cells occurs. PTD is widely used in oncology of the central nervous system (CNS). This process is made possible by the production of free oxygen radicals (ROS) and singlet oxygen, which generate oxidative stress that destroys sensitive cancer cells. In recent years, photosensitizers have also been discovered to have a strong affinity for macrophages that fill atherosclerotic plaques, making these compounds suitable for treating atherosclerosis. By inducing apoptosis of smooth muscle cells, inactivating basic fibroblast growth factor (FGF-β) and inhibiting endothelial cell hyperplasia, PDT can be used to prevent restenosis after surgical proceduresPDT appears to be a minimally invasive and highly effective therapeutic method, especially when combined with other therapeutic methods. Unfortunately, the small number of animal model studies and human clinical trials greatly limit the applicability of PDT on a wider scale. Current limitations, such as the depth of penetration, delivery of photosensitizer particles to the direct site of the lesion or the appropriate choice of photosensitizer in relation to the nature of the pathology, unfortunately make it impossible to replace current therapeutic approaches.

Background: Overt hyperthyroidism is associated with increased cardiovascular morbidity, including tachyarrhythmias and heart failure. Although standard electrocardiographic abnormalities are well recognized, data regarding advanced markers of ventricular repolarization heterogeneity remain limited. We aimed to evaluate electrocardiographic dispersion parameters as markers of altered ventricular repolarization in patients with overt hyperthyroidism. Methods: This single-centre retrospective case–control study included 97 adults: 55 patients with overt hyperthyroidism and 42 healthy euthyroid controls. Six ventricular repolarization dispersion parameters were assessed from standard 12-lead ECG recordings: QT dispersion (QTd), Bazett-corrected QT dispersion (QTcBd), Fridericia-corrected QT dispersion (QTcFd), JT dispersion (JTd), Fridericia-corrected JT dispersion (JTcFd), and Tpeak–Tend dispersion (Tp-ed). Group comparisons, correlation analyses, receiver operating characteristic (ROC) analyses, and internally validated multivariable modelling were performed. Results: All six parameters were significantly higher in overt hyperthyroidism than in controls (all p < 0.001). The best discriminatory performance was observed for JTcFd (AUC 0.813) and QTcBd (AUC 0.804). In multivariable analysis, Tp-ed remained independently associated with overt hyperthyroidism. Correlations between thyroid hormone levels and dispersion indices were weak and non-significant. Conclusions: Our findings suggest an association between overt hyperthyroidism and increased ventricular repolarization heterogeneity, as reflected by alterations in ECG-derived repolarization parameters. These results support the presence of electrophysiological changes in overt hyperthyroidism; however, the clinical implications regarding arrhythmic risk remain uncertain, as no clinical arrhythmic outcomes were assessed.

Background: Thyroid hormone excess can affect cardiac electrical activity through several mechanisms, yet its relationship with ventricular repolarization remains incompletely understood. Standard electrocardiographic intervals primarily characterize the overall duration of repolarization, whereas newer ECG-derived indices may provide additional information on its spatial and temporal heterogeneity. A better understanding of these alterations may be clinically relevant in light of emerging evidence linking circulating thyroid hormone levels with sudden cardiac death. Objectives: The aim of this study was to identify electrocardiographic parameters of ventricular repolarization that exhibit the most pronounced alterations in patients with Graves’ disease, thereby characterizing the pattern of repolarization changes associated with thyroid hormone excess. Methods: We conducted an observational analysis comparing individuals with patients with Graves’ disease with age- and sex-matched euthyroid controls. Ventricular repolarization was assessed using QT, QTc, JT, JTc, Tp-e, and Tp-e–based ratios. Group differences and discriminatory performance were evaluated using non-parametric tests and ROC analysis. Independent associations with hyperthyroidism were examined using multivariable logistic regression with entropy balancing and internal bootstrap validation. Results: Compared with controls, patients with Graves’ disease showed higher Tp-e values and Tp-e–derived ratios, consistent with greater heterogeneity of ventricular repolarization. Conversely, the raw QT and JT intervals were reduced, while their rate-corrected counterparts (QTc and JTc) showed only limited differences that varied according to the correction method. Among the evaluated ECG measures, Tp-e/QT provided the strongest separation between the groups, yielding an AUC of 0.92 (95% CI 0.84–0.97), with a sensitivity of 83% and specificity of 86% at a threshold of ≥0.24. After multivariable adjustment, Tp-e/QT remained independently related to overt hyperthyroidism (OR 1.75 for each 0.01 increment, 95% CI 1.31–2.34; p < 0.001). Heart rate was also independently associated with hyperthyroidism (OR 1.05 per 1-bpm increase, 95% CI 1.00–1.10; p = 0.046). Conclusions: In patients with Graves’ hyperthyroidism, ventricular repolarization appears to be characterized by greater electrical heterogeneity without a consistent increase in overall repolarization duration. Tp-e–derived measures may capture these abnormalities more effectively and provide additional information beyond standard ECG repolarization indices.