Cardiovascular, renal, and metabolic diseases are pathophysiologically interdependent, posing a significant global health challenge and being associated with a substantial increase in morbidity and mortality. In 2023, the American Heart Association (AHA) defined this complex network of interconnected health conditions as the cardiovascular–kidney–metabolic (CKM) syndrome. This syndrome is based on common pathophysiological mechanisms, including chronic inflammation, oxidative stress, hyperglycemia and insulin resistance, activation of the renin–angiotensin–aldosterone system (RAAS), and neurohormonal dysfunction, which trigger a vicious cycle where the impairment of one organ contributes to the progressive deterioration of the others. An integrated approach to these conditions, rather than treating them as separate entities, supports a holistic management strategy that helps to reduce the burden on public health and improve patients’ quality of life. Existing management focuses on lifestyle modification, glycemic and lipid control, and the use of nephroprotective and cardioprotective therapies. This narrative review aims to synthesize and contextualize existing information on the complex interactions between these systems and on diagnostic approaches, as well as to provide an overview of the available therapeutic options.

Amiodarone, a bi-iodinated benzofuran derivative, is among the most commonly used antiarrhythmic drugs due to its high level of effectiveness. Though initially categorized as a class III agent, amiodarone exhibits antiarrhythmic properties across all four classes of antiarrhythmic drugs. Amiodarone is highly effective in maintaining sinus rhythm in patients with paroxysmal atrial fibrillation while also playing a crucial role in preventing a range of ventricular arrhythmias. Amiodarone has a complex pharmacokinetic profile, characterized by a large volume of distribution and a long half-life, which can range from several weeks to months, resulting in prolonged effects even after discontinuation. Side effects may include thyroid dysfunction, pulmonary fibrosis, and hepatic injury, necessitating regular follow-ups. Additionally, amiodarone interacts with several drugs, including anticoagulants, which must be managed to prevent adverse effects. Therefore, a deep understanding of both oral and intravenous formulations, as well as proper dosage adjustments, is essential. The aim of this paper is to provide a comprehensive and updated review on amiodarone’s indications, contraindications, recommended dosages, drug interactions, side effects, and monitoring protocols.

(1) Background: In recent years, several studies have described various and heterogenous methods to sensitize nanoparticles (NPs) to pH changes; therefore, in this current scoping review, we aimed to map current protocols for pH functionalization of NPs and analyze the outcomes of drug-loaded pH-functionalized NPs (pH-NPs) when delivered in vivo in tumoral tissue. (2) Methods: A systematic search of the PubMed database was performed for all published studies relating to in vivo models of anti-tumor drug delivery via pH-responsive NPs. Data on the type of NPs, the pH sensitization method, the in vivo model, the tumor cell line, the type and name of drug for targeted therapy, the type of in vivo imaging, and the method of delivery and outcomes were extracted in a separate database. (3) Results: One hundred and twenty eligible manuscripts were included. Interestingly, 45.8% of studies (n = 55) used polymers to construct nanoparticles, while others used other types, i.e., mesoporous silica (n = 15), metal (n = 8), lipids (n = 12), etc. The mean acidic pH value used in the current literature is 5.7. When exposed to in vitro acidic environment, without exception, pH-NPs released drugs inversely proportional to the pH value. pH-NPs showed an increase in tumor regression compared to controls, suggesting better targeted drug release. (4) Conclusions: pH-NPs were shown to improve drug delivery and enhance antitumoral effects in various experimental malignant cell lines.

Background and objectives: Obstructive sleep apnea (OSA) in children is a debilitating disease, difficult to treat. Dental appliances have been proposed as a valid therapy for improving functional outcomes with good compliance rates. Herein, we aimed to perform a meta-analysis comparing clinical outcomes between OSA children treated with dental appliances versus controls. Materials Methods: The study was registered with PROSPERO. A systematic search was performed for all comparative studies examining outcomes in pediatric patients who underwent treatment of OSA with oral appliances versus controls. Data was extracted and analyzed using a random effects model via Rev Man 5.3. Results: Six studies including 180 patients were analyzed split into two groups: patients treated with dental appliances (n = 123) and the controls (n = 119). Therapy with dental appliances was shown to significantly improve the apnea–hypopnea index (p = 0.009) and enlarge the superior posterior airway space (p = 0.02). Maxilla-to-mandible measurements were not significantly different between the two groups, nor was the mean SO₂ (p = 0.80). Conclusions: This is the most updated meta-analysis assessing the role of dental appliances for OSA in children; it shows that such devices can improve functional outcomes by decreasing the apnea–hypopnea index.

Acute coronary syndrome (ACS) is a spectrum of clinical and paraclinical disorders arising from an imbalance of oxygen demand and supply to the myocardium. The most common cause is atherosclerosis; however, other rare causes such as carbon monoxide (CO) poisoning should be considered. Through tissue hypoxia and direct cell injury, CO poisoning can lead to a broad spectrum of cardiac disorders, especially ACS. Materials and Methods. We have conducted a retrospective study in the Toxicology Department of Saint Spiridon Emergency University Hospital, including all patients admitted through the emergency department with CO poisoning. We divided the cohort into event group (myocardial injury) and non-event group (patients without myocardial injury) and performed a subset analysis of the former. Results. A total of 65 patients were included, 22 in the event and 43 in the non-event group. The severity of poisoning did not correlate with myocardial injury; however, 50% of the event group had severe poisoning with carboxyhaemoglobin ≥ 20%. Cardiac enzyme markers (troponin and creatin-kinase MB) had a statistically significant increase in the event group compared to the non-event group (p < 0.05). Most of the patients in the STEMI (50%) and NSTEMI (66.7%) groups had severe CO intoxication. The STEMI group had a mean age of 27.7 years old and no comorbidities. Conclusions. Myocardial injury can develop in CO poisoning irrespective of the severity of poisoning, and it can be transient, reversible, or permanent. Our study introduces new information on adverse cardiac events in patients with CO poisoning, focusing on the ACS. We found that the severity of CO poisoning plays an important role in developing myocardial injury, as 50% of patients in the event group were severely intoxicated. While in-hospital mortality in our study was low, further prospective studies should investigate the long-term mortality in these patients.

Serotonin syndrome (SS) is a clinical toxidrome with high variability in clinical practice. It develops due to increased serotonin levels in the central nervous system. With an underestimated frequency, SS can develop following an overdose, a therapeutic dose increase, or drug to drug interaction of at least one serotonergic agent. It can present with autonomic signs, neuromuscular changes and an altered mental status. However, history and clinical examination are key features to formulate the diagnosis. Treatment options consist of supportive measures, discontinuation of the offending agent and certain therapeutic agents previously reported to improve outcomes. Physicians have limited experience with SS, partially due to the lack of its identification in clinical practice. Therefore, we have integrated, in a narrative review, the case of a young male with SS following an atypical antipsychotic overdose superimposed on chronic treatment with agents previously known to produce SS.