Infective endocarditis (IE) is an inflammatory disease usually caused by bacteria entering the bloodstream and settling in the heart lining valves or blood vessels. Despite modern antimicrobial and surgical treatments, IE continues to cause substantial morbidity and mortality. Thus, primary prevention and enhanced diagnosis remain the most important strategies to fight this disease. In this regard, it is worth noting that for over 50 years, oral microbiota has been considered one of the significant risk factors for IE. Indeed, among the disparate recommendations from the American heart association and the European Society of Cardiology, there are good oral hygiene and prophylaxis for high-risk patients undergoing dental procedures. Thus, significant interest has grown in the role of oral microbiota and it continues to be a subject of research interest, especially if we consider that antimicrobial treatments can generate drug-resistant mutant bacteria, becoming a severe social problem. This review will describe the current knowledge about the relationship between oral microbiota, dental procedures, and IE. Further, it will discuss current methods used to prevent IE cases that originate from oral pathogens and how these should be focused on improving oral hygiene, which remains the significant persuasible way to prevent bacteremia and systemic disorders.

The growing prevalence in the diagnosis of INOCA (Ischemia with Non-Obstructive Coronary Arteries), ANOCA (Angina with Non-Obstructive Coronary Arteries), and MINOCA (Myocardial Infarction with Non-Obstructive Coronary Arteries) highlights the need to reassess their clinical relevance. Historically regarded as benign syndromes, emerging evidence suggests that these conditions may cause serious cardiovascular events and considerable long-term disability. Additionally, emerging studies suggest that non-obstructive coronary artery disease (CAD) may have a higher prevalence compared to traditional obstructive forms of CAD. This leads to the need to better clarify the underlying pathogenic mechanisms as well as the risk factors associated with these syndromes. This is precisely the aim of this review, which focuses on the complex and heterogeneous mechanisms underlying these syndromes as well as the associated risk factors. This review also sums up the diagnostic steps necessary to achieve an accurate diagnosis, along with the interventional and pharmacological approaches to be implemented in light of the latest evidence.

Introduction: Depression is a common and severe comorbidity among individuals with heart failure (HF). Up to a third of all HF patients are depressed, and an even higher proportion have symptoms of depression. Aim: In this review, we evaluate the relationship between HF and depression, explain the pathophysiology and epidemiology of both diseases and their relationship, and highlight novel diagnostic and therapeutic options for HF patients with depression. Materials and Methods: This narrative review involved keyword searches of PubMed and Web of Science. Review search terms included [“Depression” OR “Depres*” OR “major depr*”] AND [“Heart Failure” OR “HF” OR “HFrEF” OR “HFmrEF” OR “HFpEF” OR “HFimpEF”] in all fields. Studies included in the review met the following criteria: (A) published in a peer-reviewed journal; (B) described the impact of depression on HF and vice versa; and (C) were opinion papers, guidelines, case studies, descriptive studies, randomized control trials, prospective studies, retrospective studies, narrative reviews, and systematic reviews. Results: Depression is an emergent HF risk factor and strongly relates with worse clinical outcomes. HF and depression share multiple pathways, including platelet dis-reactivity, neuroendocrine malfunction, inappropriate inflammation, tachi-arrhythmias, and frailty in the social and community setting. Existing HF guidelines urge evaluation of depression in all HF patients, and numerous screening tools are available. Depression is ultimately diagnosed based on DSM-5 criteria. There are both non-pharmaceutical and pharmaceutical treatments for depression. Regarding depressed symptoms, non-pharmaceutical treatments, such as cognitive-behavioral therapy and physical exercise, have shown therapeutic results, under medical supervision and with an effort level adapted to the patient’s physical resources, together with optimal HF treatment. In randomized clinical studies, selective serotonin reuptake inhibitors, the backbone of antidepressant treatment, did not demonstrate advantage over the placebo in patients with HF. New antidepressant medications are currently being studied and could provide a chance to enhance management, treatment, and control of depression in patients with HF. Conclusions: Despite the substantial link between depression and HF, their combination is underdiagnosed and undertreated. Considering the hopeful yet unclear findings of antidepressant trials, further research is required to identify people who may benefit from antidepressant medication. The goal of future research should be a complete approach to the care of these patients, who are anticipated to become a significant medical burden in the future.

G protein-coupled receptors (GPCRs) are the largest family of cell-surface receptors and they are responsible for the transduction of extracellular signals, regulating almost all aspects of mammalian physiology. These receptors are specifically regulated by a family of serine/threonine kinases, called GPCR kinases (GRKs). Given the biological role of GPCRs, it is not surprising that GRKs are also involved in several pathophysiological processes. Particular importance is emerging for GRK5, which is a multifunctional protein, expressed in different cell types, and it has been found located in single or multiple subcellular compartments. For instance, when anchored to the plasma membrane, GRK5 exerts its canonical function, regulating GPCRs. However, under certain conditions (e.g., pro-hypertrophic stimuli), GRK5 translocates to the nucleus of cells where it can interact with non-GPCR-related proteins as well as DNA itself to promote “non-canonical” signaling, including gene transcription. Importantly, due to these actions, several studies have demonstrated that GRK5 has a pivotal role in the pathogenesis of chronic-degenerative disorders. This is true in the cardiac cells, tumor cells, and neurons. For this reason, in this review article, we will inform the readers of the most recent evidence that supports the importance of targeting GRK5 to prevent the development or progression of cancer, cardiovascular, and neurological diseases.

Cardiovascular magnetic resonance (CMR) imaging has become a cornerstone in the diagnosis, risk stratification, and management of cardiovascular disease (CVD), particularly heart failure (HF) and cardiomyopathies. Renowned as the gold standard for non-invasive quantification of ventricular volumes and ejection fraction, CMR delivers superior spatial and temporal resolution with excellent tissue–blood contrast. Recent advancements, including T1, T2, and T2* mapping, extracellular volume quantification, and late gadolinium enhancement, enable precise tissue characterization, allowing early detection of myocardial changes such as fibrosis, edema, and infiltration. These features provide critical insights into the pathophysiological mechanisms underlying HF phenotypes and diverse cardiomyopathies, enhancing diagnostic accuracy and guiding therapeutic decisions. This review explores the expanding role of CMR in CV disease, highlighting its diagnostic value in HF and in several cardiomyopathies, as well as its contribution to improving patient outcomes through detailed tissue characterization and prognosis.

A substantial proportion of cardiovascular (CV) events occurs in individuals without previously diagnosed CV disease, underscoring the need for improved primary prevention strategies. Traditional risk scores provide probabilistic estimates but fail to directly identify the presence and heterogeneity of subclinical atherosclerosis. This review summarizes current evidence on advanced multimodality imaging approaches for identifying high-risk individuals without prior CV events. Evidence from cohort studies, randomized trials, and meta-analyses was examined to evaluate the role of coronary artery calcium (CAC) scoring, coronary computed tomography angiography (CCTA), perivascular fat attenuation index (FAI), and vascular ultrasound in risk stratification. CAC scoring remains the most validated and widely recommended tool, offering robust prognostic value and significant risk reclassification, particularly in intermediate-risk individuals. CCTA provides additional insights into plaque burden and high-risk phenotypes, while FAI enables noninvasive assessment of coronary inflammation, improving risk prediction beyond anatomical measures. Vascular ultrasound offers a radiation-free, accessible method for detecting systemic plaque burden and refining risk estimation. Overall, multimodality imaging enhances the identification of subclinical disease and supports more individualized, disease-based risk assessment. Future research should clarify cost effectiveness, optimize patient selection, and determine whether imaging-guided strategies improve long-term clinical outcomes.