Imaging is an important tool in the diagnosis and management of infective endocarditis (IE). Echocardiography is an essential examination, especially in native valve endocarditis (NVE), but its diagnostic accuracy is reduced in prosthetic valve endocarditis (PVE). The diagnostic ability is superior for transoesophageal echocardiography (TEE), but a negative test cannot exclude PVE. Both transthoracic echocardiography (TTE) and TEE can provide normal or inconclusive findings in up to 30% of cases, especially in patients with prosthetic devices. New advanced non-invasive imaging tests are increasingly used in the diagnosis of IE. Nuclear medicine imaging techniques have demonstrated their superiority over TEE for the diagnosis of PVE and cardiac implantable electronic device infective endocarditis (CIED-IE). Cardiac computed tomography angiography imaging is useful in PVE cases with inconclusive TTE and TEE investigations and for the evaluation of paravalvular complications. In the present review, imaging tools are described with their values and limitations for improving diagnosis in NVE, PVE and CIED-IE. Current knowledge about multimodality imaging approaches in IE and imaging methods to assess the local and distant complications of IE is also reviewed. Furthermore, a potential diagnostic work-up for different clinical scenarios is described. However, further studies are essential for refining diagnostic and management approaches in infective endocarditis, addressing limitations and optimizing advanced imaging techniques across different clinical scenarios.

Aortic stenosis (AS) and atherosclerosis are progressive cardiovascular conditions that frequently coexist and share multiple clinical and molecular features. Medical therapies have shown effectiveness in preventing and treating atherosclerosis and its consequences. For AS, effective pharmacological therapies remain limited. Understanding the shared risk factors and mechanisms between the two conditions may provide opportunities for therapeutic repositioning in AS. We performed a narrative review focusing on studies published from 2005 to 2025. Inclusion criteria encompassed clinical trials, experimental models, and molecular studies addressing overlapping risk factors, pathological pathways, and treatment approaches for AS and atherosclerosis. AS and atherosclerosis share key risk factors, including age, hypertension, hyperlipidemia, and diabetes. Molecular mechanisms, such as chronic inflammation, endothelial dysfunction, oxidative stress, lipid accumulation, and calcific remodeling, are common to both. Pathways involving the renin-angiotensin system, Notch signaling, and osteogenic mediators contribute to disease progression. Several drug classes, notably proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, lipoprotein(a) (Lp(a)) lowering therapies, anti-inflammatory agents, and immunomodulators, show potential for repositioning in AS management. The substantial overlap in risk factors and molecular mechanisms between AS and atherosclerosis supports a rationale for therapeutic repositioning. Targeting shared pathways could lead to innovative strategies for slowing AS progression and improving patient outcomes.

One of the most important parts of medical care is the endoscopy sector, like digestive endoscopy, which has gained extensive importance and is assumably going to increase in the future. We aimed to analyse and synthesize the impact of digestive endoscopy upon the environment and the possible measures that can be taken to minimize the negative effects of endoscopy related to environmental pollution and human health exposure. The means through which digestive endoscopy produces pollution have been analysed, considering the frame and the base of the last stage of a medical or pharmaceutical product. This research suggests a strategy for improving the impact of this sector on the sustainability of the healthcare system based on four pillars comprising the use of eco-friendly substances, materials, and devices, reducing the consumption of water and all possible devices and energy, reusing those components that can be safely reinserted in the endoscopic circuit and recycling everything that is possible. The conclusions highlight that there is a great need to take control of medical practice, admitting the impact that the healthcare system has on global warming and greenhouse gas emissions, acknowledging the limited assets and wealth of the planet, and applying standards and scales of sustainability that can lead to responsible services for patients.

Background and Objectives: Coronary atherosclerosis remains a leading cause of global morbidity and mortality. Chronic systemic inflammation has emerged as a key factor in atherosclerosis development. Tooth loss—often the final consequence of periodontitis—has been proposed as a potential clinical marker of systemic inflammation and cardiovascular risk. Objective: This narrative review synthesizes the available literature on the relationship between tooth loss and coronary artery disease (CAD) severity, exploring biological mechanisms, key epidemiological findings, and clinical implications. Materials and Methods: We reviewed observational studies, meta-analyses, and clinical reports assessing whether tooth loss is predictive of CAD severity and adverse outcomes. Results: A consistent association is reported between tooth loss and increased coronary involvement. Proposed mechanisms include periodontal inflammation, dysbiosis, systemic inflammatory responses, and translocation of oral bacteria. However, confounders such as smoking, diabetes, and socioeconomic status complicate causality. Conclusions: Tooth loss may serve as a simple, non-invasive clinical indicator of systemic inflammation and CAD severity. Incorporating oral health evaluation into cardiovascular risk assessment could enhance early detection and prevention strategies. Further longitudinal and interventional studies are required to establish causality and inform clinical guidelines.

Background: Aortic stenosis (AS) has long been considered a degenerative disease and is typically diagnosed in older men at an advanced stage. However, accumulating evidence has highlighted the similarities between AS and atherosclerosis, particularly regarding shared risk factors and overlapping pathophysiological mechanisms. This connection has led to a paradigm shift, suggesting that AS may be preventable in its early stages. Methods: This narrative review synthesizes the existing literature exploring the parallels between AS and atherosclerosis, focusing on common risk factors, pathogenic pathways, and evolving therapeutic strategies. Clinical trials and translational studies were examined to assess the effectiveness of atherosclerosis-based treatments for AS. Results: Multiple studies have confirmed the shared inflammatory, lipid-mediated, and calcific mechanisms of AS and atherosclerosis. Despite these similarities, therapeutic strategies effective in atherosclerosis, such as statin therapy, have not consistently shown benefits in AS. New medical approaches aim to delay aortic valve replacement and reduce the associated morbidity. The partially overlapping pathogenesis continues to guide future research. Conclusions: While AS and atherosclerosis share several pathogenic features, their clinical courses and treatment responses diverge. Understanding the limits and potential of their overlap may inform future preventive and therapeutic strategies. Earlier detection and targeted intervention in AS remain key goals, drawing on insights from cardiovascular disease management.

Here, we report an unusual case of a nonsmoker and hypertensive 72-year-old male who was admitted with a transient ischemic attack to the Neurology Department of Clinical County Emergency Hospital Bihor. He presented a first transient ischemic attack and paroxysmal atrial fibrilation 2 years before, when anticoagulation was started on top of his antihypertensive medication. At that time, carotid Doppler ultrasound revealed nonobstructive atherosclerosis and statin therapy was started, according to current guidelines, in order to lower the initial 70 mg/dL LDL-cholesterol level to under 55 mg/dL. Cardio-embolism was considered the mechanism of stroke at that time. Despite all the medication and the maintenance of LDL below 50 mg/dL, carotid atherosclerosis evolved to an important left internal carotid artery stenosis and transient ischemic attacks reappeared two years later. Carotid stenosis was then considered the most probable cause, although elucidating the exact mechanism was difficult. After medical treatment and subsequent endarterectomy, the patient had a good outcome. The progressive course of atheromatosis, despite maximal medication, urged us to look for further proper measures of prevention. No chronic disease was detected during the postoperative phase, except for early-stage periodontal disease, for which adequate preventive measures were applied. Considering that subclinical inflammation induced by periodontal disease can induce the progression of atherosclerosis, chronic treatment with colchicine was added, with a favorable outcome.