The role of the gut microbiome (GM) and oral microbiome (OM) in cardiovascular disease (CVD) has been increasingly being understood in recent years. It is well known that GM is a risk factor for various CVD phenotypes, including hypertension, dyslipidemia, heart failure and atrial fibrillation. However, its role in valvular heart disease (VHD) is less well understood. Research shows that, direct, microbe-mediated and indirect, metabolite-mediated damage as a result of gut dysbiosis and environmental factors results in a subclinical, chronic, systemic inflammatory state, which promotes inflammatory cell infiltration in heart valves and subsequently, via pro-inflammatory molecules, initiates a cascade of reaction, resulting in valve calcification, fibrosis and dysfunction. This relationship between GM and VHD adds a pathophysiological link to the pathogenesis of VHD, which can be aimed therapeutically, in order to prevent or regress any risk for valvular pathologies. Therapeutic interventions include dietary modifications and lifestyle interventions, in order to influence environmental factors that can promote gut dysbiosis. Furthermore, the combination of probiotics and prebiotics, as well as fecal m transplantation and targeted treatment with inducers or inhibitors of microbial enzymes have showed promising results in animal and/or clinical studies, with the potential to reduce the inflammatory state and restore the normal gut flora in patients. This review, thus, is going to discuss the pathophysiological links behind the relationship of GM, CVD and VHD, as well as explore the recent data regarding the effect of GM-altering treatment in CVD, cardiac function and systemic inflammation.

Purpose of review: Small bowel dysmotility is common in the context of neurological disorders. Overlooking it can have an adverse impact on patient's quality of life and neurological outcomes. This review focuses on describing the mechanisms and effects of enteric dysmotility in neurological patients and providing treatment options. Recent findings: Small bowel dysmotility is prevalent among neurological patients. The definition and diagnosis of small bowel dysmotility is a challenge; however, up to two-thirds of neurological patients may experience associated symptoms. Small bowel dysmotility can affect the absorption of nutrients and medication, impacts on social and professional function and can result in malnutrition and its associated morbidity and mortality. Summary: Small bowel dysmotility due to a neuropathy can result from acute or chronic disorders in the central and peripheral nervous system and includes the cerebral cortex, brain stem, spinal cord, parasympathetic (vagus) and sympathetic nerves and the myenteric and submucosal plexuses of the intestine. Generalized muscle disorders can also cause an enteral myopathy. Generally, the disorders may be degenerative or inflammatory. Both enteric neuropathy and myopathy may cause symptoms of abdominal pain, nausea/vomiting, bloating, constipation or diarrhoea and can cause malnutrition. The symptoms need to be addressed in order of importance to the patient and malnutrition prevented or treated.

Obesity is a current pandemic that sets all affected individuals at risk of heart failure (HF), and the majority of them will develop the clinical syndrome of HF with preserved ejection fraction (HFpEF). The diagnosis of HFpEF is challenging as it is based on the detection of subtle functional and structural remodeling of the heart that leads to diastolic dysfunction with increased left ventricular (LV) filling pressures and raised natriuretic peptides (NPs). The accurate diagnosis of HFpEF is even more challenging in patients who are obese, since the echocardiographic imaging quality may be suboptimal, the parameters for the evaluation of cardiac structure are indexed to the body surface area (BSA) and thus may underestimate the severity of the remodeling, and the NPs in patients who are obese have a lower normal threshold. Moreover, patients who are obese are prone to atrial fibrillation (AF) and pulmonary hypertension (PH), making the evaluation of diastolic dysfunction more strenuous. The current review aims to offer insights on the accurate diagnosis of HFpEF in patients who are obese in different clinical scenarios—patients who are obese in different clinical scenarios—such as in sinus rhythm, in atrial fibrillation, and in the case of pulmonary hypertension—by applying multimodality imaging and clinical diagnostic algorithms.

Endoscopic full-thickness resection (EFTR) has emerged as a transformative technique for managing gastrointestinal (GI) lesions, previously deemed unsuitable for endoscopic removal. Unlike conventional endoscopic resection methods, such as endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD), EFTR enables en bloc excision of both intraluminal and subepithelial lesions by resecting all layers of the GI wall, followed by defect closure to prevent complications. The introduction of the full-thickness resection device (FTRD^®) has significantly enhanced the feasibility and safety of EFTR, particularly in the colon and upper GI tract, with increasing adoption worldwide. This review provides a comprehensive analysis of FTRD^®, focusing on its clinical applications, procedural methodology, and comparative efficacy against other endoscopic resection techniques. The indications and contraindications for EFTR are explored, highlighting its utility in treating non-lifting adenomas, subepithelial tumours, and T1 carcinomas without lymph node involvement. This review synthesizes current clinical data and FTRD^® advantages. Despite its strengths, EFTR via FTRD^® incorporates challenges such as limitations in lesion size, procedural complexity, and potential adverse events. Strategies for overcoming these challenges, including hybrid techniques and modifications in procedural approach, are examined. The review also emphasizes the need for further research to optimize surveillance strategies and determine the long-term clinical impact of EFTR in GI lesion management. By integrating recent evidence, this paper provides valuable insights into the evolving role of EFTR in therapeutic endoscopy.