BACKGROUND:Emphysematous osteomyelitis of the spine is characterized by intravertebral or intraosseous air. Emphysematous pyelonephritis (EP) is the infection of the renal parenchyma and perirenal tissues caused by gas forming microorganisms and thus...

Ultra-low contrast percutaneous coronary interventions (ULPCIs) are a novel field of interventional cardiology, aiming to reduce the risk of contrast-induced nephropathy (CIN), which is a well-described adverse event after angiography. CIN is a well-described adverse event following PCI, especially in high-risk patients, i.e., patients with an already deteriorating renal function or chronic kidney disease, as well as patients of advanced age or requiring an increased amount of contrast during their intervention. Among the techniques described for ULPCI procedures, intravascular imaging guidance seems a promising option, as it allows lesion recognition and characterization, stent implantation, and PCI optimization. Intravascular ultrasound (IVUS) is the modality most commonly used, as it does not require contrast injection, contrary to optical coherence tomography (OCT). Several clinical trials, assessing IVUS in the context of ULPCI, have shown that it can be safely used in this setting while offering a substantial reduction in contrast media volume, as well as renal adverse outcomes. This review aims to describe the need for ULPCI and technical considerations regarding the use of intravascular imaging in this setting, as well as analyze the available evidence from clinical trials regarding the safety and efficacy of IVUS-ULPCI, in order to provide a comprehensive summary for practicing physicians.

Arterial hypertension is highly prevalent among individuals with chronic kidney disease (CKD), exhibiting a bidirectional association and playing a critical role in the progression of renal dysfunction. CKD affects approximately 10–12% of the global population and is often a common comorbidity in patients with true resistant hypertension. The sympathetic nervous system (SNS) plays a key role in the pathophysiological cascade of CKD-mediated hypertension. Current pharmacological therapies do not directly target SNS overactivity, highlighting the need for alternative approaches. Renal denervation (RDN), an interventional procedure that modulates both afferent and efferent renal nerve signaling, has emerged as a promising strategy for resistant hypertension with multiple pleiotropic benefits. Both preclinical and clinical trial data indicate that RDN is safe, with no significant deterioration of renal function reported in both early-stage CKD and end-stage renal disease (ESRD), as well as effective in reducing both office and ambulatory blood pressure in most studies. This review examines the pathophysiological basis for SNS overactivity in CKD, summarizes preclinical and clinical data on the safety and efficacy of RDN in this population, and discusses ongoing and future trials that may further clarify the role of RDN in CKD management and its long-term impact on renal and cardiovascular outcomes.

Renal denervation (RDN), a transcatheter renal sympathetic nerve ablation procedure, is a relatively novel established procedure for the treatment of hypertension, with it being recognized as a third option for hypertension management in the most recent European guidelines, together with pharmacotherapy, for achieving blood pressure targets. Given the relationship between both hypertension and sympathetic overdrive and the development of heart failure (HF), even studies at the dawn of research on RDN explored it as a treatment to overcome diuretic resistance in those patients. As it is now recognized that RDN does not only have organ-specific but also systemic effects, several investigators have aimed to delineate whether renal sympathetic denervation could alter the prognosis, symptoms, and adverse events of HF patients. Data are available in both HF patients with reduced and preserved ejection fraction. As the significance of neuromodulation is gaining grounds in the HF therapeutic arsenal, in this review, we aim to provide a rationale for using RDN in HF and an up-to-date overview of available data in both HF phenotypes, as well as discuss the future of neuromodulatory therapy in HF management.

Background/Objectives: Atrial fibrillation accounts for approximately 0.5–1% of emergency department visits. Contemporary ESC and ACC/AHA guidelines address acute pharmacological cardioversion, anticoagulation before cardioversion, and delayed “wait-and-see” strategies; however, real-world implementation of an early, specialist-guided pathway in the emergency department remains incompletely described. In the HEROMEDICUS study we implemented a protocol for acute management of patients presenting to the emergency department with atrial fibrillation as their main complaint. The present analysis reports the safety and efficacy of intravenous flecainide within that pathway. Methods: All patients who visited the emergency department from 8 September 2023 to 10 October 2025 with a primary diagnosis of atrial fibrillation, atrial flutter, or atrial tachycardia were screened. Patients with known heart failure (left ventricular ejection fraction < 40%), known coronary artery disease, symptoms of acute heart failure or acute coronary syndrome, or intraventricular conduction delay were excluded. Using tablet computers and an in-house application, on-duty cardiologists obtained contemporaneous electrophysiology consultation. In this institution, frontline emergency department care for arrhythmia presentations is provided by cardiologists rather than emergency-medicine physicians. Patients without prior oral loading with >300 mg propafenone or >200 mg flecainide were eligible for intravenous flecainide 2 mg/kg (maximum 150 mg) infused over 10 minutes. Follow-up at the outpatient atrial fibrillation clinic was scheduled through the application. Results: Of 277 patients screened (15 atrial tachycardia, 28 atrial flutter, 234 atrial fi-brillation - mean age 68.5±12.3 years, heart rates 122.9±25.1 bpm and CHA2DS2-VASc 2.3±1.5 points, 53% females), 85 fulfilled criteria for intravenous flecainide administration; of them, 83 had atrial fibrillation on both the triage and recruitment electrocardiograms and 2 had atrial flutter on the triage but atrial fibrillation on the recruitment electrocar-diogram – thus all patients receiving flecainide effectively had atrial fibrillation. A first-diagnosed episode was recorded in 130 patients. Sinus rhythm was restored with flecainide alone in 61/85 patients (71.8%; 95% CI 61.4–80.2%). Of the remaining 24 patients, 22 were subsequently electrically cardioverted in the emergency department and 2 failed both strategies and were discharged after rate control. Among the 26 successful pharmacological conversions with available timestamps, median time from start of in-fusion to sinus rhythm was 13 minutes. No patient developed ventricular proarrhythmia or atrial flutter with 1:1 atrioventricular conduction, at least during their stay in the emergency department. Also, no thromboembolic events occurred in the same period. None of the 85 flecainide-treated patients was admitted. Conclusions: Intravenous flecainide was safe and effective as the initial pharmacological option within the HEROMEDICUS emergency department pathway for selected patients with atrial fibrillation. Subsequent electrical cardioversion rescued most pharmacological failures. These findings apply to atrial fibrillation; they should not be extrapolated to atrial flutter or atrial tachycardia. In the absence of a control group, we report the observed absence of admissions following implementation of our protocol.

Atrial fibrillation (AF) is the most common supraventricular arrhythmia in adults, with a rising prevalence and a significant impact on quality of life and major cardiovascular outcomes. While atrial structural and electrical remodeling have long been central to AF pathophysiology, increasing evidence highlights the importance of psychological and mental health factors throughout the disease course. Depression, anxiety, and chronic stress are highly prevalent among individuals with AF and are associated with increased symptom burden, impaired quality of life (QoL), reduced treatment adherence, lower utilization of evidence-based therapies, and adverse clinical outcomes. Conversely, the diagnosis of AF itself may contribute to psychological distress, highlighting a complex bidirectional relationship between mental health and AF. This review summarizes current evidence on this interplay, with a focus on underlying mechanisms, including autonomic dysfunction and inflammation. Furthermore, the influence of mental health on outcomes and therapeutic strategies, and the clinical relevance of a multidisciplinary approach in contemporary AF management, are also examined.