Acute heart failure (AHF) is a life-threatening condition with high morbidity and mortality. Even though this pathology has been extensively researched, there are still challenges in establishing an accurate and early diagnosis, determining the long- and short-term prognosis and choosing a targeted therapeutic strategy. The use of reliable biomarkers to support clinical judgment has been shown to improve the management of AHF patients. Despite a large pool of interesting candidate biomarkers, endothelin-1 (ET-1) appears to be involved in multiple aspects of AHF pathogenesis that include neurohormonal activation, cardiac remodeling, endothelial dysfunction, inflammation, atherosclerosis and alteration of the renal function. Since its discovery, numerous studies have shown that the level of ET-1 is associated with the severity of symptoms and cardiac dysfunction in this pathology. The purpose of this paper is to review the existing information on ET-1 and answer the question of whether this neurohormone could be a promising biomarker in AHF.

Chronic kidney disease represents a complex and multifaceted pathology characterized by the presence of structural or functional renal anomalies associated with a persistent reduction in renal function. As the disease progresses, complications arise due to the chronic inflammatory syndrome, hydro-electrolytic disorders, and toxicity secondary to the uremic environment. Cardiovascular complications are the leading cause of death for these patients. Ischemic cardiac pathology can be both a consequence and complication of chronic kidney disease, highlighting the need to identify specific cardiorenal dysfunction biomarkers targeting pathophysiological mechanisms common to both conditions. This identification is crucial for establishing accurate diagnoses, prognoses, and risk stratifications for patients. This work is intended to elucidate the intricate relationship between chronic kidney disease and ischemic heart disease and to investigate the roles of cardiorenal biomarkers, including cardiac troponin, natriuretic peptides, galectin-3, copeptin, fibroblast growth factor 23 and its co-receptor Klotho, soluble suppression of tumorigenicity 2, and plasma growth differentiation factor 15.

Atrial cardiomyopathy (ACM) represents a constantly evolving concept, with increasing importance in contemporary research and clinical practice. A better understanding of the mechanisms involved in atrial remodeling and its clinical correlations especially with atrial fibrillation (AF) and other cardiometabolic comorbidities may induce a significant impact on the diagnosis, prognosis, and therapeutic approach of ACM-related comorbidities. Although initially described several decades ago, investigators have only recently highlighted that several renal, metabolic, and cardiovascular diseases are determining factors for atrial remodeling and subsequent ACM. Based on data from multiple recent studies, our research emphasizes the correlations between ACM and other coexisting pathologies including cardiovascular, respiratory, or metabolic diseases, with fibrosis being the most incriminated pathophysiological mechanism. In addition to the usual tests, the paraclinical assessment of ACM is increasingly based on the use of various cardiac biomarkers, while the cardiac magnetic resonance (CMR) has become an increasingly tempting diagnostic too for describing morphofunctional aspects of the heart chambers, with the gadolinium contrast enhanced CMR (LGE-CMR) emerging as a commonly used technique aiming to identify and quantify the precise extent of atrial fibrosis. Further research should be conducted in order to clarify our knowledge regarding atrial remodeling and, therefore, to develop new and improved therapeutic approaches in these patients.

Distal radioulnar joint (DRUJ) instability is a complex condition that can severely affect forearm function, causing pain, limited range of motion, and reduced strength. This review aims to consolidate current knowledge on the diagnosis and management of DRUJ instability, emphasizing a new classification system that we propose. The review synthesizes anatomical and biomechanical factors essential for DRUJ stability, focusing on the interrelationship between the bones and surrounding soft tissues. Our methodology involved a thorough examination of recent studies, incorporating clinical assessments and advanced imaging techniques such as MRI, ultrasound, and dynamic CT. This approach allowed us to develop a classification system that categorizes DRUJ injuries into three distinct grades. This system is intended to be practical for both clinical and radiological evaluations, offering clear guidance for treatment based on injury severity. The review discusses a range of treatment options, from conservative measures like splinting and physiotherapy to surgical procedures, including arthroscopy and DRUJ arthroplasty. The proposed classification system enhances the accuracy of diagnosis and supports more effective decision making in clinical practice. In summary, our findings suggest that the integration of advanced imaging techniques with minimally invasive surgical interventions can lead to better outcomes for patients. This review serves as a valuable resource for clinicians, providing a structured approach to managing DRUJ instability and improving patient care through the implementation of our new classification system.

The management of acute heart failure (AHF) is becoming increasingly complex, especially in patients with multiple comorbidities. Endothelin-1 (ET-1), a vasoconstrictive peptide, is an important mediator of neurohormonal activation, endothelial dysfunction, and cardiac remodeling—key processes involved in the pathogenesis of AHF. The aim of our study was to evaluate the diagnostic and prognostic performance of ET-1 in multimorbid AHF patients, compared to established markers such as amino terminal pro B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin I (hs-cTnI). We conducted a single-center prospective study including 76 patients; 54 with AHF and 22 serving as controls. Upon admission, all patients underwent a comprehensive clinical, echocardiographic, and laboratory evaluation, including plasma ET-1 measurement using the enzyme-linked immunosorbent assay (ELISA) method. Receiver operating characteristic (ROC) curve and area under the curve (AUC) analysis were performed to assess the diagnostic and prognostic performance of ET-1 in comparison to NT-proBNP and hs-cTnI. ET-1 levels were considerably higher in AHF patients than in controls (p = 0.02), with an AUC of 0.954, showing comparable diagnostic accuracy with NT-proBNP (AUC = 0.997), alongside strong correlations with signs of systemic congestion, increased hospital stay, and ventricular dysfunction. ET-1 had the strongest predictive accuracy for in-hospital mortality (AUC = 0.781, p = 0.026), outperforming NT-proBNP and hs-cTnI. For 30-day mortality, ET-1 remained a reliable predictor (AUC = 0.784, p = 0.016). However, as the follow-up period extended to one year, its predictive power declined, confirming ET-1’s prognostic efficacy only for short-term outcomes. Moreover, ET-1 levels were not influenced by the presence of comorbidities, demonstrating its potential as an independent biomarker. Our findings support that ET-1 is a valuable biomarker for both diagnosis and short-term prognosis in the assessment of multimorbid AHF patients.

Ischemia with nonobstructive coronary artery disease (INOCA) is increasingly recognized as a significant cause of angina, myocardial remodeling, and eventually heart failure (HF). Coronary microvascular dysfunction (CMD) is a major endotype of INOCA, and it is caused by structural and functional alterations of the coronary microcirculation. At the same time, atrial cardiomyopathy (ACM) defined by structural, functional, and electrical atrial remodeling has a major clinical impact due to its manifestations: atrial fibrillation (AF), atrial thrombosis, stroke, and HF symptoms. Both these pathologies share similar risk factors and have a high comorbidity burden. CMD causing INOCA and ACM frequently coexist. Thus, questions arise whether there is a potential link between these pathologies. Does CMD promote AF or the reverse? Which are the mechanisms that ultimately lead to CMD and ACM? Are both part of a systemic disease characterized by endothelial dysfunction? Lastly, which are the therapeutic strategies that can target endothelial dysfunction and improve the prognosis of patients with CMD and ACM? This review aims to address these questions by analyzing the existing body of evidence, offering further insight into the mechanisms of CMD and ACM, and discussing potential therapeutic strategies.