Search Results (715)

Non-infectious cardiac failure in feedyard cattle has become more frequently diagnosed. There is limited research assessing gross and histologic lesions in grossly abnormal hearts of harvested cattle. Cases were stratified by heart score (HS) using a scale of 1–5, with 1 representing a normal heart and 5 representing severely remodeled ventricles. Cattle were evaluated for gross lesions of the heart, lung, and liver. Samples collected from each animal for histology included cardiac (n = 4), pulmonary (n = 4), and hepatic (n = 1) tissues. Histologic evaluation scored cardiac and hepatic fibrosis and necrosis, embedded myocardial protozoal cysts (EMPCs) were quantified, and pulmonary lesions were categorized based on histologic patterns. Of 103 cases, 40 had normal HSs (NHSs) (1 or 2), and 63 had abnormal HSs (AHSs) (3, 4, or 5). There were 64 cases with normal lung deflation scores, and 39 cases with abnormal lung deflation scores. At least one cardiac section contained EMPCs in 67 cases. Cattle with abnormal lung deflation scores were more likely to have an AHS (0.76 ± 0.07, p ≤ 0.01) compared with cattle with normal deflation scores (0.52 ± 0.06). Cattle with EMPCs present in at least one cardiac section were more likely to also have an AHS (0.73 ± 0.05, p ≤ 0.1) compared with cattle without EMPCs (0.39 ± 0.08). No histological findings for the lungs or liver were associated with abnormal heart score; however, lung deflation and EMPCs were associated with abnormal heart score. Full article

Background/Objectives: Diabetes mellitus is a common chronic disease that may lead to multimorbidity and high drug use. Therefore, this study aims to examine the prevalence of polypharmacy and hyperpolypharmacy among adult patients diagnosed with type 2 diabetes mellitus (T2DM) with its associated factors. Methods: This is a retrospective cross-sectional study conducted from 1 May 2023 to 31 October 2024. The outcomes in our study were polypharmacy (from five to nine drugs) and hyperpolypharmacy (≥10 drugs). Baseline and demographic characteristics, along with multinomial logistic regression, were used to analyze the data. Results: The total number of patients with T2DM was 2435. The prevalence rate of polypharmacy was 46.98%, while hyperpolypharmacy was 24.27%. Older age was significantly associated with a higher risk of polypharmacy [OR = 1.031, 95% (1.022–1.040)] and hyperpolypharmacy [OR = 1.037, 95% (1.026–1.049)]. In addition, patients with higher levels of hemoglobin A1c showed a significantly higher risk of polypharmacy and hyperpolypharmacy ([OR = 1.162, 95% (1.105–1.221)] and [OR = 1.284, 95% (1.209–1.364)], respectively). The comorbidities that increased the odds of hyperpolypharmacy were hypertension [OR = 2.136, 95% (1.449–3.148)], pulmonary disease [OR = 2.375, 95% (1.292–4.367)], mental disorders [OR = 6.269; 95% (3.284–11.964], and congestive heart failure [OR = 8.014, 95% (2.768–23.200)]. Conclusions: The prevalence of polypharmacy and hyperpolypharmacy is high in patients with T2DM. The predictors that may play a significant role in increasing the risk of hyperpolypharmacy are the poor control of HbA1c and the coexistence of comorbidities. Providing proper prescribing of patients’ therapy plans can improve individuals’ health outcomes. Therefore, this study highlights the important role of primary care physicians in coordinating care, along with clinical pharmacists, in the identification of polypharmacy. Full article

In patients with co-morbid CHF and COPD, the diagnosis of CHF can be delayed. It is also well known that left ventricular dysfunction can arise from progressive disease-related hyperinflation. Apart from the longitudinal risk of developing CHF in some patients, a short-term or subclinical risk of cardiac events has been reported after hospitalization for COPD exacerbation. Currently there are no data or strategies to support screening for the early diagnosis of CHF in patients with COPD. Similarly, pulmonary function testing results can also be confounding and inaccurate in establishing the severity of COPD during an active exacerbation of CHF. The hyperinflation of the lungs, which can alter LV geometry and mechanics, is at the root of many of the causes of LV underfilling, which eventually contributes to CHF. Conventional echocardiography can often miss subclinical myocardial dysfunction and hence make early diagnosis even more challenging. Advanced cardiac imaging modalities and revised echocardiographic parameters can help detect subclinical LV dysfunction and PH earlier, but there are no clinical outcome data to validate their routine use in day-to-day clinical practice. Beta-blockers are generally regarded as safe to be used for appropriate cardiovascular indications in patients with COPD, and recent trials have also established the safety of long-acting beta agonists for treating COPD in patients with elevated cardiac risk. Full article

Tricuspid regurgitation (TR) is a prevalent cardiovascular disorder with significant clinical impact. TR is frequently silent and underdiagnosed and is estimated to impact over 70 million people globally. Characterized by retrograde blood flow from the right ventricle into the right atrium due to incomplete valve closure, TR leads to right heart dilation, systemic congestion, and eventually right-sided heart failure. Importantly, TR may contribute to the onset of atrial fibrillation (AF), the most common sustained arrhythmia, affecting approximately 59 million individuals worldwide. Despite its growing clinical importance, the pathophysiology of TR remains incompletely understood, and current animal models of TR, based on direct valve manipulation, limit translational applicability. We present a novel, minimally invasive porcine model of TR established via femoral/jugular vein catheterization with deployment of an inferior vena cava (IVC) filter. The filter partially impedes tricuspid valve closure, inducing TR without valvular injury. Validation was achieved through multimodal imaging, including fluoroscopy, echocardiography, and electrocardiography, confirming hallmark features of TR, including right atrial and ventricular enlargement and arrhythmic activity. This model provides a reproducible, minimally invasive platform for studying selected features of TR progression. Its minimally invasive nature and preservation of native valvular structure make it a useful preclinical platform for mechanistic and translational research. Full article

Myocardial calcification is an uncommon complication associated with end-stage chronic kidney disease (CKD) in feline patients. This report describes the clinical and multimodal imaging features of metastatic calcification in a 10-year-old castrated male mixed-breed cat. The patient presented with dyspnea and anorexia, and was diagnosed with IRIS Stage 4 CKD. Laboratory findings revealed severe hyperphosphatemia and an elevated calcium–phosphorus product (CPP) of 135 mg²/dL², based on total calcium. This value significantly exceeds 70 mg²/dL², a threshold associated with a high probability of inducing soft tissue mineralization. Echocardiography revealed extensive hyperechoic foci with posterior acoustic shadowing in the interventricular septum and left ventricular wall. Functional assessment demonstrated a restrictive diastolic filling pattern, suggesting increased myocardial stiffness and congestive heart failure. Computed tomography (CT) further visualized systemic involvement, showing diffuse, amorphous calcifications (400–900 HU) in the myocardium, multifocal aortic wall, and extracardiac tissues. Despite intensive treatment with diuretics and renal support, the patient was euthanized eight days later due to progressive renal failure. This case illustrates that the interaction between metastatic calcification and uremic cardiomyopathy (UC) can result in refractory heart failure, underscoring the value of combined echocardiography and CT in evaluating end-stage renal disease. Full article

Heart failure (HF) affects approximately 64 million people globally. HF often coexists with chronic kidney disease. HF may affect the heart during diastolic filling, systolic ejection, or both. Conventionally, HF is categorized by left ventricular ejection fraction (LVEF). One of the leading causes of death in chronic kidney disease (CKD) patients of cardiovascular origin increase hospitalizations and worsen quality of life by causing fluid and electrolyte overload. As kidney function declines, increases risk of development of HF in CKD, with a negative impact and worse prognosis in these patients. This narrative review provides healthcare professionals—including nephrologists, car-diologists, internists, and general practitioners—with evidence-based strategies to iden-tify and manage this complex comorbidity, aiming to reduce hospitalization and mor-tality in CKD patients. By synthesizing recent findings on risk stratification, diagnostic modalities, and individualized treatment—particularly for patients undergoing renal replacement therapy—clinicians can enhance volume management and optimize patient outcomes. Considering the increasing prevalence of chronic kidney disease and associated cardiovascular comorbidities, this review addresses pathogenic mechanisms, diagnostic approaches, pharmacological treatments, and dialytic therapy modifications. Full article

Background/Objectives: SGLT2 inhibitors (SGLT2i) became a cornerstone of heart failure with preserved ejection fraction (HFpEF) pharmacotherapy in the recent years However, their actual influence on pulmonary veins isolation (PVI) efficacy in this population remains unclear. The aim of the study was to evaluate an impact of SGLT2i on one-year first-time PVI efficacy and clinical course of patients with HFpEF and atrial fibrillation (AF). Methods: This is a single-center retrospective study including 105 HFpEF and AF individuals, who underwent the first-time PVI (51 (48.6%) males; mean age at PVI: 65.2 ± 9.5 years). 53 patients treated with SGLT2i (hospitalized for PVI since 2023) and 52 patients without such a treatment (2020-mid-2023) were assessed according to the clinical presentation and hard endpoints. The primary endpoint was arrhythmia recurrence rate. The secondary endpoint was a composite of major adverse cardiovascular and cerebrovascular events (MACCE). Results: SGLT2i therapy was associated with greater symptom reduction after PVI (90.6% vs. 62.7%; p < 0.001). There was a statistical trend toward reduced all-cause mortality in SGLT2i (0% vs. 5.8%; p = 0.076). Although overall AF recurrence rates were similar between subgroups, Kaplan–Meier analysis showed a non-significant trend toward lower recurrence in the SGLT2i group (p = 0.096). The analysis did not reveal significant differences in terms of cardiovascular hospitalizations, stroke/transient ischemic attack (TIA) and MACCE incidence between the subgroups. Non-vitamin K antagonist oral anticoagulants (NOACs) administration was associated with a lower risk of AF recurrence (OR 0.27; 95% CI 0.096 to 0.77; p = 0.014). MACCE occurrence was predicted by higher CHA₂DS₂-VA (Congestive heart failure, Hypertension, Age ≥ 75, Diabetes, Stroke, Vascular disease, Age 65–74) (OR 5.63; 95% CI 1.57–20.12; p = 0.008), lower left ventricular ejection fraction (LVEF) (OR 0.74; 95% CI 0.57–0.99; p = 0.028) and (vitamin K antagonists) VKA use (OR 97.44; 95% CI 3.2–2962.57; p = 0.009). Conclusions: SGLT2i pharmacotherapy in the study population was linked to higher efficacy in symptom reduction, with a probability of AF recurrence and all-cause mortality reduction, which may suggest a potential beneficial role of SGLT2i in this cohort. Full article

Renal involvement in β-thalassemia minor (β-TMin) has been described mainly in case reports and small observational studies, and its clinical significance remains incompletely characterized. Using real-world data from routinely collected electronic medical records, we performed a retrospective cohort study including 1516 adult patients with β-TMin insured by Clalit Healthcare Services to explore renal abnormalities identified during routine clinical care. Urine testing for hematuria, microalbuminuria, and proteinuria was not performed systematically but was ordered at clinicians’ discretion, resulting in evaluation of a clinically selected subset of patients. Among those tested, hematuria, microalbuminuria, and proteinuria were commonly documented, often in the absence of hypertension, diabetes mellitus, congestive heart failure, or impaired kidney function, consistent with largely subclinical renal involvement. Patients who underwent urine testing were older and had more comorbidities than untested patients, indicating potential selection bias. Correlation analyses showed weak associations between hematological and renal parameters, while ferritin levels correlated modestly with selected proteinuria measures. Due to the retrospective design and non-systematic urine assessment, population-level prevalence and clinical impact cannot be determined. Therefore, prospective studies with standardized renal evaluations are needed to better characterize the frequency, mechanisms, and clinical relevance of renal abnormalities in β-TMin. Full article

Introduction: Chronic Kidney Disease (CKD) is a leading public health problem worldwide, with limited therapeutic options to halt its progression. Recent evidence implicates non-coding RNAs (ncRNAs), specifically long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), as critical regulators in renal pathophysiology and the transition from Acute Kidney Injury (AKI) to CKD. This review aims to synthesize recent findings regarding the role of ncRNAs in CKD pathogenesis, emphasizing their potential as diagnostic biomarkers and therapeutic targets. Methods: A systematic search was conducted in the PubMed/MEDLINE and Scopus databases for original research articles published over the last five years. Studies were selected based on specific eligibility criteria focusing on the correlation of ncRNAs with the development, diagnosis, and therapy of CKD. A total of 14 studies were included in the final review. Results: This review identified a dual landscape of ncRNAs function. Several lncRNAs, including H19, MALAT1, NEAT1_2, and LINC00963, were found to act as pathogenic drivers, promoting inflammation, apoptosis, and fibrosis through pathways such as TGF-β/Smad and NF-κB. Specifically, MALAT1 and NEAT1_2 are pivotal in driving the AKI-to-CKD transition. Conversely, specific miRNAs, such as miR-204, miR-26a, miR-451, miR-101, and miR-486-5p, exhibited protective effects by attenuating oxidative stress, preserving endothelial function, and inhibiting epithelial–mesenchymal transition (EMT). Dysregulation of these molecules was also observed in systemic conditions affecting the kidney, such as congestive heart failure and β-thalassemia. Conclusions: ncRNAs are central players in the molecular mechanisms underlying renal injury and maladaptive repair. The identified lncRNAs and miRNAs offer promising avenues for non-invasive diagnosis and the development of novel targeted therapies to prevent fibrosis and slow the progression of CKD. Full article

Background/Objectives: Congestion is a hallmark of heart failure (HF) and a major determinant of outcomes. Non-invasive tools enable detection of subclinical congestion, but their correlation and prognostic relevance remain incompletely defined. The present study aimed to assess the prevalence, evolution, interrelationships, and prognostic impact of clinical and subclinical congestion markers in patients hospitalized for HF. Methods: This single-centre, prospective cohort study included adults admitted with HF who underwent serial evaluations at admission, 72 h, pre-discharge, early outpatient follow-up and at 6 months. Clinical congestion was assessed using a standardized physical examination score. Subclinical congestion was evaluated using lung ultrasound (LUS), Venous Excess Ultrasound Score (VExUS), and Remote Dielectric Sensing (ReDS). Patients were classified according to the presence of clinical and/or subclinical congestion at discharge. The primary endpoint was a composite of all-cause mortality, HF readmission, or unscheduled visits requiring intravenous diuretics within six months. Results: Ninety-four patients (mean age 74 ± 11 years, 68% male) were included. While clinical congestion improved significantly during hospitalization, approximately 30% of patients remained clinically congested at discharge. Among clinically euvolemic patients, only 47% showed no evidence of subclinical congestion. Correlations between congestion markers were weak to moderate, suggesting complementary pathophysiological information. At discharge, pulmonary B-lines were the strongest predictor of the composite endpoint (hazard ratio [HR] 3.50, 95% CI 1.41–8.72), followed by clinical congestion (HR 2.67, 95% CI 1.13–6.30). Patients with clinical and subclinical congestion exhibited lower event-free survival. Conclusions: Subclinical congestion is common despite apparent clinical euvolemia and is associated with worse outcomes. Integrating clinical assessment with non-invasive congestion markers may improve post-discharge risk stratification in HF. Full article

Chronic obstructive pulmonary disease (COPD) is increasingly recognized as a systemic disorder with clinically significant extrapulmonary manifestations. Among these, renal dysfunction—manifesting as chronic kidney disease (CKD) and acute kidney injury (AKI)—is highly prevalent, frequently underdiagnosed, and strongly associated with adverse clinical outcomes. Meta-analytic data indicate that COPD is associated with more than a twofold increase in CKD prevalence, independent of shared risk factors such as age, smoking, hypertension, and diabetes. CKD in COPD is associated with increased mortality, exacerbation burden, and healthcare utilization. AKI represents a particularly severe expression of renal involvement, occurring most commonly during acute exacerbations of COPD (AECOPD). Although the reported incidence of AKI during AECOPD varies widely by clinical setting—from approximately 2% in population-based studies to over 20% in hospitalized cohorts—its presence is consistently associated with marked increases in mortality, respiratory failure, need for mechanical ventilation, and hospital length of stay. This review synthesizes current evidence supporting a lung–kidney interorgan crosstalk framework in COPD, whereby chronic and acute pulmonary pathophysiology generates systemic disturbances that progressively impair renal structure and function. The heart is incorporated as a physiological intermediary, modulating hemodynamic transmission and venous congestion, without constituting the primary disease axis. Recognizing the role of kidney complications in COPD is crucial, as it influences how we diagnose, predict outcomes, and treat patients—especially when there are sudden flare-ups. Full article

Heart failure (HF) is a systemic syndrome in which cardiac dysfunction is closely linked to multiorgan involvement, including the gastrointestinal tract. Increasing evidence highlights the relevance of the gut–heart axis in HF pathophysiology, whereby intestinal hypoperfusion, congestion, and barrier dysfunction promote gut microbiota dysbiosis, systemic inflammation, and adverse cardiovascular outcomes. In parallel, the advent of novel HF therapies, particularly sodium–glucose cotransporter 2 inhibitors (SGLT2i) and the angiotensin receptor–neprilysin inhibitor sacubitril/valsartan, has markedly improved clinical outcomes across HF phenotypes. Beyond their established cardiovascular benefits, these therapies may exert pleiotropic effects that extend to the intestinal environment and the gut microbiota. Through integrated actions on hemodynamics, neurohormonal activation, metabolic pathways, and inflammatory processes, recent data suggest that novel HF drugs may indirectly influence the gut-microbial composition and function. Conversely, the gut microbiota may modulate drug efficacy and result in interindividual variability in therapeutic responses, suggesting a bidirectional interaction between pharmacological treatment and the gut ecosystem. This narrative review summarizes current evidence of gut microbiota alterations in HF and critically examines emerging data on interactions between the gut microbiota and novel HF therapies, focusing on SGLT2 inhibitors and sacubitril/valsartan. Understanding this crosstalk may support the development of microbiota-informed, personalized therapeutic strategies in heart failure. Full article

Background: Systemic venous congestion is a key driver of organ dysfunction in heart failure (HF), yet accurate non-invasive quantification remains challenging. Recognizing residual congestion is critical, since it predicts HF readmissions and mortality. Traditional assessments (physical exam, jugular venous pressure, inferior vena cava [IVC] size) are imprecise. The Venous Excess Ultrasound Score (VExUS) is a semi-quantitative point-of-care ultrasound (POCUS) protocol that integrates IVC diameter with Doppler flow patterns in the hepatic, portal and intrarenal veins to grade systemic venous overload. Methods: We conducted a narrative review of literature (2018–2025) regarding the usefulness of VExUS in HF, covering congestion pathophysiology, clinical evidence (hemodynamic correlations, organ dysfunction, outcomes), potential applications, integration with lung ultrasound, echocardiography and biomarkers, limitations of its assessment and future directions. Results and Discussions: In HF, elevated right atrial pressure causes venous congestion. VExUS integrates IVC diameter with Doppler waveforms of hepatic, portal, and intrarenal veins to grade congestion. Emerging evidence shows higher VExUS grades correlate with elevated filling pressures, renal dysfunction, and worse outcomes. Its use may guide diuretic therapy, aid discharge planning, and monitor outpatient congestion, especially when combined with lung ultrasound and biomarkers. However, VExUS has limitations: it is technical and operator-dependent. Importantly, large trials validating VExUS-guided management are lacking. Future directions include AI-driven automation of Doppler analysis and integration with multimodal congestion monitoring to provide a comprehensive congestion assessment. Conclusions: VExUS is a promising noninvasive tool for quantifying congestion in HF. Higher grades are associated with organ dysfunction and poor prognosis. Incorporating this technique into HF care may improve congestion-guided therapy, but large-scale validation is required before routine use. Full article

Background: Renal function deterioration during hospitalization for acute heart failure (AHF) is common and is traditionally classified as acute kidney injury (AKI) or worsening renal function (WRF) based on changes in serum creatinine (Cr). However, Cr-based definitions may inadequately reflect the complex cardiorenal interactions occurring in AHF. Purpose: This narrative review summarizes and compares definitions of AKI and WRF used in AHF, evaluates their prognostic significance, and explores whether renal function deterioration should be interpreted as a marker of cardiorenal disease severity rather than isolated kidney injury. Methods: A narrative review of randomized trials, observational studies, post hoc analyses, and meta-analyses was conducted, focusing on Cr-based and nephrology-derived AKI definitions (RIFLE, AKIN, KDIGO), timing and baseline selection, congestion status, and the role of biomarkers and imaging in clinical interpretation. Results: The most widely used definition of WRF is an absolute increase in serum Cr ≥ 0.3 mg/dL. Multiple studies demonstrate that such changes frequently occur during effective decongestion and are not independently associated with adverse outcomes in the absence of residual congestion. In contrast, persistent congestion, impaired diuretic response, reduced renal reserve, and advanced cardiorenal comorbidity consistently predict worse prognosis. Nephrology-derived AKI definitions identify higher-risk patients but incompletely account for the hemodynamic and therapeutic context of AHF. Conclusions: In AHF, AKI and WRF often act as markers of underlying cardiorenal disease severity rather than direct indicators of irreversible kidney injury. Interpretation of renal function deterioration should be contextual, integrating congestion status, perfusion, renal reserve, and dynamic response to therapy. Achieving effective and complete decongestion remains the primary therapeutic objective in AHF, even in the presence of transient Cr increases. Full article

Background/Objectives: Acute heart failure (AHF) is a leading cause of hospitalization and mortality among very old patients, yet this group is underrepresented in prognostic studies. Carbohydrate antigen 125 (CA125) has emerged as a potential biomarker of congestion and inflammation, but its value in patients aged 80 years and over remains unclear. We aimed to evaluate the prognostic value of plasma CA125 measured at admission for 12-month all-cause mortality and the composite outcome of mortality or heart failure (HF) readmission in very elderly patients hospitalized for AHF. Methods: We conducted a prospective observational study of patients aged ≥80 years admitted to an acute geriatric unit for AHF. CA125 and NT-proBNP were measured within 24 h of admission. Outcomes were assessed at 12 months. Survival analyses were performed using Kaplan–Meier curves, Cox regression models, and restricted cubic splines. Results: A total of 210 patients (mean age 89.8 ± 5.3 years; 75.3% females; 88.1% frail) were recruited. During the one-year follow-up, 70 deaths (37.2%) and 68 HF hospital readmissions (36.1%) were recorded. Patients in the highest CA125 tertile had an increased cumulative mortality risk (log-rank p = 0.061). A CA125 value ≥ 100 U/mL independently predicted both mortality (HR 1.88, 95% CI 1.15–3.09; p = 0.012) and the composite endpoint (HR 1.54, 95% CI 1.04–2.29; p = 0.031). Measures of functional dependence and frailty demonstrated greater discriminative ability than biomarkers. Conclusions: In very elderly patients hospitalized for AHF, elevated CA125 at admission independently predicted 12-month mortality and HF readmission. CA125 provides complementary prognostic information to geriatric assessment and may support risk stratification in this vulnerable population. Full article