Pericardial diseases comprise a heterogeneous spectrum, ranging from self-limited acute pericarditis to recurrent inflammatory syndromes, large pericardial effusions, cardiac tamponade, and chronic constrictive pericarditis. Although acute pericarditis is often considered a benign condition, a substantial proportion of patients develop recurrent or persistent disease with prolonged symptoms and an impaired quality of life. Diagnostic uncertainty and suboptimal early management, particularly excessive corticosteroid use, may further contribute to the development of chronic disease and treatment resistance. Recent advances in cardiovascular imaging and anti-inflammatory therapy have substantially transformed the management of pericardial diseases. Multimodality imaging, including echocardiography, cardiac computed tomography (CT), and cardiac magnetic resonance (CMR) imaging, plays a central role in anatomical assessment, evaluation of hemodynamic impact, and differentiation of active inflammation from irreversible fibrotic remodeling. Meanwhile, an improved understanding of the autoinflammatory pathways involved in recurrent pericarditis has led to the development of targeted therapies, most notably interleukin -1 (IL-1) inhibitors, which have demonstrated robust efficacy and meaningful steroid-sparing effects in refractory disease. This review summarizes contemporary diagnostic and therapeutic strategies for pericardial diseases, with an emphasis on recurrent pericarditis and imaging-guided management. We propose a stepwise, precision-based approach that integrates clinical risk stratification, multimodality imaging, and targeted anti-inflammatory therapy to optimize patient outcomes.

Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide. Ischemic heart disease and diabetic cardiomyopathy are two CVDs characterized by prominent myocardial injuries. Calcium overload, mitochondrial damage, the accumulation of reactive oxygen species (ROS), and abnormal programmed cell death (PCD) pathways, such as autophagy, pyroptosis, apoptosis, and ferroptosis, are recognized as the major mechanisms of myocardial injury. Dexmedetomidine (DEX) is a selective α2-adrenergic receptor agonist that is often administered to surgical patients due to the associated sedative, analgesic, and anxiolytic properties. Recent studies have indicated that DEX can exhibit more beneficial effects in patients, including reducing myocardial and vascular damage in CVD patients. Mechanistically, DEX reduces levels of oxidative stress markers and inflammatory cytokines and improves mitochondrial function. Numerous studies have revealed novel regulatory roles for DEX in mediating ferroptosis. This study summarizes the expression and functions of ferroptosis in ischemic heart disease and diabetic cardiomyopathy and discusses the regulatory mechanism of DEX in ferroptosis.

The iatrogenic acute aortic syndrome is one of the fatal complications of the endovascular procedure. Identifying and managing such complications is crucial for optimal patient outcomes.

We report a case of left lateral accessory pathway with successful ablation and perforation of a branch of the descending thoracic aorta during the procedure, which was treated by implanting an endovascular stent graft in the thoracic aorta.

Appropriate imaging and early intervention with endovascular repair can be key to the successful management of patients with aortic perforation.

Aortic computed tomography angiography is the gold standard method for diagnosis, and the endovascular approach could be a therapeutic option in these cases.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are widely used metabolic therapies for type 2 diabetes and obesity, with well-established cardiovascular benefits. Beyond glycemic control, accumulating experimental and clinical evidence suggests that GLP-1RAs exert pleiotropic actions relevant to neurological diseases. Metabolic dysfunction, chronic inflammation, oxidative stress, mitochondrial impairment, and neurovascular injury represent convergent mechanisms that contribute to neurodegeneration, cerebrovascular pathology, and metabolism-related brain disorders. Notably, these processes overlap with pathways modulated by GLP-1 signaling across systemic and central compartments. GLP-1 receptors are expressed in neurons, glial cells, and components of the neurovascular unit, providing a biological basis for possible neurological effects. Preclinical studies suggest that GLP-1RAs can reduce neuroinflammation and oxidative stress, support mitochondrial function, and help maintain blood-brain barrier integrity. Clinical findings, however, remain inconsistent. Studies in Parkinson's disease have reported encouraging signals, but biomarker evidence for disease modification is still limited. In Alzheimer's disease, clinical trials have produced mixed or negative results. These differences may reflect disease stage, patient selection, drug-specific pharmacology, central nervous system exposure, endpoint sensitivity, and treatment duration. Overall, GLP-1RAs may influence neurological disease through metabolic, inflammatory, and vascular pathways, but their clinical role remains unsettled. Future studies should use biomarker-informed designs, prespecified neurological endpoints, appropriate drug selection, and sufficiently long follow-up to determine which patients and disease stages are most likely to benefit.

Primary aldosteronism (PA), a renin-independent state of aldosterone excess, is associated with excess risk of stroke, myocardial infarction, atrial fibrillation, heart failure, and chronic kidney disease compared with essential hypertension. Emerging evidence suggests that renin-independent aldosterone excess exists on a continuum rather than as a dichotomous disease state, including subclinical primary aldosteronism (sPA), even in normotensive individuals. Whether sPA is associated with major adverse cardiovascular events (MACE) prior to overt hypertension remains incompletely characterized.

To synthesize available evidence linking renin suppression and mild aldosterone excess to cardiovascular outcomes.

A narrative review of the literature was conducted using PubMed/MEDLINE, the Cochrane Library, and Web of Science from inception through May 2025, to identify cohort studies evaluating renin phenotype, aldosterone levels, and cardiovascular outcomes.

Suppressed renin and higher aldosterone levels, even within conventionally normal ranges, are associated with incident hypertension, left ventricular hypertrophy (LVH), atrial fibrillation, and cardiovascular events. In overt PA, significantly higher rates of cardiovascular diseases have been observed compared with blood pressure-matched essential hypertension. Emerging population-based data suggest a graded cardiovascular risk extending below traditional diagnostic thresholds.

Biochemical phenotypes consistent with sPA may represent an early cardiometabolic state associated with elevated risk of MACE, even before overt PA criteria are met. The absence of standardized diagnostic thresholds and randomized interventional data currently limits clinical translation. Prospective trials evaluating renin-guided screening and early mineralocorticoid receptor antagonism are needed to determine whether intervention at the subclinical stage reduces long-term cardiovascular harm.

To describe the clinical characteristics of a Swedish cohort of patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) and kidney involvement and to study long-term survival and predictors of all-cause mortality.

An observational study including patients with AAV and kidney involvement between 1993 and 2023 from two centres in mid-Sweden. Data were obtained from electronic health care records and follow-up visits. Multivariable Cox regression models and Kaplan-Meier analysis were performed to evaluate risk factors of interest predicting all-cause mortality.

Among 190 patients (56% men, median age 67 years, 43% PR3-ANCA (Proteinase 3 Anti-Neutrophil Cytoplasmic Antibody), and 57% MPO -ANCA (Myeloperoxidase Anti-Neutrophil Cytoplasmic Antibody) positive, estimated glomerular filtration rate at diagnosis was 23 ml/min/1.73 m² [interquartile range (IQR) 11-42] and 16% required dialysis. Median follow-up 20 was 7.5 years (IQR 3.6-12.3) and 106 deaths occurred. Main causes of death were infections (28%), cardiovascular disease (24%) and malignancy (18%). Cox hazard regression models showed that older age [hazard ratio (HR) 1.10, 95% CI 1.06-1.14] was a strong, consistent, and independent predictor of all-cause mortality, irrespective of sex, ANCA type, and kidney function. In the Uppsala cohort (n = 91) serum albumin levels at diagnosis emerged also as an independent risk factor when adjusting for age, kidney function and other inflammatory parameters (HR 0.86, 95% CI 0.79-0.94).

Long-term patient and kidney survival was associated mainly with age and serum albumin levels at diagnosis in this Swedish cohort of patients with AAV. Infections and cardiovascular disease were the most common causes of death, underscoring the importance of infection monitoring and cardiovascular risk management.

Mineralocorticoid receptor antagonists, spironolactone, eplerenone, and finerenone, are cornerstone therapies in cardiovascular and renal diseases. While their efficacy is established, a systematic, head-to-head comparison of their post-marketing safety profiles based on large-scale real-world data is lacking.

This study comprehensively compared the post-marketing safety profiles of spironolactone, eplerenone, and finerenone using 11,556 primary suspect reports from the FAERS database (Q1 2004-Q3 2025).

Disproportionality analyses revealed distinct adverse event (AE) signatures. Spironolactone exhibited the broadest safety profile, with disproportionate reporting indicating congenital malformations, acute pulmonary edema, serious cutaneous reactions, and antiandrogenic effects including rare signals such as endometriosis in males. Eplerenone showed a more focused yet severe profile, with signals for serious cardiac events and renal/hepatic failure. Finerenone demonstrated the most targeted profile, with signals predominantly confined to renal and metabolic domains. Hyperkalemia was a consistent moderate-priority signal across all three drugs, and several high-signal, unlabeled AEs were identified. Network toxicology analysis further supported these findings by linking shared and drug-specific molecular targets to key pathways (e.g., aldosterone-regulated sodium reabsorption, MAPK signaling).

These hypothesis-generating findings underscore the need for personalized safety monitoring, potential label updates, and independent validation in other pharmacovigilance databases before clinical or regulatory conclusions can be drawn.

Atrial fibrillation (AF), the most prevalent cardiac arrhythmia, is strongly associated with atrial fibrosis. Salvianolic acid B (Sal-B), a bioactive compound extracted from Salvia miltiorrhiza, demonstrates cardioprotective properties, though its specific role in AF remains to be elucidated.

Transcriptome analysis of the GSE115574 dataset was performed to identify COL1A2 as a differentially expressed gene in patients with AF. Molecular docking simulations were performed to evaluate the binding affinity between Sal-B and COL1A2. For in vitro experiments, an injury model was established in AC16 cardiomyocytes using Angiotensin II (Ang-II) treatment, followed by intervention with either Sal-B (80 μg/mL) or COL1A2 siRNA. Cellular viability, apoptosis, migration capacity, and fibrosis markers (COL1A1, α-SMA, and collagen III) were subsequently assessed. In vivo studies employed an ACh-CaCl₂-induced AF rat model, with cardiac function evaluated through electrocardiography (ECG) and echocardiography. Myocardial tissue damage was examined via hematoxylin-eosin (HE) staining and Masson's trichrome staining. Western blot analysis was used to determine COL1A2 expression and PI3K-AKT pathway activity.

COL1A2 expression was significantly upregulated in AF, and molecular docking demonstrated its strong binding affinity for Sal-B. Sal-B treatment rescued Ang-II-induced cardiomyocyte damage, reduced apoptosis, and suppressed fibrosis marker expression. In rat models, either Sal-B or si-COL1A2 alone shortened the AF duration, improved cardiac function (attenuated the elevated E/E^' ratio while restoring the ejection fraction), and reduced fibrosis and inflammation. The combined treatment synergistically restored sinus rhythm and normalized collagen deposition, suggesting a modulatory role of Sal-B in these processes.

Sal-B alleviates AF in association with COL1A2 modulation and PI3K-AKT signaling pathway inhibition, which may contribute to reducing atrial fibrosis.

In patients with atrial fibrillation (AF) and heart failure with reduced ejection fraction (HFrEF), atrioventricular node ablation (AVNA) and permanent pacing are often pursued when rhythm control is not pursued. Biventricular pacing (BiVP) has demonstrated benefits over right ventricular pacing, while conduction system pacing (CSP) has emerged as an alternative. However, evidence directly comparing CSP with BiVP in this high-risk population remains inconsistent.

To compare CSP versus BiVP in patients with AF and HFrEF undergoing AVNA, focusing on cardiac function, clinical outcomes, and procedural metrics.

Following PRISMA guidelines, we searched PubMed, Scopus, and Web of Science through February 2026 for studies comparing CSP and BiVP in adults with AF and HFrEF undergoing AVNA. Outcomes included all-cause mortality, heart failure hospitalization (HFH), changes in left ventricular ejection fraction (LVEF), QRS duration, New York Heart Association (NYHA) class, pacing threshold, procedure duration, and fluoroscopy duration. A random-effects model was used to pool mean differences (MDs) or risk ratios (RRs) with 95% confidence intervals (CIs).

Six studies (one randomized crossover trial and five observational studies; N = 766 patients: CSP = 356, BiVP = 410) were included. All-cause mortality was significantly reduced in favor of CSP (RR 0.64 [CI: 0.44 to 0.94], p = 0.02, I² = 0%). There was also a trend towards lower HFH, but it marginally missed statistical significance (RR 0.77 [CI: 0.58 to 1.03], p = 0.08; I² = 0%). Additionally, CSP decreased NYHA class (MD -0.64 [CI: -1.18 to -0.10], p = 0.02; I² = 85%) and significantly reduced QRS duration (MD -33.56 ms [CI: -52.36 to -14.76], p = 0.0005; I² = 97%). LVEF improvement did not significantly differ between groups (MD 4.51% [95% CI: -1.50 to 10.52], p = 0.14; I² = 98%). Procedure duration and fluoroscopy times did not show statistically significant difference between the two groups (MD -11.54 min [CI: -50.05 to 26.97], p = 0.56, I² = 96%), and (MD -5.75 min [CI: -13.13 to 1.63], p = 0.13, I² = 88%), respectively. Overall pacing thresholds did not significantly differ between CSP and BiVP; however, modality-specific subgroup analysis showed comparable thresholds between HBP and BiVP, whereas LBBP was associated with significantly lower pacing thresholds than BiVP.

Among patients with AF and HFrEF undergoing AVNA, CSP may offer symptomatic and electrocardiographic advantages over BiVP, with a possible signal toward improved major clinical outcomes that requires confirmation in larger randomized studies.

Cardiovascular diseases, such as hypertension, coronary artery diseases (CAD), arrhythmias, and chronic heart failure (CHF), often require treatment with beta-blockers. These conditions frequently coexist with chronic obstructive pulmonary disease (COPD), which can complicate therapeutic decisions. Indeed, patients with moderate-to-severe COPD are frequently not given these agents out of concern for possible bronchoconstriction arising from blockade of β₂-adrenoceptors in the airways. Observational studies, and meta-analyses support the cardiovascular benefits of β-blockade in people with COPD and cardiovascular diseases. Recent trials evaluating cardioselective β-blockade suggest that cardioselective beta-blockers such as bisoprolol, metoprolol and nebivolol are safe and likely beneficial in those patients that would benefit from their intake due to presence of cardiac comorbid diseases. The aim of this systematic review is to summarise the recent trials and indications for use of cardioselective β-blockers in patients with COPD.