Iron overload cardiomyopathy (IOC) remains an important cause of morbidity and mortality in patients with hereditary haemochromatosis and transfusion-dependent conditions such as haemoglobinopathies. The condition arises when excess iron, due to increased intestinal iron absorption or repetitive transfusions, saturates transferrin-binding capacity, generating non-transferrin-bound iron. This form of iron enters cardiomyocytes through L-type and T-type calcium channels, divalent metal transporter 1, and ZIP14 and triggers oxidative stress via the Fenton reaction, mitochondrial dysfunction, calcium dysregulation, and ferroptosis. The resulting clinical spectrum ranges from diastolic dysfunction to overt heart failure and fatal arrhythmias. Cardiac magnetic resonance T2* has revolutionized diagnosis and risk stratification, enabling MRI-guided chelation strategies that have dramatically reduced cardiac mortality over the past decades. Phlebotomy remains the cornerstone of treatment in primary haemochromatosis, while iron chelators, including deferoxamine, deferiprone and deferasirox, is the standard for transfusion-dependent patients. Adjunctive amlodipine has also emerged as a strategy to reduce myocardial iron accumulation. Novel disease-modifying or curative treatments for thalassaemia, such as luspatercept, mitapivat and gene therapy offer the prospect of addressing the root cause of iron loading. This review provides an updated comprehensive, evidence-based overview of the pathophysiology, diagnosis, and management of IOC.

Heart failure accounts for more than 43% of annual deaths worldwide, and isdriven by widespread pathological remodeling, in which myocardial fibrosis plays an important role. Currently, accurate clinical diagnosis of myocardialfibrosis (MF) remains difficult, with even greater challenges in differentiating among lesser-understood etiologies, such as cardiac sarcoidosis (CS) andcardiac amyloidosis (CA).

To investigate the capability of high-resolution magic angle spinning (HRMAS) nuclear magnetic resonance (NMR)spectroscopy to differentiate amongst patients with MF of different origins (CS, CA) using blood sera.

HRMAS NMR spectroscopy of 10 ìL ofblood sera from three patient groups, with matched controls, was conducted:1)MF due to common causes including hypertension and coronary arterydisease (n = 13),2)transthyretin CA (n = 18), and3)CS (n = 12). NMR spectra were analyzed as regions of interest (ROIs). ROIAL-NMR was used toidentify metabolites present in the determined ROIs. Statistical analysis, such as hierarchical clustering, Wilcoxon/Kruskal-Wallis tests (paired andunpaired), and unsupervised multivariate principal component analyses (PCA), were performed to distinguish diseased individuals from their matchedcontrols.

Analysis of NMR spectra identified 61 ROIs highlighting metabolite alterations such as changes in fatty acids, branched chain aminoacids, and markers of energy and inflammatory states, that may contribute to disease-specific metabolic signatures.

HRMAS NMRmetabolomics results may enhance our understanding of the patho-mechanisms underlying myocardial fibrosis across etiologies and serve as a clinicallypractical tool to improve diagnostic precision and identify new therapeutic targets.

Treatment for heart failure with mildly reduced ejection fraction (HFmrEF) and preserved ejection fraction (HFpEF) has evolved significantly in recent years. This period of therapeutic progress follows a span of over two decades during which randomized controlled trials (RCTs) of neurohormonal blockade and other therapies failed to definitively demonstrate clinical benefits. As such, traditionally, management guidelines for HFmrEF and HFpEF were limited to recommendations focused on optimization of volume status with diuretics, management of comorbidities, and consideration of certain medications such as angiotensin receptor-neprilysin inhibitor (ARNi) or steroidal mineralocorticoid receptor antagonists (MRA) to subsets of patients. After definitive results from multiple RCTs, sodium-glucose cotransporter 2 inhibitors (SGLT2i) are currently a main pillar in treating HFmrEF and HFpEF in European and American guidelines. However, other therapies, including non-steroidal mineralocorticoid receptor antagonists (nsMRA) and glucagon-like peptide-1 receptor agonists (GLP-1 RA), are proving to be additional effective treatments for HFmrEF and HFpEF and preventing the progression of cardiovascular-kidney-metabolic (CKM) syndrome. There is now increasing justification for combining multiple proven treatments for HFmrEF and HFpEF to maximize potential benefits.

Sports cardiology is a cardiovascular subspecialty that cares for competitive athletes and highly active individuals with cardiovascular risk factors and/or disease. Exercise can lead to physiological, structural, and electrical cardiac remodeling while also contributing to maladaptive changes, including arrhythmias. These nuances have contributed to the emergence of sports electrophysiology as a specialized extension within sports cardiology, dedicated to understanding arrhythmias, including best practices in arrhythmia management in this patient group. Although the diagnosis and treatment of arrhythmias in athletes often parallel standard electrophysiological practices, there are differences and factors to be taken into account. Examples include exercise type and intensity; potential performance effects and side effects of antiarrhythmic therapies; timing and indications for catheter ablation; device selection and programming for cardiac implantable electronic devices when applicable; interpretation of cardiovascular testing; and return-to-play guidance. In this state-of-the-art review, athletic electrical remodeling, clinical considerations for arrhythmia management in athletes, device-related matters, and future directions for the evolving field of sports electrophysiology are discussed. This document builds on recent clinical references by providing practical clinical guidance for electrophysiologists and cardiovascular clinicians who care for athletic patients with arrhythmias and formally introduces the concept of "sports electrophysiology" within sports cardiology as a novel discipline.

Despite advances in endovascular technologies, microsurgical clipping is still a relevant treatment for cerebral aneurysms. Blood flow reduction techniques become necessary in some cases (no adequate proximal and distal blood flow control). Rapid ventricular pacing is a new effective technique for controllable hypotension and aneurysm sac relaxation.

To demonstrate successful rapid ventricular pacing in microsurgical clipping of a large aneurysm of vertebrobasilar confluence in acute period of SAH.

A 64-year-old patient with SAH from vertebrobasilar confluence aneurysm underwent successful microsurgical treatment.

The patient underwent surgery on the second day after hemorrhage. Surgery was performed through a right-sided retrosigmoid approach. Two episodes of rapid ventricular pacing were used to relax the aneurysm and reduce the risk of intraoperative rupture. The effect was achieved almost immediately after initiation with episodes lasting no more than 50 seconds. Controllable hypotension minimized bleeding. There were no postoperative neurological complications. CT angiography showed complete exclusion of aneurysm. The patient was discharged after 10 postoperative days.

Rapid ventricular pacing may be justified in the treatment of complex cerebral aneurysms when surgical blood flow control is difficult. Large-scale studies are needed to develop patient selection algorithms for this surgery.

To describe a rare complication of non-penetrating traumatic brain injury.

We present a 16-year-old patient with multiple skeletal lesions and mild traumatic brain injury (TBI). Two weeks after injury, clinical status suddenly worsened due to large subdural hematoma without signs of subarachnoid hemorrhage despite normal neuroimaging data at baseline.

Examination revealed pericallosal artery aneurysm. Microsurgical intervention with aneurysm excision was performed. Histological examination revealed thrombotic masses containing fibrin and no vascular walls of aneurysm. Therefore, the aneurysm was regarded as traumatic false aneurysm resulting from detachment of small artery. There were no neurological disorders at discharge.

Acute subdural hematoma in delayed period after TBI requires CT angiography to rule out traumatic aneurysm.

To analyze the factors contributing to postoperative anosmia and to evaluate the effectiveness of preventive strategies in microsurgery for cerebral aneurysms.

The study included 117 patients with unruptured anterior circulation aneurysms who underwent surgery at the Burdenko Neurosurgery Center in 2024-2025. All patients underwent olfactometric assessment preoperatively, after 5-7 postoperative days and 6 months after surgery. Clinical, anatomical (CT angiography) and intraoperative factors were analyzed.

Postoperative anosmia occurred in 55 (47%) patients with bilateral involvement in 11 (20%) cases. Anosmia developed in 70.2% of patients with anterior communicating artery (ACoA) aneurysms. Significant anatomical predictors were superior (p=0.01) and anterior (p=0.01) ACoA aneurysm dome orientation. Intraoperative risk factors included nerve compression by brain spatula (p<0.001) and arachnoid dissection of the nerve. In some cases, we noted a single-stage flow of blood along anterior cranial fossa base from olfactory tract during frontal lobe traction and arterial dissection. This «red drop» sign was an intraoperative marker of nerve injury (p=0.04). Transsylvian approach for middle cerebral artery aneurysms ensured 100% preservation of olfactory function (p<0.001). After 6 months, olfactory function recovered in 33.3% of patients. Previous COVID-19 was associated with worse recovery (p=0.05).

Postoperative anosmia is a frequent complication in aneurysm surgery. The main predictors are ACoA aneurysm and intraoperative traction-induced avulsion of the nerve. Preventive strategies include selection of less traumatic approach and minimized pressure on olfactory nerve. Arachnoid dissection of the nerve is not recommended.

Triggering receptor expressed on myeloid cells 2 (TREM2) is a key transmembrane immune receptor that is specifically highly expressed in myeloid cells, particularly macrophages, within atherosclerosis (AS) plaques. Advances in single-cell sequencing technology have clearly defined TREM2-high macrophages as a distinct subpopulation known as lipid-associated macrophages. TREM2 exhibits stage-specific bidirectional regulatory effects during the progression of AS. In the early stage of the disease, TREM2 promotes cholesterol uptake by upregulating the scavenger receptor CD36, thereby accelerating foam cell formation and lesion expansion. In the advanced stage, however, its protective effects become prominent: TREM2 enhances macrophage survival, drives reverse cholesterol transport, and improves efferocytosis efficiency, thereby effectively inhibiting necrotic core expansion and maintaining plaque stability. At the molecular level, the TREM2-DAP12 complex upregulates CD36-mediated lipid uptake through the p38 mitogen-activated protein kinase/peroxisome proliferator-activated receptor gamma (PPARγ) axis, whereas deficiency of liver X receptor (LXR) can weaken its protective effects. Mitochondrial reactive oxygen species (mtROS) drive the transition of macrophages toward a pro-inflammatory foam cell phenotype through signal transducer and activator of transcription 5 (STAT5). In addition, ferroptosis-related mitochondrial dysfunction promotes the death of advanced foam macrophages and aggravates plaque instability. In terms of clinical translation, soluble TREM2 (sTREM2) levels are associated with the risk of coronary heart disease and adverse cardiovascular events, suggesting that sTREM2 may serve as a potential biomarker reflecting plaque inflammation and cellular injury and may provide incremental predictive value beyond high-sensitivity C-reactive protein. TREM2 agonists, such as AL002a, can reprogram foam macrophages and enhance efferocytosis and necrotic core clearance, thereby improving plaque stability and showing potential for precision intervention. In summary, TREM2 shows a "double-edged sword" role at different stages of AS, and precise stage-specific modulation of TREM2 may represent a new direction for immunotherapy in AS.

Hypertensive retinopathy is a microvascular complication caused by systemic hypertension and can lead to severe visual impairment. At present, the molecular mechanisms of this disease remain incompletely understood, particularly the global expression profiles and regulatory networks of non-coding RNA (ncRNA). This study aims to comprehensively analyze the genome-wide differential expression profiles of messenger RNA (mRNA), microRNA (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA) in retinal tissues from a spontaneously hypertensive rat (SHR) model of hypertensive retinopathy, and to observe transcriptomic changes after treatment with the calcium channel blocker lacidipine, thereby revealing their potential roles in disease pathogenesis and identifying possible therapeutic targets.

SHRs were used as a model of hypertensive retinopathy, and normotensive Wistar-Kyoto (WKY) rats were used as controls. Rats were divided into 3 groups: A control group (WKY), a model group (SHR), and a treatment group (SHR+lacidipine). Rats in the treatment group received lacidipine by gavage at 0.5 mg/(kg·d) for 8 consecutive weeks. At the end of the experiment, retinal tissues were collected for histopathological examination by hematoxylin and eosin (HE) staining and for high-throughput sequencing. The lncRNA library was used to analyze mRNA, lncRNA, and circRNA expression profiles, and the small RNA (sRNA) library was used to analyze miRNA expression profiles. Differential expression analysis was performed using DESeq2. The screening criteria were |log₂ fold change (FC)|≥1 and false discovery rate (FDR) significance criteria for mRNAs and lncRNAs, and |log₂FC|≥1 and P<0.05 for miRNAs and circRNAs as exploratory candidates. Differentially expressed RNAs were subjected to Gene Ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Competing endogenous RNA (ceRNA) regulatory networks involving lncRNA/circRNA-miRNA-mRNA were constructed through target prediction and co‑expression analysis. Ten mRNAs whose expression changes were reversed after treatment were selected for validation by real-time reverse transcription polymerase chain reaction (real-time RT-PCR; n=6 per group). Comparisons among multiple groups were performed using one-way analysis of variance and post hoc multiple-comparison tests.

1) Verification of the animal model: Blood pressure was significantly higher in the model group than in the control group. The model group exhibited edema of the retinal nerve fiber layer, dilation of vascular lumens, and increased retinal thickness. Lacidipine treatment reduced blood pressure and alleviated these pathological changes. 2) Differential expression of mRNAs: Compared with the control group, 870 mRNAs were significantly downregulated and 1 018 mRNAs were significantly upregulated in the model group. Compared with the model group, 2 644 mRNAs were significantly downregulated and 186 mRNAs were significantly upregulated in the treatment group. GO analysis showed that upregulated mRNAs in the model group were enriched in immune-inflammatory processes, such as leukocyte activation, chemotaxis, defense response, and regulation of tumor necrosis factor (TNF) production, whereas downregulated mRNAs were enriched in G protein-coupled receptor (GPCR) signaling, glycoprotein synthesis, ion channel activity, and related processes. KEGG analysis revealed that upregulated mRNAs in the model group were enriched in interleukin-17 (IL-17), TNF, oxidative stress, and lipid inflammatory mediator metabolic pathways, whereas downregulated mRNAs were enriched in phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) signaling, vascular smooth muscle contraction, extracellular matrix (ECM)-receptor interaction, and related pathways. In the treatment group, the downregulated mRNAs were mainly enriched in pathways related to immune-inflammatory activation, such as mast cell degranulation and leukocyte degranulation. 3) Treatment-reversed mRNAs: A total of 67 genes that were upregulated in the model group and downregulated after treatment were identified; these genes were mainly enriched in endoplasmic reticulum stress-associated apoptotic signaling, mitophagy, ubiquitin ligase activity, and related processes. In addition, 54 genes that were downregulated in the model group and upregulated after treatment were identified; these genes were mainly enriched in amino acid transport, integrin complex, focal adhesion, glutamate transport activity, and related processes. Real-time RT-PCR validated the expression changes of Med22, Rmt1, Sytl3, Itgb7, and Slc1a3 which were decreased in the model group and increased after treatment, as well as Rnf183, Lrrc29, Lat2, Hist1h4m, and Dpm3, which were increased in the model group and decreased after treatment. These findings were consistent with the sequencing results. 4) Differential expression of miRNAs: Compared with the control group, 30 miRNAs were downregulated and 26 miRNAs were upregulated in the model group. Compared with the model group, 14 miRNAs were downregulated and 53 miRNAs were upregulated in the treatment group. Treatment-reversed miRNAs were identified: Rno-miR-1-3p, novel_miR_1203, and novel_miR_1417 were upregulated in the model group and downregulated after treatment, whereas novel_miR_107 and novel_miR_905 were downregulated in the model group and upregulated after treatment. Their target genes were enriched in regulation of retinal cone/rod cell differentiation, ECM remodeling, the Notch pathway, fatty acid synthesis, and related processes. 5) Differential expression of lncRNAs: Compared with the control group, 786 lncRNAs were downregulated and 764 lncRNAs were upregulated in the model group. Compared with the model group, 217 lncRNAs were downregulated and 230 lncRNAs were upregulated in the treatment group. A total of 55 lncRNAs that were upregulated in the model group and downregulated after treatment, and 76 lncRNAs that were downregulated in the model group and upregulated after treatment, were identified. Their target genes were enriched in immune regulation, wound healing, vascular remodeling, retinol metabolism related to rod-mediated scotopic vision, glutamatergic neuron differentiation, the forkhead box O (FoxO) pathway, retinoic acid-inducible gene I (RIG-I)-like receptor signaling, and related processes. 6) Differential expression of circRNAs: Compared with the control group, 45 circRNAs were downregulated and 47 circRNAs were upregulated in the model group. Compared with the model group, 25 circRNAs were downregulated and 22 circRNAs were upregulated in the treatment group. Eleven circRNAs that were downregulated in the model group and upregulated after treatment, and 10 circRNAs that were upregulated in the model group and downregulated after treatment, were identified. Their host genes were enriched in regulation of synaptic neural signaling, second messenger transmission, calcium signaling, and vascular endothelial growth factor (VEGF) signaling pathways. 7) Construction of ceRNA networks: Based on expression patterns and target prediction, multiple lncRNA/circRNA-miRNA-mRNA regulatory networks were constructed. For example, the networks composed of rno_circ_Rims2_10, rno-miR-1-3p, and related mRNAs, such as Mmp14 and Fasn, as well as the novel_miR_1417 related network, may be involved in retinal stress responses, inflammatory regulation, and neurovascular remodeling.

This study is the first to integrate and analyze retinal transcriptomic profiles of mRNAs, miRNAs, lncRNAs, and circRNAs in an SHR model of hypertensive retinopathy, and it reveals RNA expression changes associated with lacidipine treatment. The results suggest that immune-inflammatory activation, neurovascular dysfunction, and ncRNA-mediated ceRNA regulatory networks may participate in the pathogenesis of hypertensive retinopathy. The identified differentially expressed molecules and predicted regulatory axes provide a candidate molecular basis for further mechanistic validation and screening of potential therapeutic targets.

Cardiovascular disease (CVD) accounts for approximately 40% of deaths among patients with rheumatoid arthritis (RA), yet the burden of heart failure (HF) within this population remains poorly characterized. Using the KURAMA cohort, we aimed to quantify the prevalence of HF among RA outpatients and develop a practical HF screening tool that uses variables readily available to rheumatologists in routine clinical practice.

A cross-sectional study of 542 outpatients with RA was conducted. Their HF status was determined using a prespecified multistep algorithm that integrated clinical history, loop diuretic use, N-terminal pro-B-type natriuretic peptide (NT-proBNP), echocardiography, and careful differentiation from interstitial lung disease (ILD). Adaptive LASSO regression was applied to identify independent factors associated with HF and construct a detection score using non-cardiac variables.

Heart failure was detected in 26.5% of patients with RA. Older age, lower haemoglobin (Hb) levels, higher serum creatinine (CRE) levels, and higher Simplified Disease Activity Index (SDAI) were identified as independent non-cardiac factors associated with HF. A 4-factor HF detection score was constructed based on adjusted odds ratios. The area under the receiver operating characteristic curve (AUC) for the discrete score based on variables routinely available in rheumatology clinics was 0.793, comparable to that of NT-proBNP ≥ 125 pg/mL alone (AUC = 0.814).

HF affects over one in four RA outpatients. A simple 4-factor score may serve as a practical first-line triage tool to identify patients who warrant further cardiac evaluation and cardiology referral.