Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and a leading cause of cardioembolic stroke. In nonvalvular atrial fibrillation (NVAF), thrombus formation occurs predominantly within the left atrial appendage (LAA), making it a key therapeutic target. While oral anticoagulation remains standard for thromboembolic risk reduction, contraindications, elevated bleeding risk, and therapy intolerance drive the need for nonpharmacologic alternatives. This review examines the role of the WATCHMAN left atrial appendage occlusion (LAAO) device in NVAF-related stroke prevention, encompassing pathophysiologic rationale, device design, procedural technique, clinical evidence, post-implantation management, and outstanding evidence gaps. The PROTECT AF and PREVAIL trials established WATCHMAN-based LAAO as noninferior to warfarin for prevention of stroke, systemic embolism, and cardiovascular death, though early procedural complications underscored the importance of operator experience. Subsequent real-world registries confirmed safety and effectiveness in higher-risk, anticoagulation-ineligible populations. Newer-generation platforms including the WATCHMAN FLX and FLX Pro, demonstrate improved sealing performance and procedural safety, while contemporary randomized trials further define LAAO's role relative to DOAC therapy. WATCHMAN-based LAAO represents an important alternative for carefully selected patients, particularly those with high bleeding risk. Optimal patient selection, antithrombotic regimens, and long-term outcomes warrant continued investigation.
Pulmonary artery banding (PAB) remains an important palliative strategy in congenital heart disease (CHD), particularly for temporary modulation of pulmonary blood flow and pressure during staged management. Over the past two decades, catheter-based pulmonary flow restrictors (PFRs) have emerged as less invasive alternatives to surgery, expanding treatment options for fragile infants and selected older patients. This review traces the evolution of transcatheter PFR, from early experimental concepts to off-label use of manually fenestrated Medtronic microvascular plugs (MVPs). It examines device mechanics, fenestration geometry and technique, implantation strategies, pulmonary vascular interaction, complications, antithrombotic management, retrieval, and long-term limitations. Key challenges include non-standardized fenestration, device-vessel mismatch, progressive loss of restriction with growth, anatomy-dependent performance, and increasingly time-dependent retrieval difficulty. The principal strength of the MVP-based approach is its intraprocedural adaptability, allowing fenestration to be tailored to individual anatomy, hemodynamics, and therapeutic goals. Given the dynamic and heterogeneous physiology of CHD, future dedicated platforms should preserve this adaptability rather than impose a fixed design. Technical refinement should therefore remain embedded within a patient-centered strategy that allows ongoing adjustment. Multicenter registries and purpose-built platforms may help define the future of controlled and durable transcatheter pulmonary flow modulation.
IntroductionR-loops, RNA-DNA hybrid structures with a displaced single-stranded DNA loop, are key regulators of transcriptional control, chromatin architecture, and genome stability and have emerging roles in inflammatory signaling. However, the relationship between R-loop abundance and strongly modulated inflammatory effector genes in metabolic inflammation and influenza virus infection remains underexplored.MethodsWe performed a locus-centric integrative analysis combining robust differentially expressed genes (DEGs) from multiple inflammatory and infection-related murine and human transcriptomic disease models with experimentally validated multi-cell R-loop annotations from the reference atlas RLoopBase. Our correlation framework evaluated the directional relationship between R-loop abundance and inflammatory gene expression rather than assuming disease-sample-matched R-loop measurements. We further analyzed R-loop regulatory proteins, NRF2-associated R-loop regulators, and overlaps between R-loop regulators and CRISPRi-identified mitochondrial and cellular reactive oxygen species (ROS) regulators.ResultsIn angiotensin II-infused apolipoprotein E-deficient (ApoE−/−) mice, a model of abdominal aortic aneurysm (AAA), genomic regions encoding the top significantly upregulated genes exhibited significantly fewer R-loops than those encoding downregulated genes at days 14 and 28. Similarly, in atherosclerotic ApoE−/− mice fed a high-fat diet for 32 and 78 weeks, upregulated genes were associated with fewer R-loops than downregulated genes. Reduced R-loop abundance was also observed in genomic regions encoding the top significantly upregulated genes in liver tissues from patients with non-alcoholic steatohepatitis (NASH), as well as in monosodium urate (MSU)-stimulated lymphatic endothelial cells (LECs) and influenza virus-infected human umbilical vein endothelial cells (HUVECs). R-loop regulatory proteins upregulated during metabolic inflammation were enriched in immune and inflammatory pathways. NRF2 was identified as a regulator of 27 R-loop regulatory proteins, including 10 positively and 17 negatively regulated proteins. Furthermore, 54 R-loop regulatory proteins overlapped with CRISPRi-identified mitochondrial and cellular ROS regulators, suggesting potential reciprocal regulation between R-loop homeostasis and ROS signaling. Disease-associated changes in pro-ROS and anti-ROS R-loop regulatory proteins further linked R-loop regulation to inflammatory and oxidative stress pathways.DiscussionThese findings identify reduced R-loop abundance at genomic regions encoding strongly upregulated inflammatory genes as a shared feature across multiple models of metabolic inflammation and influenza virus infection. The results further suggest that immune-associated R-loop regulatory proteins and the NRF2–ROS axis may contribute to R-loop remodeling during inflammatory disease. This integrative framework provides new insight into the potential role of R-loops and ROS-sensitive R-loop regulators in inflammatory and metabolic diseases and identifies candidate pathways for future mechanistic investigation and therapeutic targeting.
BackgroundLeft bundle branch area pacing (LBBAP) has emerged as a physiological pacing strategy. LBBAP has been predominantly performed using the lumen-less lead.ObjectivesThis study aims to explore the efficacy and safety of LBBAP performed with stylet-driven leads (SDL) via site-selective pacing catheter (SSPC) sheaths.MethodsWe evaluated consecutive 79 patients undergoing LBBAP using standard stylet-driven active leads via SSPC sheaths. Pacing parameters (threshold, R-wave amplitude, impedance), QRS morphology and duration, left ventricular activation time in lead V5 and complication rates were analyzed. Postoperative measurements of lead parameters and complications were recorded at 1, 3, 6, and 12 months.ResultsLBBAP was successfully achieved in 69 of the 79 patients (87.3%), with 7742 leads via SSPC sheaths, with 52 patients (65.8%) showing visible left bundle branch potentials. Mean paced QRS duration and left ventricular activation time in lead V5 were 111.1 ± 27.2 ms and 69.0 ± 11.7 ms. Intraoperative electrode parameters for SDL-LBBAP, including pacing threshold (0.8 ± 0.2 V at 0.4 ms), impedance (792.5 ± 140.7 ohms), and sensing amplitude (14.0 ± 5.9 mV), remained stable during the 12 month follow up. Intraoperative ventricular septal perforation occurred in six patients (7.6%), with no subsequent persistent ventricular septal defects. Procedural time and fluoroscopy exposure time were lower in the latter 39 patients, declining markedly as operator experience accumulated.ConclusionsThe application of SDL in LBBAP is safe and feasible, with excellent success rates and stable long term electrical performance.
ObjectiveTo investigate the role of a multimodality imaging approach in detecting subclinical cardiac impairment in systemic sclerosis (SSc) patients.MethodsBetween 2017 and 2019 we retrospectively collected data related to 50 consecutive SSc patients who underwent Doppler echocardiography and cardiac magnetic resonance (CMR). The data was compared with 50 controls matched for age, sex and cardiovascular risk predictors.ResultsCMR revealed late gadolinium enhancement (LGE) (30% vs. 8%, p = 0.005), myocardial edema (14% vs. 0%, p = 0.006), and pericardial effusion (18% vs. 4%, p = 0.026) in a significantly higher number of SSc subjects, compared to matched controls. A positive linear correlation has been observed between disease duration and LGE progression from basal to apical left ventricular segments (r = 0.82, p < 0.001). The lower the ejection fraction, the longer the disease duration (r = −0.69, p = 0.004), and the higher the number of LGE segments (r = −0.78, p < 0.001). Multivariate analysis confirmed disease duration as independent predictor of myocardial fibrosis after adjustment for confounders (p < 0.001), as well as the independent association of both LGE and disease duration with impaired left ventricular ejection fraction in SSc subjects (p < 0.001). Doppler echocardiography showed a significantly lower E/A ratio (1.0 ± 0.3 vs. 1.3 ± 0.6, p = 0.002), higher E/e’ ratio (10.9 ± 2.5 vs. 6.8 ± 1.1, p < 0.0001) and systolic peak tricuspid regurgitation velocity (2.7 ± 0.6 m/s vs. 2.3 ± 0.5 m/s, p = 0.005) among SSc patients compared to controls. LGE-positive SSc subjects showed a higher E/e’ ratio compared to other SSc patients (13.5 ± 2.4 vs. 9.7 ± 1.4, p < 0.0001).ConclusionsThese data confirm the significant prevalence of imaging findings of subtle cardiac impairment in SSc patients, thus suggesting the role of multimodality imaging by Doppler echocardiography and CMR as a potential screening approach in this subset population.
ObjectiveThis study aimed to perform hemodynamic simulations using patient-specific models of abdominal aortic aneurysms (AAA) following endovascular aneurysm repair (EVAR) to investigate the association between energy loss (EL) and Type I endoleak.MethodsPre- and post-EVAR models were reconstructed from computed tomography angiography (CTA) for four patients with Type I endoleak and four without. Component quantification of EL, along with wall shear stress (WSS)-related hemodynamic parameters, were employed to evaluate the potential of endoleak.ResultsEndoleaks following EVAR tended to occur at the junction of stent grafts, where high time-averaged wall shear stress (TAWSS), high turbulence EL, and high mean flow EL were observed. The turbulence EL values for the main stents, left iliac branch stents, and right iliac branch stents in the endoleak group were 516 ± 183*10−6 W, 828 ± 195*10−6 W, and 609 ± 193*10−6 W, respectively, and the mean flow EL for those regions were 363 ± 125*10−6 W, 631 ± 138*10−6 W, and 352 ± 162*10−6 W, respectively. Compared with the no endoleak group, the endoleak group exhibited significantly higher turbulence EL and mean flow EL at the iliac branch and main stent, whereas no significant difference in TAWSS was found.ConclusionComponent quantification of EL demonstrated preliminary feasibility for evaluating Type I endoleak in patients with EVAR for AAA, demonstrating greater advantages over WSS-related hemodynamic parameters. This method may provide valuable support for clinicians in assessing surgical prognosis.
BackgroundDepression is a common comorbidity in cardiovascular disease; however, its prognostic impact in peripheral artery disease (PAD) remains uncertain. This study evaluated the association between depression and clinical outcomes in patients with PAD.MethodsPubMed, Embase, Web of Science, Cochrane Library, and ClinicalTrials.gov were systematically searched from inception to December 2025. Observational studies comparing PAD patients with and without depression were included. Primary outcomes included all-cause mortality, major adverse cardiovascular events (MACE), major amputation, and major adverse limb events (MALE). Random-effects meta-analyses were performed.ResultsThirteen studies involving 681,959 patients were included. Compared with those without depression, PAD patients with depression were generally younger and had a higher burden of cardiovascular and metabolic comorbidities. Depression was not significantly associated with all-cause mortality in pooled analyses of either odds ratios (OR = 2.01; 95% CI: 0.77–5.27; p = 0.15) or hazard ratios (HR = 1.15; 95% CI: 0.97–1.36; p = 0.11). However, depression was significantly associated with worse limb-related outcomes, including major amputation (OR = 1.25; 95% CI: 1.15–1.37; p < 0.001, HR = 1.36; 95% CI: 1.21–1.54; p < 0.001) and MALE (OR = 1.24, 95% CI: 1.16–1.33, p < 0.001). Depression was also associated with a higher risk of MACE in both pooled OR analysis (OR = 1.82; 95% CI: 1.02–3.26; p = 0.04) and time-to-event analysis (HR = 1.24; 95% CI: 1.15–1.35; p < 0.001).ConclusionsIn PAD, comorbid depression was associated with higher MALE and MACE risks, but not all-cause mortality. These findings suggest that mental health assessment may be considered as part of comprehensive PAD care.
Coronary artery bypass grafting (CABG) remains central for multivessel coronary artery disease, but durable benefit depends on graft patency. Patency reflects interacting anatomical, technical, haemodynamic, biological and patient-level determinants. The endothelium offers a useful, metabolically active interface because it regulates vascular tone, thrombosis, inflammation, leukocyte trafficking and repair. This Review examines how conduit choice, harvesting, preservation, anastomotic geometry, target anatomy, operative strategy and comorbidity drive early thrombosis, intermediate intimal hyperplasia and late atherosclerosis. Particular emphasis is placed on oxidative stress, endothelial nitric oxide synthase dysfunction, reduced endothelial nitric oxide (eNO) bioavailability and pathological reactive oxygen species (ROS) signalling. Accordingly, we focus on endothelial nitric oxide synthase (eNOS) dysfunction, reduced eNO bioavailability and pathological ROS signalling, and present an eNO/ROS-centred research framework, requiring local delivery, temporal control and CABG-specific validation.
ObjectiveAdverse pregnancy outcomes (APOs) are independent risk factors for cardiovascular disease in women. Within the novel cardiovascular-kidney-metabolic (CKM) framework, evidence linking APOs to advanced CKM (stages 3–4) remains limited.MethodsThis study used data from the Kailuan Cohort and combined cross-sectional and longitudinal designs. The cross-sectional analysis included 2,738 women with singleton deliveries. For the longitudinal analysis, 2,575 women without advanced CKM at baseline were followed up for a median of 11.68 years. A history of APOs was the primary exposure. Multinomial logistic regression and Cox proportional hazards models were used.ResultsCross-sectionally, APOs were positively associated with baseline CKM stage severity, with odds ratios increasing across stages (Stage 1: odds ratio [OR] 1.42, 95% confidence interval [CI] 1.03–1.96; Stage 2: OR 1.65, 95% CI 1.26–2.17; advanced CKM: OR 2.93, 95% CI 1.74–4.94). Women with APOs had a higher incidence of advanced CKM than those without (13.39 vs. 8.42 per 1,000 person-years). After multivariable adjustment, a history of APOs was associated with a 27% increased risk of incident advanced CKM (hazard ratio 1.27, 95% CI 1.01–1.61). Sensitivity analyses excluding participants with less than 4 years of follow-up and those taking medications at baseline yielded results consistent with the primary analysis. In the exploratory analyses, we further evaluated the association between a history of APOs and incident CKM stages 3 and 4. A history of APOs was associated with an increased risk of incident CKM Stage 4, whereas no statistically significant association was observed with incident CKM Stage 3.ConclusionA history of APOs was associated with greater baseline CKM severity and an increased risk of developing advanced CKM. Therefore, APOs may serve as early markers for identifying women at risk of progressive CKM.
Epigenetics modulates gene expression and plays a pivotal role in numerous immune disorders. Over the past two decades, increasing evidence has indicated that epigenetic regulation contributes to transplant rejection and immune tolerance. Four primary epigenetic mechanisms—DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs (ncRNAs)—exert distinct effects on rejection after transplantation. Therefore, understanding the epigenetic mechanisms of rejection provides novel avenues for inducing immune tolerance and developing strategies to prolong graft survival and patient longevity. This review outlines the history of epigenetics and highlights landmark events since the term was coined. Furthermore, we summarize epigenetic research methodologies and describe the four primary general mechanisms of epigenetic regulation. We subsequently focus on recent studies supporting the role of epigenetic regulation in distinct pathological processes of solid organ transplantation (namely, ischemia‒reperfusion injury, acute rejection, and chronic rejection) and graft-vs.-host disease following hematopoietic stem cell transplantation. Finally, we discuss the clinical applications of epigenetics in transplant rejection, including predictive diagnostics and the induction of immune tolerance, to guide the future development of improved rejection suppression therapies.
BackgroundThe role of epicardial adipose tissue (EAT) and gut microbiota (GM) in heart failure (HF) and atrial fibrillation (AF) have been extensively researched, but the role of them in individuals with concurrent HF with reduced ejection fraction (HFrEF) and AF (HFrEF_AF) is still unclear. Furthermore, the role of SGLT2i in HFrEF_AF patients is also not fully understood. The purpose of this study is to compare the differences in EAT and GM between HFrEF_AF and HFrEF patients without AF (HFrEF_NAF), and to analyse the relationship between them and the patients' heart structure, as well as the changes of them after SGLT2i treatment.Methods45 HFrEF_NAF patients and 39 HFrEF_AF patients were continuously recruited, with 26 patients from each group meeting the selection criteria. Fecal samples and CT scans were collected at baseline and after SGLT2i treatment for 3 months, respectively. The 16S rRNA gene of fecal samples was sequenced, and EAT volume (EATV) and EAT volume index (EATVI) values were measured and calculated with CT. These patients were followed up for up to 12 months to assess their long-term re-hospitalization rates.ResultsThe results showed that EATV [191.75 (119.59, 222.44) vs. 141.99 (97.10, 183.75)] and EATVI [105.07 (82.90, 116.39) mL/m2 vs. 81.03 (55.12, 108.74) mL/m2] in HFrEF_AF patients were significantly higher than in HFrEF_NAF patients. After adjusting for Age, Gender, CHD and BMI, Spearman correlation analysis showed that EATVI was significantly negatively correlated with post-conversion abundance of Escherichia coli (R = −0.496, P = 0.019) and Escherichia Shigella (R = −0.472, P = 0.027) in HFrEF_AF patients. The mediation analysis showed that Escherichia Shigella in HFrEF_AF patients had a significant indirect effect on LAAD through EATVI (ACME = −0.553, P = 0.042), but the direct and total effects were not significant. After 3 months of SGLT2i treatment, the connection between Escherichia Shigella, EATVI and LAAD disappeared in HFrEF_AF patients. Moreover, after SGLT2i treatment, harmful AF-related bacteria such as Catenibacterium are no longer enriched in HFrEF_AF patients, whereas beneficial bacteria such as Blautia are enriched. The 12 months follow-up showed no significant difference in re-hospitalization rate between HFrEF_NAF and HFrEF_AF patients.ConclusionEATV and EATVI in HFrEF_AF patients were significantly higher than in HFrEF_NAF patients. There may be an abnormal “Escherichia Shigella-EAT-LAAD” axis in HFrEF_AF patients, and SGLT2i may benefit HFrEF_AF patients differently than HFrEF_NAF patients by inhibiting this axis.Clinical Trial Registrationhttps://www.chictr.org.cn/showproj.html?proj=240632, ChiCTR2400088128.
Background and aimsDelayed extubation of the endotracheal tube (DE) can occur after surgical anesthesia. There has been particular interest in DE among patients with obesity (defined as BMI ≥ 30 kg/m² according to World Health Organization criteria), but the risk factors remain unclear.Methods and resultsWe aimed to identify risk factors for DE after abdominal laparoscopic gastrointestinal surgery. The incidence of DE in this setting was approximately 10%. Through multiple logistic regression, we identified multiple risk factors for DE. In the overall gastrointestinal cohort, BMI and age showed the strongest correlation with DE, with a combined AUC of 0.875. The cutoff values for BMI (31.765) and age (53.5 years) represent risk-discrimination thresholds for identifying patients at higher risk of DE. In the bariatric subgroup, the factors that showed the strongest discriminatory ability were BMI, age, male sex, propofol dosage, sevoflurane dosage, and fasting blood glucose, with a combined AUC of 0.920. The exploratory cutoffs—BMI 36.32, age 41.5 years, male sex, propofol 107.5 mL, sevoflurane 35 mL, and fasting blood glucose 5.935 mmol/L—may help identify patients at relatively higher risk of DE.ConclusionsBMI and age are the most reliable predictors of DE in patients undergoing gastrointestinal surgery. In addition to BMI and age, other important factors include male sex, dosages of propofol and sevoflurane, and fasting glucose levels. For patients with obesity, the combined influence of these factors yielded an AUC of 0.920 for predicting delayed extubation.
BackgroundRotational atherectomy (RA)-induced coronary perforation (CP) represents a dreaded complication, with incidence rates remaining constant and non-negligible for patient safety.ObjectiveIn 2020, we published a paper on four mechanisms of RA-induced CP. In this paper, we hypothesized that modifying practice through general awareness of the mechanisms of RA-induced CP and providing mentorship could lead to a reduction in the incidence of CP.MethodsConsecutive RA patients were recruited and stratified into two groups: January 2009 to December 2019 (Period I) and January 2020 to February 2024 (Period II). During Period II, efforts (structured education, case advice, and case review) to promote general awareness of the four mechanisms of the RA-induced CP were made and mentorship from experienced operators was provided to ensure adherence to good RA practice.ResultsA total of 877 patients were recruited: 510 in Period I and 367 in Period II. Most RA procedures were performed for single vessels in both periods. For non-left main vessels, more distally located and bifurcation lesions were treated in Period I, but the incidence of severe calcification was slightly higher in Period II than in Period 1. Less RA was performed for side branches only, and the use of only the 1.25 mm burr increased in Period II. RA could be successfully completed in a high percentage of patients in both periods (98.4% vs. 98.4%, p = 0.938). The final stent size and total stent length were similar in the two periods. Baseline and gain in Syntax scores were higher in Period I than in Period II, but the residual Syntax scores were similar. More patients were prophylactically put on mechanical circulatory support for CHIP in Period II. Acute slow/no flow (4.9% vs. 9.0%, p = 0.021), RA-induced CP (0.3% vs. 2.0%, p = 0.027), and acute heart failure/pulmonary edema (0.3% vs. 2.9%, p = 0.004) were significantly reduced in Period II. No CP events occurred secondary to wire tip injury, wire transection, burr oversizing, or bias cutting in Period II.ConclusionModifying RA practice through general awareness of the four mechanisms of RA-induced CP and provision of mentorship from experienced operators helped lower the incidence of this fearful complication.
ObjectiveTo observe the efficacy of drug-coated balloon (DCB) in the treatment of in situ short (reference diameter ≥2.8 mm) and long lesions (reference diameter ≥2.8 mm, length ≥20 mm) of large coronary artery vessels.MethodsA total of 126 patients who were diagnosed and treated in the Department of Cardiology, Affiliated Hospital of Hangzhou Normal University from April 2021 to December 2024 were selected, and all of them were treated with DCB for in situ primary coronary artery lesions. Computer-based quantitative coronary angiography analysis software was used to analyze the coronary angiography images of included patients obtained at three different time points; pre-interventional procedure, immediate post-interventional procedure, and follow-up. The selected patients were divided into two groups according to the length of target vessel lesions, namely the lesion length <20 mm group (n = 68) and the lesion length ≥20 mm group (n = 58). The inter-group comparison was performed to evaluate the efficacy of DCB in long in situ coronary artery lesions.ResultsThe average length of the target vessel lesion in the included cases was 16.64 ± 5.65 mm, and the reference diameter of the target vessel lesion was 3.19 ± 0.35 mm. During follow-up of 14.80 ± 8.55 months, none of the patients suffered acute myocardial infarction or severe arrhythmia, cardiogenic shock, and stroke. None of the cases showed revascularization of the target vessel at follow-up, and the late lumen loss during follow-up was −0.03 ± 0.23 mm. There was no significant difference in late lumen loss between the two groups of patients with different lesion lengths [−0.03 ± 0.21 mm vs. −0.02 ± 0.25 mm, P = 0.803].ConclusionsDCB is safe and effective in treating in situ short and long lesions of large coronary artery vessels, and it can reduce the late lumen loss in coronary target lesions.
Diabetic cardiomyopathy refers to myocardial structural, functional, and metabolic abnormalities enriched in people with diabetes that are not fully explained by obstructive epicardial coronary artery disease, significant valvular disease, or other established cardiac conditions. In clinical practice, diabetic myocardial dysfunction frequently overlaps with obesity, hypertension, chronic kidney disease, coronary microvascular dysfunction, and heart failure with preserved ejection fraction (HFpEF)-type cardiometabolic phenotypes. Among the mechanisms implicated in this condition, advanced glycation end products (AGEs) and receptor for advanced glycation end products (RAGE) signaling constitute a biologically plausible framework linking chronic hyperglycemia and dicarbonyl stress to myocardial injury. This review distinguishes RAGE-independent AGE-mediated injury, including extracellular matrix cross-linking and intracellular protein modification, from RAGE-dependent multiligand signaling, which may amplify oxidative, inflammatory, mitochondrial, calcium-handling, endothelial, and profibrotic responses. We further discuss RAGE as a multiligand pattern-recognition receptor and its interactions with danger signaling, innate immune pathways, and inflammasome activation within a broader inflammatory–oxidative network. In addition, we evaluate therapeutic strategies aimed at reducing glycation burden, interrupting matrix cross-linking, or inhibiting receptor-related signaling, and assess circulating and tissue-related biomarkers for phenotypic stratification and therapeutic monitoring. The review further considers methylglyoxal, glyoxal, 3-deoxyglucosone, and glyoxalase-1-dependent detoxification as components of dicarbonyl stress. Although experimental evidence supports biological plausibility, human evidence remains predominantly associative, circulating biomarkers lack cardiac specificity, and DCM-specific therapeutic trials are scarce. Future studies should use phenotype-enriched, multimodal biomarker strategies and mechanism-matched endpoints to determine whether selected patient subgroups may benefit from AGE- or RAGE-directed intervention.
BackgroundRadial access is currently the approach of choice for coronary interventional procedures. However, puncture and hemostasis are not exempt from access site complications. This study evaluated the efficacy and safety of two radial hemostasis devices used after percutaneous coronary intervention (PCI) in routine clinical practice.MethodsA prospective, single-center, real-world cohort study was carried out. Consecutive patients undergoing coronary angiography or PCI via radial access between February 2023 and October 2024 were included. Depending on the hemostasis technique used, the patients were assigned to TR-Closure band™ or a dedicated pad (VIRUNDA®). Access site complications were assessed at the time of device removal.ResultsA total of 597 patients were included (TR-Closure band™ n = 282; VIRUNDA® n = 315). The median age was 71 years (63–78); 409 (68.5%) were male. Compression time was shorter with VIRUNDA® [median 113 [90–133] vs. 148 [125–180] minutes; p < 0.001]. VIRUNDA® was associated with lower bleeding rates [Bleeding Academic Research Consortium (BARC) score 1: 9.8% vs. 58.2%], less pain during compression (10.5% vs. 19.9%) and after compression (5.4% vs. 13.8%), and less paresis (2.5% vs. 8.5%) (all p ≤ 0.001). Hematoma was more frequent with TR-Closure band™ (27.7% vs. 19.4%; p = 0.009). The immediate radial artery occlusion rates were similar (9.2% vs. 4.6%; p = 0.143). The multivariate analysis identified the use of VIRUNDA® as an independent protective factor (RR 0.171; 95%CI 0.119–0.245; p < 0.001).ConclusionsCompared with TR-Closure band™, VIRUNDA® reduced bleeding, pain and paresis, and shortened compression time, without a significant increase in immediate radial occlusion. These findings support its use as a safe and efficient hemostatic alternative in routine practice.
Sepsis-induced cardiomyopathy (SIC) is an acute reversible myocardial dysfunction complicating sepsis. With impaired cardiac systolic and diastolic function, it greatly increases the risk of multiple organ failure and mortality in septic patients. This systematic review outlines the overall research landscape of SIC, including pathological mechanisms, epidemiological profiles, updated diagnostic systems and innovative therapeutic strategies, as well as existing challenges and future research priorities. Five major pathological pathways jointly mediate SIC progression, and its prevalence and mortality differ substantially across regions, populations and infectious pathogens. The diagnostic framework has been updated to a multi-dimensional evaluation system, and emerging imaging techniques and combined biomarker panels have greatly improved early diagnostic performance. Therapeutic concepts have transformed from conventional symptomatic care to mechanism-oriented precise intervention, with multiple new therapies and intelligent medical tools applied clinically. At present, inconsistent diagnostic criteria, insufficient specific medications and unbalanced medical resources worldwide hinder clinical management. Future studies aim to standardize diagnostic criteria, explore molecular mechanisms, accelerate the clinical application of targeted drugs, and popularize advanced technologies in under-resourced areas to improve patient outcomes.
Interventional treatment for hemodynamically unstable pulmonary embolism (PE) is now common due to the fact that unstable PE carries a significant 30-day mortality. Unstable PE is characterized by acute right ventricular failure, hypotension, and hypoxia, leading to cardiovascular collapse and cardiac arrest. Implementation of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) acutely provides oxygenation support to improve hypoxia and offload the right ventricular (RV) pressure in the belief that rapid reduction of hypoxia and right ventricular (RV) pressure will provide a window for intervention. There are two strategies for using VA-ECMO during percutaneous pulmonary mechanical thrombectomy: VA-ECMO-assisted mechanical thrombectomy and mechanical thrombectomy with standby VA-ECMO. While the application of VA-ECMO in percutaneous mechanical thrombectomy is usually short-term, providers must be cognizant that it can be associated with substantial multisystem morbidity due to a systemic inflammatory response, hemorrhagic stroke, renal dysfunction, and bleeding, and these factors will impact outcomes. The evolving paradigm positions VA-ECMO combined with percutaneous pulmonary mechanical thrombectomy as the preferred combination for the high-risk PE patients (acute right ventricular failure, refractory shock, and cardiac arrest), while percutaneous pulmonary mechanical thrombectomy alone with standby VA-ECMO suffices for most intermediate PE patients.
IntroductionCoronary artery disease (CAD) remains the leading cause of cardiovascular mortality worldwide, and early accurate risk stratification for major adverse cardiovascular events (MACE) is critical for improving clinical outcomes. Coronary computed tomography angiography (CCTA) is the cornerstone of non-invasive plaque assessment, yet conventional morphological evaluation fails to capture plaque microheterogeneity, limiting the accuracy of traditional risk prediction. We developed and validated a multidimensional model integrating clinical, plaque morphological, and CCTA-derived radiomic features to predict MACE, and quantified the incremental prognostic value of radiomics.MethodsA total of 567 patients with CCTA-confirmed CAD were retrospectively enrolled and randomly split 7:3 into training (n = 398) and test (n = 169) sets. From 1,833 extracted radiomic features, hierarchical dimensionality reduction selected core features to construct a radiomic score. Four models were established: clinical + plaque, clinical + radiomics, plaque + radiomics, and all features. Model performance was assessed using area under the receiver operating characteristic curve (AUC), calibration curves, and decision curve analysis. Incremental value was evaluated via the DeLong test, integrated discrimination improvement (IDI), and net reclassification improvement (NRI). Model interpretability was elucidated via SHapley Additive exPlanations (SHAP).Results and DiscussionIn the test set, the full model achieved an AUC of 0.840 (95% CI: 0.774–0.907), accuracy of 0.822, and Brier score of 0.150, significantly outperforming the clinical + plaque model (AUC = 0.771, P = 0.016). The full model yielded an IDI of 0.203 (95% CI: 0.151–0.256), categorical NRI of 0.379 (95% CI: 0.245–0.508), and continuous NRI of 1.151 (95% CI: 0.88–1.416). SHAP analysis identified texture features reflecting plaque grayscale heterogeneity as the primary drivers of MACE prediction. These findings demonstrate that combining clinical, plaque, and radiomic features significantly improves MACE prediction in CAD, and that radiomics offers substantial incremental prognostic value, providing a reliable non-invasive risk stratification tool.
