Mitral commissural prolapse or flail, characterized by intricate and diverse anatomical features, poses a significant challenge in mitral transcatheter edge-to-edge repair (M-TEER). Previous studies have largely focused on central mitral regurgitation with favorable valve anatomy or a general broad spectrum of complex mitral regurgitation. However, no established approach is currently available for M-TEER in commissural degenerative mitral regurgitation (DMR).
Therefore, this study aimed to evaluate the efficacy and safety of a novel morphology classification-guided M-TEER strategy for treating commissural DMR using the MitraClip system. This prospective, multicenter, single-arm, objective performance criteria study involved 12 experienced centers in Asia, primarily located in China. Patients with symptomatic moderate-to-severe (3+) and severe (4+) native DMR and commissural involvement were stratified into three morphological categories based on an echocardiographic core laboratory analysis, and tailored M-TEER strategies were proposed. The primary endpoint is the proportion of patients achieving a mitral regurgitation (MR) grade of ≤1+ without repeat mitral intervention at one-year follow-up. Clinical, echocardiographic, functional, and quality-of-life outcomes were assessed over one year.
Based on statistical power calculations, a total of 148 patients are required to achieve adequate power to test the primary efficacy hypothesis, accounting for an estimated 10% attrition rate at 12 months.
The morphology classification system enhances M-TEER for commissural DMR by addressing the unique challenges of this approach, enabling tailored interventions that optimize procedural success and patient outcomes.
ChiCTR2400090258, https://www.chictr.org.cn/showproj.html?proj=239191.
Continuous-flow left ventricular assist devices (LVADs) represent a leading option in the treatment of end-stage heart failure (HF), provided that right ventricular (RV) contractile function is sufficiently preserved to ensure cardiac output after LVAD implantation. In this context, evaluating the RV before surgery is crucial, as the onset of early right heart failure (RHF) following LVAD placement is linked to increased mortality and morbidity. Unfortunately, the contractile performance of the RV is a difficult issue to evaluate and requires a multimodal approach based on the application of multiple diagnostic tools, including clinical assessment, echocardiography, right heart catheterization (RHC), and risk models, all of which have variable predictive power in the currently available literature. Pre-implantation RV assessment is even more challenging and misleading in patients with hemodynamic instability under extracorporeal membrane oxygenation (ECMO) support, a situation characterized by complete right heart unloading, which renders most assessment techniques unreliable. The present paper proposes a simple and comprehensive preoperative appraisal strategy for the RV, which is adapted to the clinical status (critical or more stable) of the patient, based on a review of the advantages and limitations of each diagnostic modality and derived parameters.
Pulmonary hypertension (PH) is a progressive disease caused by structural and functional changes in the pulmonary vasculature resulting from diverse etiologies. PH ultimately leads to increased right ventricular (RV) afterload, RV hypertrophy, fibrosis, and right heart failure (RHF). Moreover, RV fibrosis initially serves as a protective mechanism against pressure overload-induced RV dilatation, but eventually progresses to excessive fibrosis, which impairs cardiac function. This review explores the relationship between RV fibrosis and RV function in PH patients, examines the clinical relevance of this relationship, evaluates techniques for quantifying RV fibrosis, and presents potential therapeutic strategies aimed at preserving right heart function in PH patients.
Cardiac amyloidosis, once considered a rare and untreatable disorder, is now increasingly recognized as a significant cause of heart failure, particularly in older adults. The two most clinically relevant subtypes of cardiac amyloidosis—immunoglobulin light-chain amyloidosis (AL) and transthyretin-related amyloidosis (ATTR)—differ in pathogenesis, natural history, and management strategies, thereby necessitating a tailored approach to diagnosis and therapy. Advances in multimodality cardiac imaging, including echocardiography, cardiac magnetic resonance, and nuclear scintigraphy, have enabled earlier detection and improved differentiation between subtypes. Management of AL centers on rapid initiation of plasma cell-directed therapies to suppress light-chain production, with autologous stem cell transplantation and novel chemotherapeutic regimens improving survival. In contrast, ATTR management focuses on stabilizing or reducing transthyretin deposition through disease-modifying agents, such as stabilizers, gene-silencing therapies, and emerging fibril-disrupting approaches. Supportive care, including guideline-directed heart failure therapies and arrhythmia management, as well as advanced therapies such as transplantation, remains essential across both subtypes, albeit with unique considerations due to amyloid-related hemodynamics. This review synthesizes current evidence on the diagnosis and treatment of AL and ATTR, highlights recent therapeutic breakthroughs, and discusses ongoing challenges in optimizing patient outcomes, from equitable access to therapies to the integration of multidisciplinary care.
The association between elevated perfusion pressure and neurological outcomes in out-of-hospital cardiac arrest (OHCA) survivors remains unclear. Specifically, to our knowledge, no studies have currently investigated whether the duration of elevated perfusion pressure influences neurological prognosis following OHCA. Thus, this study aimed to examine the association between the duration of a mean arterial pressure (MAP) >80 mmHg during the first 48 hours after return of spontaneous circulation (ROSC) and neurological outcomes in OHCA survivors.
This observational study included adult patients (≥18 years) with OHCA treated between January 2019 and May 2021. The cumulative duration of a MAP >80 mmHg was recorded during the 0–24, 25–48, and 0–48 hour intervals following ROSC. The primary outcome was the neurological status at 6 months, with good outcomes defined as Cerebral Performance Category (CPC) scores of 1 or 2.
Among the 468 patients with OHCA, 132 (28.2%) achieved good neurological outcomes. The duration of a MAP >80 mmHg over 0–48 hours was significantly longer in the good outcome group compared with the poor outcome group (35 (26–42) vs. 28 (16–39) hours; p < 0.001). In the multivariable analysis after adjusting for confounders, longer durations of a MAP >80 mmHg at 0–48 hours (odds ratio (OR): 1.047, 95% confidence interval (CI): 1.021–1.073) and 25–48 hours (OR: 1.086, 95% CI: 1.042–1.131), but not at 0–24 hours, were associated with good neurological outcomes at 6 months.
The duration of a MAP >80 mmHg during the 0–48 and 25–48 hour periods after ROSC was associated with good neurological outcomes at six months in OHCA survivors.
The implementation of the fibrosis 4 (FIB-4) index was initially associated with hepatic dysfunction; however, this index may also provide prognostic information in heart failure (HF). Thus, this study aimed to assess whether combining the FIB-4 and carbohydrate antigen 125 (CA125) indices in patients hospitalized for acute heart failure (AHF) can identify subgroups with differing risks of morbidity and mortality.
This retrospective study included 402 patients consecutively admitted for AHF between January 2023 and December 2024, after excluding elective admissions (n = 403), inter-hospital transfers (n = 232), and low-output cases (n = 51). Patients were stratified into four groups according to the FIB-4 score (<1.3 or high) and CA125 value (≤50 U/mL or high): Group 1 (low FIB-4 + low CA125; n = 43), Group 2 (low FIB-4 + high CA125; n = 57), Group 3 (high FIB-4 + low CA125; n = 117), and Group 4 (high FIB-4 + high CA125; n = 185). Clinical, echocardiographic, therapeutic, and laboratory variables were analyzed, as well as morbidity (HF-related emergency visits and readmissions) and all-cause mortality.
Patients with both elevated FIB-4 and CA125 values had a higher prevalence of systemic/mixed congestion (p < 0.01), higher N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels (p < 0.01), and less frequent inspiratory inferior vena cava (IVC) collapse (p < 0.01). Although no survival differences were observed (p = 0.29), morbidity was significantly higher in group 4: more worsening episodes per patient (p = 0.0001), increased HF readmissions (p = 0.004), and more emergency visits (p = 0.001). The FIB-4 index correlated positively with worsening episodes (p < 0.0001), and the CA125 value showed a trend with mortality. No significant correlation was found between FIB-4 and CA125 or between FIB-4 and mortality (p > 0.1).
The FIB-4 index may be a useful indicator in AHF. Elevated values at admission for decompensation, in combination with high CA125 levels, can be used to identify a subgroup of patients with poor short- to medium-term outcomes, particularly in terms of worsening. Further studies are needed to determine the actual utility of the FIB-4 index in the context of AHF.
Significant differences often exist between estimated glomerular filtration rates (eGFR) calculated using various biomarkers. However, the relationship between these eGFR methods and atrial fibrillation (AF) recurrence after radiofrequency catheter ablation (RFCA) remains unclear.
Thus, this study employed a retrospective analysis of 523 patients with AF who underwent an initial RFCA between July 2019 and October 2022. The eGFR was calculated using three methods based on the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula: serum creatinine (eGFRcr), serum cystatin C (eGFRcys), and a combination of both (eGFRcrcys). Cox regression models were used to explore the relationship between eGFR and AF recurrence.
Over a 1-year follow-up period, 174 (33.3%) patients experienced AF recurrence after RFCA. Multivariable Cox regression analysis indicated that only eGFRcys showed a consistent, significant inverse association with AF recurrence (hazard ratio (HR) = 0.990, 95% confidence interval (CI): 0.982–0.998, p = 0.019). In contrast, eGFRcrcys showed borderline significance after full adjustment (p = 0.067). Meanwhile, stratifying by optimal cutoff values identified an association for eGFRcys ≤64.280 mL/min/1.73 m2, and eGFRcrcys ≤76.093 mL/min/1.73 m2 with significantly higher recurrence risks after full adjustment (p = 0.008 and p = 0.036, respectively). Additionally, incorporating eGFRcys or eGFRcrcys into the baseline risk model led to a greater improvement in predictive accuracy than adding eGFRcr.
The association between eGFR and AF recurrence after ablation appears to vary depending on the measurement methods; eGFRcys seems to provide the most reliable information. Incorporating eGFRcys into the pre-ablation risk stratification may enhance patient management and improve outcomes for patients undergoing AF ablation.
Predicting cardiac death in patients with acute myocardial infarction (AMI) remains a major challenge. The Coronary Artery Tree description and lesion evaluation (CatLet) angiographic scoring system can describe the variability in coronary artery anatomy, the degree of stenosis of the affected coronary artery, and the subtended myocardial territory. Therefore, this study aimed to establish an effective and interpretable machine learning (ML) model to explore the relationship between the CatLet score and cardiac death in patients with AMI.
The CatLet score was calculated in 767 consecutively enrolled patients with AMI. Cox regression analysis, Kaplan–Meier survival analysis, and restricted cubic spline analysis were used to explore the association between the CatLet score and cardiac death in patients with AMI. Six ML methods were used to build predictive models. The Shapley Additive Explanations (SHAP) analysis was used to visualize model features and individual case predictions.
Compared to the lowest CatLet score of tertile 1, patients with the highest CatLet score (tertile 3) had a higher risk of cardiac death (hazard ratio (HR) = 3.71; 95% confidence interval (CI) = 1.36–10.08; p = 0.010). Restricted cubic spline analysis indicated a linear association between the CatLet score and cardiac death. The ML results showed that the adaptive boosting (Adaboost) model had the most reliable performance with an area under the curve (AUC) of 0.927, a sensitivity of 0.902, and a specificity of 0.796. The SHAP analysis showed that the CatLet score was a significant contributor to the cardiac death outcome.
The Catlet score positively correlates with the risk of cardiac death in patients with AMI, while the use of ML modeling can effectively predict the risk of cardiac death.
Atrial fibrillation (AF) represents a major public health burden, especially in its long-standing persistent form, which is often resistant to pharmacological or catheter-based therapies. Hybrid ablation, which integrates minimally invasive surgical and endocardial catheter techniques, has been introduced to address these complex cases. However, data evaluating the long-term comparative effectiveness of immediate versus staged ablation strategies remain limited, and the specific contribution of adjunctive targets, such as Bachmann's bundle (BB), remains unclear.
In this single-center retrospective cohort study, we analyzed 60 patients with long-standing persistent AF who underwent hybrid ablation between 2008 and 2020. All patients received thoracoscopic epicardial ablation followed by endocardial catheter ablation either during the same hospitalization (“immediate group”, n = 20) or ≥4 weeks later (“staged group”, n = 40). A subset of patients underwent adjunctive BB ablation. The primary outcome was freedom from documented AF recurrence. Secondary outcomes included procedural complications, hospitalization duration, and long-term survival.
At a mean follow-up of 106 ± 12 months, sinus rhythm was maintained in 90.0% of patients in the immediate group and 62.5% in the staged group (p = 0.034). BB ablation was associated with significantly improved rhythm control (90% vs. 70%; p = 0.04). No major adverse events or procedural mortality were reported. The immediate group had significantly shorter hospital stays (5.6 ± 1.5 vs. 8.8 ± 1.3 days; p < 0.001). Subgroup analyses did not reveal significant differences in recurrence among patients without BB ablation.
Hybrid ablation provides durable rhythm control and excellent safety over long-term follow-up. BB ablation enhances success and should be considered in procedural planning. Immediate catheter ablation may be a viable strategy in appropriately selected patients, potentially reducing hospitalization time and healthcare resource utilization. Our findings support the need for individualized ablation strategies in complex AF management and underscore the importance of integrating adjunctive targets, such as BB, into advanced procedural workflows.
Modern medicine increasingly offers the potential to individualise patient care and tailor therapies to meet specific patient needs. Catheter ablation in atrial fibrillation has undergone radical evolution since the advent of early ablative therapies; however, more comprehensive or extensive strategies are now possible. Moreover, novel energy sources, catheters, and mapping platforms are being developed and implemented, raising the potential to deliver ablation strategies more effectively, durably, quickly, and potentially more extensively. This poses the challenge of whether to prioritise anatomical landmark-based ablation or pursue individual mechanisms of arrhythmia on a personalised basis. Thus, this review aims to summarise the current state-of-the-art developments in catheter ablation for atrial fibrillation, recent advances, and developments in both the ablation and understanding of arrhythmia pathophysiology.
The urinary sodium-to-potassium (UNa/UK) ratio reflects the dietary sodium and potassium balance and may serve as a biomarker for hypertension (HTN). An imbalance in the dietary sodium–potassium ratio may contribute to systemic inflammation, alterations in gut microbiota (GM), and related metabolic disorders. This study aimed to investigate the relationship between the UNa/UK ratio, HTN, inflammation, GM, and metabolic abnormalities using cross-sectional and Mendelian randomization (MR) analyses.
We included 1210 hospitalized patients (median age, 51 (43–57) years; 57.9% male) who underwent 24-hour urine electrolyte measurement. Participants were grouped by the median UNa/UK ratio (4.40) for subsequent analysis, with 605 participants in each group. Additionally, we performed two-sample MR analyses to evaluate causal relationships between the UNa/UK ratio and HTN, circulating inflammatory proteins and immune cells, GM, and plasma metabolites.
A cross-sectional analysis revealed significant associations between the UNa/UK ratio and HTN prevalence, inflammation scores, and metabolites. Logistic regression confirmed the UNa/UK ratio as an independent predictor of HTN (odds ratio (OR): 1.076; 95% confidence interval (CI): 1.037–1.116). Spearman correlation analysis showed a positive correlation between the UNa/UK ratio and several inflammatory scores. The MR analyses indicated a causal effect of the UNa/UK ratio on HTN (inverse-variance weighted method: OR: 1.5130, 95% CI: 1.1613–1.9712), inflammatory proteins, immune cells, GM, and plasma metabolites.
The UNa/UK ratio was significantly associated with HTN risk, systemic inflammation, GM dysbiosis, and metabolic disorders. Integrating both cross-sectional and MR approaches, our findings highlight the UNa/UK ratio as a clinically relevant biomarker and reinforce the role of dietary sodium–potassium balance in modulating HTN through underlying mechanisms involving inflammation, GM alterations, and metabolites.
In the era of mitral transcatheter edge-to-edge repair (M-TEER), growing evidence continues to support a shift from a binary classification of mitral regurgitation (MR) into primary and secondary forms toward a more refined, subtype-based approach. Additionally, anatomical and pathophysiological heterogeneity significantly influences procedural complexity, durability of repair, and clinical outcomes within both primary and secondary MR. Furthermore, recent trials suggest that the timing of the intervention is as critical as patient anatomy; delaying treatment until advanced ventricular remodeling has occurred may limit the benefits of MR reduction. Moreover, long-term data on durability and device-failure management remain limited, particularly in secondary MR, where the progression of the underlying cardiomyopathy largely determines the outcomes. Thus, this review underscores how integrating MR subtyping with intervention strategies may influence patient selection and highlights the need for future research to adopt a more individualized, mechanism-driven approach.
This study aimed to systematically investigate the association between serum branched-chain amino acids (BCAAs) and the risk of chronic rheumatic heart disease (RHD), as well as to explore potential mediating mechanisms through immune markers.
The data utilized in this prospective cohort study were derived from the UK Biobank. Serum BCAAs (leucine, isoleucine, and valine) were measured using metabolic profiling of nuclear magnetic resonance data. Chronic RHD cases were identified through hospital inpatient records and death registries. Multivariable Cox regression models were used to analyze the association between BCAAs and RHD risk. Causal mediation analysis was employed to investigate the mediated role of immune markers.
A total of 273,595 participants were included, with 6051 (2.21%) participants developing chronic RHD. Each one-unit standard deviation increase in total BCAAs was associated with a 4.8% increased risk of RHD (hazard ratio (HR) = 1.048, 95% confidence interval (CI): 1.023–1.074). Among individual BCAAs, valine exhibited the strongest association (HR = 1.061, 95% CI: 1.035–1.088). Subgroup analyses revealed significantly stronger associations in participants aged <65 years compared to those aged ≥65 years (p for interaction = 0.032). Mediation analysis demonstrated that immune markers significantly mediated the BCAA–RHD association, with lymphocyte-to-C-reactive protein ratio accounting for 30.8% of the total effect.
Observational data suggest serum BCAAs correlate with increased RHD risk, especially in individuals aged <65 years; however, causation requires experimental verification. Immune markers significantly mediate the BCAA–RHD association, indicating that immunomodulatory pathways may be potential therapeutic targets. These findings provide novel insights into RHD pathogenesis and may inform risk stratification and prevention strategies.
The study aimed to compare the differences in reverse left ventricular (LV) remodeling following transcatheter aortic valve replacement (TAVR) between patients with the bicuspid aortic valve (BAV) and those with tricuspid aortic valve (TAV), both with aortic stenosis, in a Chinese population.
A total of 137 patients were enrolled who were treated with a self-expandable Venus A valve at our center, who underwent TAVR from January 1, 2019, to June 30, 2022. We retrospectively included patients with BAV and TAV who underwent echocardiographic follow-ups at baseline and at least 6 months after the procedure.
Patients with a BAV were younger than those with a TAV. The BAV patients had a larger aortic root diameter (ARD), although the size of valve implantation was comparable between the two groups. Patients with a BAV might experience less reverse LV remodeling post-TAVR than patients with a TAV during the one-month follow-up (140.09 ± 36.94 g/m2 vs. 126.36 ± 26.96 g/m2; p = 0.044). There were no significant differences in the LV mass index (LVMi) between the two groups throughout the 24 hours or the six-month follow-up post-TAVR. Patients with a higher mean pressure gradient (MPG) (95% confidence interval (CI): 0.112–0.581; p = 0.004) and a larger ARD (95% CI: 0.519–5.573; p = 0.019) before TAVR had favorable mid-term LV reverse remodeling (ΔLVMi within 6 months) post-TAVR. Patients with much more severe aortic stenosis (AS) had favorable mid-term LV reverse remodeling post-TAVR.
Patients with BAV might experience less reverse LV remodeling post-TAVR than patients with TAV during a short-term follow-up, but similar remodeling during mid-term follow-ups.
The efficacy of beta-blockers in stable coronary artery disease (CAD) patients with preserved left ventricular function remains controversial. We aimed to evaluate the cardiovascular associations of beta-blocker therapy in this population through a comprehensive meta-analysis.
We conducted a systematic review and meta-analysis following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, searching PubMed, EMBASE, Web of Science, Scopus, Google Scholar, and Cochrane databases from inception to May 2025, updating and extending the previous meta-analysis. We included observational studies comparing beta-blocker therapy versus control in stable CAD patients, defined as those without acute coronary syndrome manifestations for a sufficient period (typically >6 months) to ensure clinical stability, with preserved left ventricular ejection fraction (left ventricular ejection fraction >50%). Primary outcome was cardiac death. Secondary outcomes included all-cause mortality, heart failure, myocardial infarction (MI), and stroke. Random-effects models were used for all analyses. Subgroup analyses were conducted for cardiac and all-cause death stratified by propensity score matching status and prior beta-blocker use exclusion criteria. Publication bias was assessed using funnel plots and Peter's test.
Nine observational studies encompassing 903,870 patients (616,645 beta-blocker users vs. 287,225 controls) were included. Beta-blocker therapy showed no significant association with the primary endpoint: cardiac death (hazard ratio (HR) 0.98, 95% CI: 0.93–1.04, p = 0.54). Secondary outcomes similarly demonstrated no significant associations: all-cause mortality (HR 0.98, 95% CI: 0.91–1.05, p = 0.49), MI (HR 1.02, 95% CI: 0.93–1.11, p = 0.72), stroke (HR 1.02, 95% CI: 0.97–1.08, p = 0.43), and heart failure (HR 1.10, 95% CI: 0.95–1.27, p = 0.20). Substantial heterogeneity was observed for all-cause death (I2 = 87%) and heart failure (I2 = 95%). Subgroup analyses failed to identify populations with clear associations between beta-blocker therapy and improved outcomes.
Beta-blocker therapy was not significantly associated with cardiovascular benefits in stable CAD patients with preserved left ventricular function. These findings provide additional contemporary evidence supporting current guideline recommendations from both American Heart Association (AHA)/American College of Cardiology (ACC) and European Society of Cardiology (ESC) regarding beta-blocker use in this population. Clinicians should conduct individualized risk-benefit assessments rather than adopting routine prescribing patterns.
CRD420251141812, https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=1141812.
Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and frequently co-occurs with metabolic diseases, such as diabetes and obesity. Due to the intricate and multifactorial pathophysiology of AF, this disorder often eludes effective prevention and durable control with current therapeutic strategies; thus, these strategies may not consistently mitigate the onset, persistence, and related adverse outcomes of AF. Moreover, atrial metabolic remodeling and mitochondrial stress can promote the development of atrial cardiomyopathy and AF through electrophysiological and structural changes. Hence, targeting these metabolic alterations may prevent the onset of this arrhythmia. A contemporary therapeutic paradigm prioritizes restoration of metabolic homeostasis, led by sodium–glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists and complemented by emerging mitochondria-targeted strategies with potential for incremental disease modification. Concurrently, integrative multi-omics is mapping atrial metabolic diversity in AF to support biomarker-guided, individualized interventions, while next-generation imaging is enhancing the detection of pathologic substrates and refining risk assessment. This review provides a comprehensive analysis of the mechanisms through which metabolic remodeling and mitochondrial stress cause AF, evaluates current experimental and diagnostic methods, and discusses emerging substrate-targeted therapies.
Coronary artery disease is a leading cause of morbidity and mortality in patients with type 2 diabetes mellitus. Indeed, diabetic patients often present with silent or atypical symptoms and are more likely to develop complex, diffuse, rapidly progressive, and recurrent atherosclerosis. While current guidelines favor coronary artery bypass grafting in diabetic patients with multivessel disease, advances in percutaneous coronary intervention technology have broadened the range of revascularization options for this high-risk population. Nevertheless, despite major improvements in stent platforms over the past two decades, diabetic patients continue to experience higher rates of in-stent restenosis and adverse cardiovascular events compared to non-diabetics, in part, because of the permanent metallic scaffold. Therefore, novel strategies, including drug-coated balloons, minimize chronic inflammation and eliminate permanent vessel caging, thereby offering promising alternatives in this setting, particularly for lesion subsets typical of diabetic patients. This review discusses the current landscape and future directions of percutaneous coronary revascularization in diabetic patients, outlining the evolution from drug-eluting stents to emerging metal-sparing technologies, and highlighting the persistent challenges in achieving optimal outcomes in this population.
Patients bridged to heart transplantation (HTx) and patients with primary graft dysfunction (PGD) after HTx are typically treated with circulatory support. However, the survival of patients in both indications might depend on the type of circulatory support. Thus, this meta-analysis aimed to investigate the survival of HTx patients supported during bridging with a durable left ventricular assist device (d-LVAD), a temporary LVAD (t-LVAD), or venoarterial extracorporeal membrane oxygenation (VA-ECMO). We also investigated the survival rate of patients with PGD by type of circulatory support device.
We performed a random-effects meta-analysis.
We included four studies evaluating bridging to HTx (n = 1678 patients) and three studies for the PGD analysis (n = 35 patients). The 1-year survival after HTx was significantly higher in patients bridged with a t-LVAD (92.7%; 95% confidence interval (CI): 89.2 to 95.6%; p = 0.027) and with a d-LVAD (86.8%; 95% CI: 75.8 to 94.8%; p = 0.001) compared to VA-ECMO (71.6%; 95% CI: 63.7 to 78.9%). The 30-day survival in patients with PGD and t-LVAD was 100% (95% CI: 59.2–100%), while with PGD and VA-ECMO, survival was 92.4% (95% CI: 66 to 100%).
Both d-LVAD and t-LVAD bridging methods appear to have comparable 1-year survival rates, which are higher than those after VA-ECMO bridging. Nonetheless, more prospective clinical studies are needed to investigate outcomes after using circulatory support devices for PGD after HTx. The PROSPERO registration: CRD420251149065, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251149065.
Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide, creating an urgent demand for small-diameter vascular substitutes with durable long-term patency. Large-caliber synthetic grafts, such as polyethylene terephthalate (PET) and ePTFE, are well established in clinical practice; however, these synthetic grafts fail in small-diameter applications due to thrombosis and intimal hyperplasia. Moreover, autologous grafts are constrained by limited availability and variable quality. Recently, synthetic degradable polymers (e.g., polycaprolactone (PCL), poly(lactic-co-glycolic acid) (PLGA)), and extracellular matrix-derived natural materials (collagen, gelatin, silk fibroin, bacterial cellulose) have drawn increasing attention, as each offers distinct advantages and limitations in terms of mechanics, biocompatibility, and degradation behavior. Meanwhile, emerging fabrication technologies, including electrospinning, thermally induced phase separation, microfluidic spinning, and three-dimensional printing, are advancing the structural biomimicry and functional optimization of artificial vascular grafts. Thus, building on these developments, this review further examines the design strategies of tissue-engineered vascular grafts (TEVGs), focusing on cell sourcing, in vitro and in situ endothelialization, antithrombotic modification, and the prevention of intimal hyperplasia, while also summarizing outcomes from preclinical models and early clinical trials. Despite promising progress, the widespread clinical translation of TEVGs remains limited by prolonged manufacturing cycles, high costs, and insufficient long-term patency. Hence, future efforts toward standardized cell sources, integrated structure, function design, and multicenter clinical validation are critical to the development of next-generation vascular grafts.
This study aimed to decode the spatiotemporal trajectory of atrial fibrillation/flutter (AF/AFL) burden (1990–2021) through hierarchical quantification of socioeconomic health gradients and Bayesian projection modeling across 204 countries and territories until 2036.
This study, based on data from the 2021 Global Burden of Disease (GBD) study, systematically investigates the geopolitical and temporal dynamics of AF/AFL from 1990 to 2021. This study quantified the impact of population structure, age distribution, and disease rates on the disease burden, assessed the inequality of burden among different countries, and predicted the disease trends for the next 15 years.
From 1990 to 2021, when the age-standardized death rate (ASDR) was the only indicator showing an upward trend (estimated annual percentage change (EAPC) = 0.1 (0.06–0.13)), the absolute number of AF/AFL cases continued to rise. Decomposition analysis revealed that population growth (43.17%) and aging (56.31%) were the primary drivers of the global AF/AFL burden in 2021. The study found that from 1990 to 2021, inequality in the social indicators index (SDI) worsened, whereas the slope index of inequality (SII) values for AF/AFL incidence (41.68 vs. 81.71), prevalence (499.54 vs. 1076.65), mortality (3.23 vs. 8.50), and disability-adjusted life years (DALYs) (82.36 vs. 189.81) all increased. Notably, the global AF/AFL burden is projected to continue rising through 2036. The age-standardized incidence rate (ASIR) (52.36 vs. 56.07) for AF/AFL is expected to increase annually, while the ASDR (4.12 vs. 3.93) and age-standardized DALYs rate (ASDAR) (107.45 vs. 90.87) are projected to decline. However, the number of cases is expected to maintain growth.
This study shows that the global burden of AF/AFL has an overall increasing trend from 1990 to 2021, primarily driven by population growth and aging. Countries with a high SDI bear a disproportionately high burden of AF/AFL, while SDI-related inequalities among countries have worsened over time. This study highlights the significant challenges in the prevention and management of AF/AFL, including the rising number of cases and the unequal distribution of the subsequent burden worldwide. These findings may be instructive for developing more effective public health policies and reasonably allocating medical resources.
Left atrial appendage aneurysm (LAAA) is a rare cardiac abnormality associated with thromboembolic events and arrhythmias. This systematic review aimed to provide a comprehensive evaluation of literature reports on the demographics, clinical presentation, electrocardiographic and imaging findings, treatment, and outcomes of patients with LAAA.
A literature search was conducted using the PubMed, MEDLINE, and Scopus databases through September 2025. Only case reports and series explicitly describing LAAA were included. Extracted data included age, sex, clinical symptoms, electrocardiogram (ECG) characteristics, imaging findings, associated cardiac abnormalities, treatment modalities, and outcomes.
A total of 216 cases were included. The mean age at diagnosis was 30.41 ± 22.39 years, with a slight predominance of males (50.5%). Symptoms included palpitations (32.4%), dyspnoea (17.2%), and thromboembolic events (7.8%). Atrial fibrillation and flutter were the most commonly detected arrhythmias. Echocardiography was the most frequently used initial diagnostic tool, with computed tomography (CT) and magnetic resonance imaging (MRI) providing additional anatomical details. Chest X-rays often yielded non-specific findings. The mean aneurysm diameter was 6.87 ± 2.64 cm. Surgical treatment, mainly aneurysm resection, was the most commonly used approach (72.7%), while conservative and device-based therapies were applied selectively. Concomitant cardiac anomalies were present in 13.7% of cases and influenced case management. The mortality rate was 4.6%, although significant morbidity was observed. Multivariate logistic regression analysis revealed that atrial fibrillation/flutter was the sole variable significantly linked with clot formation/embolism (p < 0.05).
LAAA is a rare, although clinically significant, entity with variable presentation and management challenges. However, early recognition and individualized treatment are essential. Further research is needed to define standardized diagnostic criteria and treatment guidelines.
Evidence is accumulating that shows spontaneous coronary artery dissection (SCAD) as a recognized cause of acute coronary syndrome (ACS), disproportionately affecting younger people and women. Moreover, despite continuing progress, the understanding of the pathophysiology, diagnosis, and management of SCAD remains limited. SCAD, by definition, is a non-atherosclerotic formation of an intramural hematoma or intimal tear, yet current diagnostic criteria and management are derived from atherosclerotic ACS guidelines. This review encompasses the current understanding of the condition, including risk factors, diagnostic and imaging modalities available for detection, differentials to be considered, associations with other comorbidities, prognostic factors, and management options for both the short and long term, encompassing both medical and interventional therapies. Meanwhile, a lack of research in key populations, such as non-pregnant women, postmenopausal women, and men, prevents the generalizability of these findings and has been highlighted. However, by identifying and conceptualizing existing evidence, this review aims to provide direction to future research.
Acute Stanford type A aortic dissection (ATAAD) is a life-threatening cardiovascular emergency that demands prompt and accurate diagnosis due to a high associated mortality. Although imaging remains the diagnostic gold standard, the limited accessibility and time sensitivity of this technique underscore the need for reliable serum biomarkers. D-dimer is the most widely used biomarker, offering high sensitivity; however, the limited specificity of using D-dimer has prompted a search for novel biomarkers with greater diagnostic precision. Interestingly, proteoglycans (PGs) are essential constituents of the extracellular matrix (ECM) and have emerged as promising candidates for ATAAD, as PGs are released into the circulation during medial degradation, a defining histological feature of ATAAD. Moreover, emerging evidence suggests that specific PGs exhibit favorable specificity and stability, potentially enabling distinction between ATAAD and other acute cardiovascular syndromes. Additionally, in contrast to D-dimer, which is rapidly cleared within 8 hours, certain PGs, such as aggrecan, remain stable for up to 72 hours, offering an advantage for detecting ATAAD in patients presenting beyond the early acute phase. This review summarizes the potential of aortic PGs as biomarkers of medial degeneration and circulating PGs as serum diagnostic markers of ATAAD. Future research is warranted to establish PGs as clinically reliable biomarkers, with the potential to enhance current diagnostic frameworks and support an earlier, more accurate identification of ATAAD.
Hypertension is a prominent cardiovascular risk factor, especially among patients with diabetes and obesity. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are a class of drugs originally developed to improve glycemic control in patients with diabetes; however, these agonists have subsequently demonstrated additional cardioprotective effects, including modest reductions in blood pressure (BP). This literature review examines the various mechanisms through which GLP-1 RAs reduce BP, including weight loss, improved endothelial function, and renal sodium management. While GLP-1 RAs are less potent in BP reduction compared to conventional antihypertensive agents, the broader metabolic benefits of these agonists make this class of drug a valuable adjunct in managing hypertension, particularly in patients with metabolic syndrome. Nonetheless, further studies are needed to explore the long-term effects of BP and optimize patient selection for maximal cardiovascular benefit.
Cardiovascular diseases (CVDs) are a leading cause of mortality, significantly influencing quality of life and causing a burden on the healthcare system. Current treatment strategies utilize modern therapeutics, such as sodium–glucose cotransporter 2 (SGLT2) inhibitors and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, which are both effective and safe. However, despite current medicines, acute cardiovascular events and chronic complications of CVDs remain significantly prevalent. Furthermore, CVDs are strongly linked to metabolic and inflammatory conditions that create a pathophysiological network of interactions, worsening the health of individuals. Therefore, identifying novel therapeutic targets and treatment combinations is of great importance to further mitigate the harmful effects of CVDs. Recently, aprocitentan, an endothelin-1 inhibitor, was approved to treat arterial hypertension. Meanwhile, endothelin has become a therapeutic target in CVDs, with inhibitors previously registered and used to treat pulmonary hypertension. Thus, this review aims to comprehensively discuss the role of endothelin-1 as a therapeutic target in CVDs and related disorders.
Infective endocarditis (IE) is a life-threatening cardiac infection. The incidence of IE is increasing due to complex sociodemographic shifts, including increases in intravenous drug use (IVDU) attributed to opioid epidemics. Cardiac rehabilitation (CR) is a comprehensive form of secondary prevention for heart disease. Current guidelines suggest that CR may be beneficial in the recovery from IE, but supporting evidence is limited. Given the utility of CR in the recovery from other cardiac conditions and the unique characteristics of patients with IE, this narrative review summarizes the existing data on the use of CR following surgical treatment of IE. The existing literature is limited to the CopenHeartIE randomized clinical trial (RCT) and four case reports. Thus, to our knowledge, this represents the first review to focus specifically on CR in the context of IE. The CopenHeartIE RCT found that patients receiving CR showed greater improvements in levels of physical fatigue, general fatigue, maximal power, systolic blood pressure, and some questionnaire scores than the control group. The results of multiple case reports represent unique and extreme cases of IE from which support for the use of CR following IE can be drawn from the relative successes of each patient. Moreover, it is important to consider that the complex social needs of the IE population may require additional psychosocial support, which can be achieved by integrating social workers into the multidisciplinary CR team. While further research is warranted, the existing evidence supports the use of CR as part of the comprehensive recovery from IE.
Takotsubo syndrome (TTS) is an acute, reversible form of left ventricular dysfunction, typically triggered by emotional or physical stress. The hallmark feature is reversible regional wall motion abnormality extending beyond a single coronary distribution, most commonly presenting with an apical ballooning pattern. The pathophysiology is multifactorial, encompassing neurohormonal dysregulation, catecholamine-mediated toxicity, microvascular dysfunction, oxidative stress, inflammation, and metabolic disturbances. Nonetheless, despite growing recognition, an evidence gap persists in diagnosing TTS. Meanwhile, TTS is classified within myocardial infarction with non-obstructive coronary arteries (MINOCAs) and frequently treated as a diagnosis of exclusion. Further complicating the diagnostic algorithm, emerging evidence indicates that TTS and coronary artery disease (CAD) may coexist, suggesting a potential bidirectional relationship rather than a bystander phenomenon. Moreover, TTS shares several pathophysiological mechanisms with coronary microvascular dysfunction syndromes: angina with non-obstructive coronary arteries (ANOCAs) and ischemia with non-obstructive coronary arteries (INOCAs). These overlaps underscore the need for rigorous differential diagnosis and careful comprehensive evaluation of hemodynamic significance, plaque morphology, and microvascular phenotyping to enhance clinical recognition and optimize therapeutic decision-making. This review synthesizes current evidence on the diagnosis and management of TTS, emphasizing the intersection between TTS and coronary and microvascular disorders to promote a more targeted, mechanism-based therapeutic approach.
Coronary heart disease (CHD), one of the most severe cardiovascular conditions, poses a significant threat to the health and survival of older adults. Numerous studies have confirmed that diabetes, inflammation, and dyslipidemia are key risk factors for CHD. However, the relationship between the C-reactive protein–triglyceride glucose index (CTI) and CHD risk in older adults across different glucose metabolism statuses remains unexplored. Thus, this study aimed to investigate the correlation between the CTI and CHD risk in older adults with varying glycemic statuses.
Patients aged ≥60 years, who underwent coronary angiography between January 2019 and December 2023, were enrolled. A diagnosis of CHD was performed when the coronary angiography demonstrated ≥50% stenosis in at least one major epicardial vessel. Demographic characteristics, medical history, laboratory data, and procedural records were systematically collected. Least absolute shrinkage and selection operator (Lasso) and multivariate logistic regression identified potential predictors. Receiver operating characteristic (ROC) curves were employed to assess the clinical value of CTI in predicting CHD risk. A restricted cubic spline (RCS) was used to examine all nonlinear relationships. A nomogram for the occurrence of CHD in older adults was constructed, and a subgroup analysis was performed.
A total of 1204 patients were included (919 diagnosed with CHD, 285 non-CHD (NCHD) controls). The CTI was identified as an independent risk factor for CHD (odds ratio (OR) = 4.88, 95% confidence interval (CI): 3.59–6.62). The CTI, analyzed both as a continuous and categorical variable, showed significant associations with CHD incidence across various adjusted models. The RCS analysis across different glucose metabolism statuses revealed a nonlinear relationship between the CTI and coronary artery stenosis severity in the overall population. The nomogram model based on multivariate logistic regression demonstrated good predictive accuracy for CHD in older adults.
A positive correlation exists between the CTI and both CHD risk and the severity of coronary stenosis in older adults.
Atrial fibrillation (AF) is the most common sustained arrhythmia and a major cause of cardioembolic stroke, with the left atrial appendage representing the predominant site of thrombus formation. Oral anticoagulation (OAC)—particularly with direct oral anticoagulants—remains the cornerstone of stroke prevention; however, contraindications and bleeding risks limit the use of OAC in selected patients. Percutaneous left atrial appendage closure (LAAC) has emerged as a device-based alternative to oral anticoagulation. Moreover, the indications of LAAC are expanding to include recurrent ischemic stroke despite adequate anticoagulation and patients with advanced chronic kidney disease. Thus, this review synthesizes the current evidence on LAAC and provides a practical, step-by-step procedural roadmap, from preprocedural imaging with transesophageal echocardiography or cardiac computed tomography and anatomical sizing, to transseptal puncture, device selection, deployment, and release criteria, as well as intraprocedural imaging and hemodynamic assessment. Advances in imaging modalities, procedural planning, and device technology have improved both efficacy and safety. However, postprocedural antithrombotic strategies remain heterogeneous and the subject of ongoing clinical trials. Future research is expected to refine patient selection, optimize pharmacotherapy after LAAC, and further define the role of LAAC in the contemporary management of AF.
Transthyretin cardiac amyloidosis (ATTR-CA) is an increasingly recognized and underdiagnosed cause of heart failure (HF), encompassing both preserved (HFpEF) and reduced (HFrEF) ejection fraction phenotypes. Once identifiable only following a biopsy, the advent of bone scintigraphy has dramatically improved noninvasive detection and detected a higher community prevalence, particularly among older patients with unexplained left ventricular hypertrophy. ATTR-CA arises from misfolding of transthyretin (TTR), leading to amyloid fibril deposition within the myocardium, which impairs cardiac compliance, conduction, and output. This review explores the evolving epidemiology of ATTR-CA in HF, mechanisms of disease progression, and key features for screening, emphasizing clinical red flags, biomarkers, and imaging features. This review also addresses the nuanced role of guideline-directed medical therapy in this population, where neurohormonal agents may offer limited benefit or be poorly tolerated due to restrictive physiology and autonomic dysfunction. Crucially, the emergence of amyloid-specific therapies, including TTR silencers, stabilizers, and degraders, has transformed the therapeutic landscape, offering mortality and morbidity benefits that were previously unavailable. Early diagnosis and individualized management, integrating conventional and amyloid-targeted approaches, are essential to improving outcomes in this complex and increasingly treatable cardiomyopathy.
Traditional parameters, such as left atrial size or volume, typically reflect chronic pressure and volume overload; however, these abnormalities only become evident at advanced stages, often missing early signs of dysfunction. In contrast, left atrial reservoir strain (LASr), measured by speckle-tracking echocardiography, offers a sensitive and dynamic assessment of atrial mechanics, integrating atrial compliance with left ventricular diastolic interaction. Moreover, impaired LASr reflects atrial stiffness and fibrosis, and correlates with elevated filling pressures, making the LASr parameter a comprehensive biomarker of left-sided cardiac function. Indeed, LASr has demonstrated diagnostic and prognostic value across a wide spectrum of conditions. In heart failure with preserved ejection fraction, LASr refines the assessment of diastolic dysfunction and predicts hospitalization and mortality. In atrial fibrillation, reduced strain correlates with atrial fibrosis and left atrial appendage dysfunction, identifying patients at increased risk of arrhythmia recurrence and thromboembolism. In valvular disease, LASr uncovers subclinical remodeling and stratifies risk even in patients with apparently moderate aortic stenosis. Meanwhile, in addition to cardiovascular disease, LASr can detect early atrial impairment in systemic disorders such as hypertension, diabetes, obesity, and amyloidosis, often before structural enlargement becomes evident. Our group has shown that LASr predicts persistent hypertension after gestational hypertensive disorders, reveals subclinical diastolic dysfunction in idiopathic pulmonary fibrosis, non-invasively predicts left atrial appendage thrombus in atrial fibrillation, stratifies outcomes in moderate aortic stenosis, and provides prognostic information in acute ischemic stroke. This narrative review outlines the physiological basis, technical considerations, and clinical applications of LASr, discusses its limitations and future perspectives—including multimodality imaging and artificial intelligence—and underscores its transition from a research metric to a dynamic biomarker ready for clinical practice.
Biological age (BA) more accurately reflects the true ageing status of the body compared with chronological age. While biological aging is associated with various cardiovascular diseases, the relationship between BA and abdominal aortic aneurysms (AAAs) remains unclear.
This study utilized data from the UK Biobank for analysis. Telomere length (TL) and BA acceleration, calculated using the Klemera-Doubal method (KDM) and phenotypic age (PhenoAge) methods, were used as surrogate measures of biological aging. Cox regression was primarily performed to explore the association between biological aging and AAA risk. Genetic susceptibility was assessed by constructing a polygenic risk score (PRS).
This study included 311,646 participants with a median age of 58 years. A total of 1339 new cases of AAA (4.33‰) were reported over a median follow-up period of 12.54 years. Each standard deviation (SD) increase in TL was associated with a 17% decreased risk of AAA (hazard ratio (HR) = 0.83, 95% confidence interval (CI) = 0.79–0.88). Each SD increase in BA acceleration in the KDM was associated with a 21% increased risk (HR = 1.21, 95% CI = 1.12–1.29), and and each SD increase in acceleration in the PhenoAge method was associated with a 40% increased risk (HR = 1.40, 95% CI = 1.32–1.48). These associations were independent of genetic risk, as assessed by the PRS, and a joint effect on AAA occurrence was observed. Additionally, we identified a sex-specific modification in the association between telomere shortening and AAA risk, with a significant association observed exclusively in men.
Accelerated biological aging was longitudinally associated with an increased risk of AAA, suggesting that BA may be a significant factor and a potential biomarker for AAA.
Cardiac computed tomography (CT) has become an essential imaging modality in structural cardiac interventions, providing high-resolution anatomical and functional assessments. Moreover, the role of cardiac CT spans pre-procedural planning, intra-procedural guidance, and post-procedural follow-up in interventions such as transcatheter aortic valve implantation (TAVI), mitral, tricuspid, and pulmonary valve interventions, left atrial appendage occlusion (LAAO), atrial septal defect (ASD), and paravalvular leak (PVL) closures. Furthermore, compared to traditional imaging techniques, cardiac CT offers superior spatial resolution, precise anatomical characterization, and improved procedural success rates by minimizing complications. Additionally, advances in artificial intelligence (AI)-driven CT analysis, perfusion imaging, and four-dimensional cardiac CT are expanding the associated applications. This review discusses the current role, benefits, limitations, and future perspectives of cardiac CT in guiding structural heart interventions.
Electrocardiograms (ECGs) remain a foundational pillar of cardiovascular diagnostics, providing rapid, non-invasive diagnosis and being universally accessible to all clinicians. An ECG captures the electrical signals of the heart via a standard 12-lead configuration, offering insights into arrhythmias, conduction delays, ischemic injury, structural remodeling, and systemic pathologies with cardiac implications. This review presents a structured framework for ECG interpretation by discussing general approaches to rate, rhythm, axis, intervals, and repolarization dynamics, and by outlining both cardiac and non-cardiac conditions associated with ECG abnormalities. We explore the accelerating pace of innovations in artificial intelligence (AI) for ECG analysis. Deep learning algorithms now rival and, in select domains, surpass expert clinicians in detecting left ventricular systolic and diastolic dysfunction, hypertrophic obstructive cardiomyopathy, and acute myocardial infarction. The integration of AI-enhanced ECG interpretation enables earlier disease recognition, refined risk stratification, and optimized clinical decision-making across acute and chronic care settings. This review systematically guides readers through ECG interpretation, linking fundamental principles with nuanced clinical patterns using AI to enhance accurate diagnosis and improve patient outcomes across a wide range of cardiovascular conditions.
Pulsed field ablation (PFA) is a novel ablation technique for atrial fibrillation (AF). Indeed, PFA utilizes cell electroporation and exhibits selectivity for myocardial tissue, depending on the method used to deliver the pulsed electric field, potentially sparing surrounding non-cardiac structures. Recent clinical trials have demonstrated the non-inferiority of PFA compared with conventional thermal ablation for arrhythmia recurrence, including radiofrequency and cryoballoon ablation. Currently, large registry data present an acceptable safety profile. However, PFA is not without risk, and some unique, albeit infrequent complications have been recognized with this ablation modality, including stroke, coronary artery spasm, and intravascular hemolysis. Thus, given the associated safety, efficacy, and improved procedural workflow of this technique, the advent of PFA will likely lower the threshold for patient selection for AF ablation, particularly owing to the growing burden of AF in our community. This review provides an overview of the biophysics of PFA, various catheter designs, clinical trial and registry data, potential complications associated with PFA, and future directions in this promising area of AF management.