Stage-Dependent Diastolic Recovery and Reverse Remodeling After Atrial Fibrillation Ablation Across the Spectrum of Left Ventricular Diastolic Dysfunction.

Right Ventricular Dysfunction in Bone Marrow Transplantation: An Emerging Component of Cancer Therapy-Related Cardiotoxicity.

Mechanical ventilation patterns and outcomes in patients with right ventricular (RV) dysfunction: A cohort study.

The Right Ventricle, the Forgotten Chamber or Not.

Summary of the International Society for Heart and Lung Transplantation (ISHLT) Consensus Conference on Graft Dysfunction within the First 72 hours after Heart Transplantation: A 10-year Update.

Cardiac adaptation to chronic pressure overload is traditionally viewed as a uniform concentric hypertrophy; however, growing evidence suggests that the myocardium responds in a spatially heterogeneous manner. This study aimed to systematically map regional and temporal adaptation patterns of the left ventricle (LV) under experimental pressure overload using high-resolution multiparametric cardiac MRI, with the hypothesis that distinct regional adaptation phenotypes contribute to both local functional differences and global ventricular dysfunction. Thirty-seven male 129/SvEv mice underwent transverse aortic constriction (TAC) surgery and were followed longitudinally over 7 weeks. Cine imaging, T1- and T2-mapping were performed at baseline, 3 days, 4 weeks and 7 weeks using a 9.4 T small-animal scanner. A 200-sector LV segmentation enabled quantitative regional analysis of wall thickness, fractional shortening (FS) and relaxation times. Global and regional imaging parameters were correlated with histological and biochemical indices at study termination, and statistical analyses were performed using the Mann-Whitney test and correlation modelling, with p < 0.05 considered significant. All TAC animals developed global LV hypertrophy and an early increase in LV mass (+62% ± 15% at Week 7, p < 0.001). Unexpectedly, in 18 animals (49%), a discrete basolateral LV segment failed to hypertrophy (spared hypertrophy, SH) despite uniform pressure elevation. This region exhibited markedly reduced regional FS (10.2% ± 3.1% vs. 24.9% ± 2.2%, p = 0.01) and was associated with lower global ejection fraction (32.5% ± 1.8% vs. 49.8% ± 4.1%, p < 0.05) and LV dilatation. Parametric MRI revealed distinct tissue signatures: T1 increased in hypertrophied sectors (+22.6% ± 1.1%), whereas it decreased in SH sectors (-5.1% ± 1.7%, p < 0.01) over the 7-week observation period. Sector-wise correlations linked T1 shortening with reduced FS (R2 = 0.58, p = 0.002), suggesting maladaptive regional remodeling. In conclusion, pressure overload elicits diverse regional adaptation, and failure to hypertrophy identifies myocardial territories prone to early dysfunction and global decline. Recognizing hypertrophy as an essential adaptive mechanism shifts the paradigm of pressure-overload remodeling. Multiparametric MRI provides a translational platform for detecting regional vulnerability and guiding early intervention.

P8. Choice of Revascularization Strategy Impacts Outcomes in Patients with Ischemic Left Ventricular Dysfunction

Integrated metabolomic and proteomic analysis of cardiac tissues in a murine model of Kawasaki disease.

46. Impact of Age at Pulmonary Artery Banding on Left Ventricular Dysfunction After Anatomic Repair of Congenitally Corrected Transposition with Intact Ventricular Septum

Hemodynamic transitions in pulmonary artery pulsatility index and compliance in advanced heart failure.

Mavacamten improves symptoms in obstructive hypertrophic cardiomyopathy, but real-world prescription patterns, safety profile, and the effect of atrial fibrillation (AF) on outcomes remain unclear. An observational multicenter analysis using patient-level data from the TriNetX database (2011-2023) compared patients with obstructive hypertrophic cardiomyopathy treated with mavacamten versus those not treated with mavacamten (controls). Multivariable logistic regression identified predictors of mavacamten use. Propensity-score matching was used to reduce confounding bias. Outcomes included acute heart failure, left ventricular systolic dysfunction, cardiovascular hospitalization, new-onset AF, and all-cause mortality. Outcomes were also stratified by AF history. Among 15 145 patients, 509 (3.5%) received mavacamten; 502 matched to 1475 weighted 1:3 controls (equivalent to 502). Black patients were significantly less likely to receive mavacamten compared with White patients (odds ratio, 0.45 [95% CI, 0.33-0.63]). Of the 502 mavacamten recipients, 4.8% experienced acute heart failure, 8.3% experienced systolic dysfunction, 10.8% experienced cardiovascular hospitalization, 6.4% experienced new-onset AF, and 1.4% died. Overall outcomes were similar between both groups except for a higher incidence of systolic dysfunction in mavacamten patients (log-rank P<0.001). Among mavacamten patients, those with baseline AF (28%) had significantly higher rates of acute heart failure (7.8% versus 3.6%; P=0.047), systolic dysfunction (12.8% versus 6.4%; P=0.02), cardiovascular hospitalization (27.7% versus 4.2%; P<0.01), and mortality (5% versus 0%; P<0.01). Older age independently predicted acute heart failure, whereas baseline AF predicted both cardiovascular and all-cause hospitalization. Black patients have markedly lower access to mavacamten. Preexisting AF was associated with a higher risk of adverse outcomes for patients on mavacamten, highlighting the need for careful monitoring.

Right ventricular pacing leads to left ventricular (LV) dyssynchrony, which is a critical factor in the pathophysiology of pacing-induced LV dysfunction (PIVD) and cardiomyopathy (PICM). This study aimed to determine the incidence of PIVD and PICM and evaluate the prognostic value of the real-time three-dimensional echocardiography (RT3DE)-derived systolic dyssynchrony index (SDI), measured shortly after pacemaker implantation, in predicting their development. In this prospective observational study, 108 patients undergoing permanent RV pacing. Only 60 patients with preserved baseline LV ejection fraction (LVEF ≥ 50%) were enrolled. Comprehensive echocardiography, including global longitudinal strain (GLS) and RT3DE for SDI (Tmsv 16-SD) calculation, was performed at baseline, 7-10 days, and 6 months post-implantation. Patients were classified at 6 months as preserved (LVEF reduction ≤ 10%, final LVEF ≥ 50%), PIVD (LVEF reduction > 10%, final LVEF ≥ 50%), or PICM (LVEF reduction > 10%, final LVEF < 50%). The patients' mean age was 62.4 ± 16.3 years, 32 patients were males (53.3%). Mean follow-up was 6.53 ± 0.75 months. Twenty-five patients (41.7%) developed LV impairment; of them, 16 (85%) patients had PIVD, and nine (15%) patients had PICM. While baseline characteristics were similar, the dysfunction group exhibited significantly higher SDI and worse GLS as early as 7-10 days post-pacing. At 6 months, there were significant differences between the preserved group (35 patients) and impaired LV group regarding LV EF (63.6 ± 5 vs. 49.8 ± 11.6, p < 0.001), GLS (- 15.6 ± 3 vs. - 10.9 ± 3.8, p < 0.001), SDI% (2.4 ± 1.2 vs. - 7.9 ± 5.9, p < 0.001), and excursion (5.8 ± 2.23 vs. 3.2 ± 2.1, p < 0.001). In multivariate analysis, both SDI (odds ratio [OR], 5.38; 95% CI, 1.56-18.52; p = 0.008) and GLS (OR, 1.39; 95% CI, 1.02-1.90; p = 0.040) at 7-10 days were independent predictors of 6-month dysfunction. Receiver operating characteristic analysis showed that an SDI > 1.49% predicted dysfunction with an area under the curve of 0.843 (84% sensitivity, 71% specificity). A clear gradient of worsening SDI and GLS was observed from Preserved to PIVD to PICM. Mechanical dyssynchrony quantified by RT3DE-derived SDI is a powerful, independent predictor of pacing-induced LV dysfunction, identifiable within the first week after implantation. This early measurement offers a critical opportunity for risk stratification and guided intervention to prevent the progression to overt cardiomyopathy.

Acute respiratory distress syndrome (ARDS) remains a major challenge in critical care, with mortality exceeding 40%. Its diagnosis and management depend on multi-step procedures, invasive arterial blood gas analysis, and subjective CT interpretation, often leading to inconsistency, delayed intervention, and increased procedural burden. To address these limitations, we develop AutoARDS, an all-in-one foundation model that transforms routine chest CT into a quantitative platform, enabling integrated and reproducible assessment of diagnosis, progression, oxygenation, physiology, and prognosis within a single, non-invasive workflow, thereby supporting faster and more standardized critical-care decisions. Technically, AutoARDS proposes to employ a multi-task pretraining strategy with adversarial perturbation, distilling routine but unstructured clinical data into unified representations for fine-grained pathological learning. Trained on over 50,000 CT volumes and validated across six medical centers (6,153 individuals), AutoARDS (1) established a reproducible CT-derived biomarker linking morphological injury with disease severity, enabling standardized tracking of pulmonary progression; (2) accurately diagnosed acute respiratory failure and ARDS (AUCs = 0.97 and 0.87), facilitating early recognition and reducing diagnostic delay; (3) directly estimated the P/F ratio (PCC = 0.83), outperforming SpO2-based monitoring for noninvasive severity stratification and ventilation management; and (4) predicted 28-day outcomes (time-averaged AUC = 0.79), providing complementary risk assessment for clinical planning. Further analyses confirm generalizability to ARDS-associated right ventricular dysfunction (AUC = 0.76) and revealed a positive shift image-derived age residuals, reflecting disease-related imaging patterns that resemble pulmonary aging. By bridging visual information with quantitative physiology, AutoARDS exemplifies a scalable blueprint for transforming chest CT into an integrated, quantitative platform for precise and reproducible critical-care management.

Type 2 diabetes mellitus (T2DM) is a globally prevalent metabolic disorder frequently complicated by cardiovascular pathologies, notably left ventricular diastolic dysfunction (LVDD), which can progress to heart failure with preserved ejection fraction (HFpEF). There is emerging evidence of a crucial interplay between autonomic dysfunction and chronic low-grade inflammation in the pathogenesis of LVDD in T2DM patients. The bidirectional crosstalk between the autonomic nervous system and the immune system has been a novel area explored in preclinical studies. Autonomic dysfunction, as evidenced by reduced heart rate variability and impaired baroreflex sensitivity, is common among patients with T2DM. The interaction between the autonomic nervous system and inflammation is altered in T2DM, shifting towards vagal withdrawal and the release of pro-inflammatory cytokines (e.g., TNF-α, IL1β, IL-6, and TGF-β), which can promote myocardial stiffening and fibrosis. These pathophysiological mechanisms, together with metabolic and hemodynamic dysfunction in T2DM, can lead to HFpEF. Neuromodulation techniques, such as vagal nerve stimulation, have shown promise in reducing myocardial fibrosis and HFpEF in preclinical studies. Vagal nerve stimulation is thought to dampen the pro-inflammatory responses, thereby promoting tissue repair and protecting against cardiac dysfunction. In this review, we explore how inflammation-autonomic crosstalk represents a pivotal mechanism in the development of LVDD in T2DM, providing a scientific rationale for neuro-modulatory interventions.

SIRT5 (sirtuin 5) is a member of the sirtuin family known to regulate cardiac metabolism, aging, and function. However, its role in cardiac fibroblast (CFB) metabolism, activation, and fibrosis remains elusive. Expression changes of SIRT5 in CFBs from cardiac tissue of human and mouse with heart failure were determined. The functional role of SIRT5 in cardiac fibrosis was evaluated through CFB-specific knockout and overexpression of Sirt5 in mice. The involvement of succinylation of lysine 489 (Lys489) on PCK2 (phosphoenolpyruvate carboxykinase 2) in SIRT5-mediated regulation of cardiac fibrosis was assessed by introducing the Lys489-to-arginine mutation of PCK2 in Sirt5-deficient CFBs and in CFB-specific Sirt5 knockout mice. SIRT5 expression was markedly reduced in CFBs from humans and mice with heart failure and showed a negative correlation with cardiac fibrosis severity. Loss of Sirt5 in CFBs exacerbated left ventricular dysfunction, cardiac hypertrophy, and cardiac fibrosis in mice subjected to transverse aortic constriction, whereas overexpression of Sirt5 in CFBs significantly attenuated these pathological changes. Sirt5 deficiency promoted CFB activation by driving a metabolic shift from oxidative phosphorylation to glycolysis. Mechanistically, Sirt5 deficiency increased the succinylation of PCK2 at Lys489, a key enzyme linking glycolysis and the tricarboxylic acid cycle, which consequently inhibited this enzyme activity in CFBs. Importantly, this specific modification at the Lys489 mutation that prevents succinylation effectively reversed both the metabolic reprogramming and the hyperactivation of CFBs induced by Sirt5 knockout. In vivo, introducing the Pck2 K489R mutation fully rescued the exacerbated cardiac fibrosis and dysfunction observed in Sirt5-deficient mice after transverse aortic constriction. By desuccinylating PCK2 at Lys489, SIRT5 prevents the metabolic reprogramming and subsequent activation of CFBs, protecting against cardiac fibrosis.

Functional tricuspid regurgitation in the setting of right ventricular (RV) remodelling remains one of the least standardized challenges in valvular surgery. Surgeons are often confronted with complex anatomy and limited formal training in advanced tricuspid reconstruction. This review seeks to consolidate the evolving surgical knowledge base and provide a structured reference for the full spectrum of repair strategies beyond annuloplasty. A targeted literature review was performed to identify key reports on surgical tricuspid valve interventions. These were synthesized narratively to outline the principles, indications, and anatomical rationale for current techniques, including edge-to-edge repair, leaflet augmentation, papillary muscle relocation, approximation, suspension, bundling, and annular repositioning. Collectively, these approaches form a growing surgical armamentarium aimed at restoring normal leaflet geometry and subvalvular alignment in the setting of RV dilatation. Understanding the interplay between annular, leaflet, and subvalvular distortion is essential for achieving functional and durable repair that can rival evolving transcatheter options. This review unifies previously scattered concepts into a practical framework for anatomy-guided tricuspid reconstruction, offering surgeons an accessible reference for managing complex, RV-dependent tricuspid valve disease.

Heart failure with preserved ejection fraction is the fastest-growing subtype of heart failure, especially among the elderly. It is aimed to determine whether the addition of 10mg of Dapagliflozin for HFpEF patient can lead to a decrease in epicardial adipose tissue volume. this non-randomized clinical trial included 60 patients presented with left ventricular diastolic dysfunction (30 patients fulfilling HFpEF diagnostic criteria received dapagliflozin 10mg once daily in addition to standard medical therapy and 30 patients with LV diastolic dysfunction who did not meet HFpEF criteria received standard medical care only). The mean EAT volume was significantly (p < 0.001) higher in the HFpEF + dapagliflozin group vs. standard care group at baseline while it was comparable in the two groups at follow-up (p = 0.081). For within group comparisons, insignificant (p = 0.124) change was recorded for the standard care group while there was significant reduction in the HFpEF + dapagliflozin arm (p < 0.001). Additionally, EAT reduction in the HFpEF + dapagliflozin group was confirmed by the interaction between time and treatment modality (p < 0.001). SGLT2 inhibitor use was associated with a significant reduction in epicardial adipose tissue, a fat depot implicated in HFpEF pathophysiology. This finding suggested a possible structural association that warrants confirmation in randomized out-come driven trials. NO. (NCT06510270) (first submitted date 15/7/2024, first posted date 19/7/2024).

Obesity-induced left ventricular diastolic dysfunction (LVDD), associated with ectopic fat and dysfunctional epicardial adipose tissue (EAT), is emerging as a key research area due to its increasing prevalence and links to metabolic-associated steatotic liver disease (MASLD) and type 2 diabetes mellitus (T2DM). This underscores the importance of early risk assessment and intervention to prevent the progression of LVDD. We developed an interpretable machine learning (ML) model combining cardiac magnetic resonance (CMR) radiomics and clinical data to assess LVDD risk in MASLD/T2DM patients, enabling proactive treatment customization. We prospectively analyzed 175 MASLD/T2DM patients, splitting them into training and external validation groups. After categorizing them as LVDD+ or LVDD-, we collected clinical data and extracted standardized CMR radiomics features to develop ML models. The optimal model was internally validated, interpreted using Shapley Additive Explanations (SHAP), and externally validated. LVDD prevalence was similar in both cohorts (45.5% vs 46.2%, χ2 = 0.108, P = 0.743) among 175 MASLD/T2DM patients. The extreme gradient boosting (XGBoost) model, combining CMR radiomics and clinical data, outperformed in both internal and external validations. SHAP analysis revealed five critical determinants of LVDD: three radiomics features from CMR images and two clinical variables. The XGBoost model, incorporating radiomics from CMR images and clinical data, outperformed other ML models in predicting LVDD risk in patients with T2DM and MASLD, enhancing risk assessment accuracy. This improvement allows for timely treatment adjustments, potentially preventing LVDD progression more effectively.

Atrial fibrillation (AF) frequently coexists with pulmonary hypertension (PH) and is associated with clinical deterioration, right ventricular dysfunction, and increased mortality. While catheter ablation has demonstrated superiority over anti-arrhythmic drug (AAD) therapy in select AF populations, outcomes in patients with concurrent PH remain poorly characterized. We performed a retrospective cohort study using the TriNetX Research Network. Adults with AF and PH were identified and stratified by treatment with catheter ablation plus AAD or AAD therapy alone. After 1:1 propensity score matching for demographics, comorbidities, and medication use, 9759 patients were included in each cohort. The primary outcomes were major adverse cardiovascular events (MACE) and right heart failure. Secondary outcomes included all-cause mortality, acute myocardial infarction (MI), and stroke. Kaplan-Meier models were used as the primary analysis, with Cox proportional hazards and E-value analysis as sensitivity. Competing risk analyses were performed using Fine-Gray models. Ablation was associated with a 50% reduction in MACE (HR 0.497 [0.467, 0.528], p < 0.001) and 35% reduction in right heart failure (HR 0.647 [0.573, 0.732], p < 0.001). There were also significant reductions in all-cause mortality (HR 0.469 [0.454, 0.488], p < 0.001) and stroke (HR 0.819 [0.728, 0.922], p = 0.001). There was no difference in acute MI (HR 0.982 [0.891, 1.082], p = 0.710). Findings were consistent across Cox sensitivity analyses, E-value analysis, and competing-risk models. In AF patients with PH, catheter ablation with AAD therapy was associated with substantially lower risks of adverse cardiovascular outcomes compared with AAD therapy alone. These findings suggest that catheter ablation is associated with lower risks of adverse cardiovascular outcomes in this high-risk population.

Surgical repair of CDH is associated with early postoperative changes in echocardiographic indices of biventricular systolic performance and pulmonary vascular loading. Paired echocardiography allows quantification of early hemodynamic adaptation following repair. • Pulmonary hypertension and ventricular dysfunction are major contributors to early morbidity and mortality in infants with congenital diaphragmatic hernia (CDH). • The early hemodynamic impact of surgical repair, assessed using paired preoperative and postoperative echocardiography within individual infants, has not been well characterized. • Surgical repair of CDH is associated with early postoperative changes in echocardiographic indices of biventricular systolic performance, septal geometry, and pulmonary hypertension. • Changes in pulmonary vascular loading were closely associated with directional changes in ventricular systolic performance indices, highlighting the importance of ventricular-vascular interaction in early postoperative hemodynamic adaptation.