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Journal articlePalermi S, Zeidaabadi B, Vecchiato M, et al., 2026, , Int J Cardiol, Vol: 461
BACKGROUND: Pre-participation screening (PPS) in competitive athletes aims to identify cardiovascular diseases associated with sudden cardiac death (SCD). Although the 12‑lead electrocardiogram (ECG) represents the cornerstone of PPS, structural abnormalities may demonstrate limited or incomplete electrical expression, particularly in asymptomatic athletes with physiological remodeling. Artificial intelligence (AI)-enabled ECG models have shown promising performance in hospital-based populations, but their transportability to low-prevalence athlete screening environments remains uncertain. OBJECTIVES: To develop and externally validate a deep learning (DL)-based AI-ECG ensemble model for detecting imaging-confirmed structural heart disease in competitive athletes undergoing PPS. METHODS: A convolutional neural network (CNN) ensemble was trained using hospital-derived ECG images from Beth Israel Deaconess Medical Center (BIDMC, Boston, USA) and externally validated in the Italian Team for Athlete CARDiac evaluation and AI-based Risk prediction (ITACARD-AI) registry. Separate CNNs were developed for valvular heart disease (VHD) and cardiomyopathies (CM) and combined using XGBoost meta-learning. Model performance was assessed using area under the receiver operating characteristic curve (AUROC), subgroup analyses, and threshold-based evaluation. RESULTS: The ITACARD-AI cohort included 1115 competitive athletes (mean age 26 ± 13 years; 70% male), including 48 athletes (4.3%) with VHD and 30 (2.7%) with CM. External validation demonstrated substantial performance degradation compared with hospital-based internal validation. AUROC values decreased to 0.70 (95% CI 0.64-0.75) for VHD and 0.69 (95% CI 0.60-0.78) for CM, indicating only modest discrimination in the screening population. Threshold analyses showed high negative predictive values (∼99%) but persistently low positive predictive values (≤8%), reflecting limited disease enrichment and st
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Journal articleRisum N, Philbert BT, Svendsen JH, et al., 2026, , Am Heart J, Vol: 300
BACKGROUND: Cardiac resynchronization therapy (CRT) using biventricular pacing (BiV-CRT) is an established treatment for patients with symptomatic heart failure, reduced left ventricular ejection fraction, and left bundle branch block (LBBB), leading to improvements in symptoms, ventricular function, exercise capacity and survival. Despite these benefits, up to one third of patients fail to respond optimally with no clinical improvement despite meeting current criteria for implantation. Conduction system pacing (CSP), delivered via His bundle pacing or left bundle branch area pacing, has emerged as an appealing alternative by directly engaging the native His-Purkinje system. However, randomized data directly comparing CSP-based CRT with conventional BiV-CRT remain limited. STUDY DESIGN: His-Alternative II is an investigator-initiated, multicenter, randomized non-inferiority trial designed to evaluate whether CRT delivered via CSP is non-inferior to conventional biventricular pacing with respect to left ventricular reverse remodeling. The study enrolls patients with symptomatic heart failure (New York Heart Association class II to III), left ventricular ejection fraction ≤35%, strict LBBB by electrocardiographic criteria, and optimal medical therapy. A total of 150 patients were randomized with a 1:2 randomization ratio to receive BiV-CRT or CSP-based CRT (His bundle pacing or left bundle branch pacing) and followed for 6 months. The primary endpoint is change in left ventricular end-systolic volume assessed by echocardiography; a surrogate endpoint consistently associated with long-term outcomes in CRT populations. Secondary endpoints include functional capacity, symptomatic status, quality of life, electrical resynchronization, and device-related complications. CONCLUSIONS: His-Alternative II is designed to determine whether CSP-based CRT can achieve left ventricular reverse remodeling comparable to that obtained with conventional BiV-CRT. The study will provide
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Journal articleAdami E, Kim Y, Zheng SL, et al., 2026, , Sci Transl Med, Vol: 18
Hypertrophic cardiomyopathy (HCM) is marked by asymmetric cardiac wall thickening, hypercontractility, diastolic dysfunction, and fibrosis. Pathogenic sarcomere gene variants cause HCM, but comparable abnormalities occur in patients with unexplained disease, albeit with fewer adverse events. To investigate stage- and genotype-specific disease mechanisms, we performed single-nucleus RNA sequencing of cardiac tissues from 47 patients with HCM, spanning obstructive HCM with preserved systolic function and end-stage HCM, and compared them with nonfailing donor and dilated cardiomyopathy hearts. We identified transcriptional programs associated with cardiomyocyte hypertrophy, fibrosis, and vascular remodeling. Pathogenic variant-positive early-stage HCM samples showed reduced cardiomyocyte abundance and expansion of a proarrhythmogenic cardiomyocyte state. We identified proline-rich 16 (PRR16) as a cardiomyocyte growth-associated gene in HCM and validated its increased expression by RNA in situ hybridization and in a human induced pluripotent stem cell-derived cardiomyocyte HCM model. In HCM samples, fibroblast compositional shifts were associated with profibrotic activation and adverse extracellular matrix remodeling, accompanied by reduced collagen IV (COL4A1/COL4A2) expression and ultrastructural basement membrane abnormalities. HCM samples also exhibited extensive vascular alterations, including shifts in endothelial cell subpopulations, reduced pericyte abundance suggestive of microvascular dysfunction, and increased lymphangiogenic vascular endothelial growth factor C signaling. Unsupervised and supervised machine learning approaches distinguished HCM from dilated cardiomyopathy and accurately predicted genotype status in early-stage HCM from cell type-resolved transcriptional profiles, revealing widespread genotype-driven remodeling. Together, our findings uncover multicellular, genotype-associated remodeling programs in HCM, providing insight into mechanisms unde
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Journal articleHunt SE, Lemos D, Pericherla SR, et al., 2026, , J Mol Biol, Vol: 438
To facilitate both disease research and personalised medicine, there is an urgent need for accessible, structured data models describing the molecular basis of genetically determined disease. Gene2Phenotype is a database of expert-curated monogenic gene-disease associations, which was established in 2012 to enable efficient prioritisation of likely diagnostic genomic variants. Initially focused on developmental disorders, it has since been extended to support cardiac, eye, skeletal and skin disorders and germline cancer predisposition. We have redesigned and extended Gene2Phenotype, which now openly shares standardised, structured models of rare monogenic diseases, detailing genotype, molecular mechanism and associated phenotypes, curated from scientific literature. The updated platform, which includes a new API, enabling programmatic access, improves the findability, accessibility, interoperability and reusability of detailed rare monogenic disease association data. These data have the potential to accelerate disease research, clinical diagnosis, treatment selection and the development of novel therapies. Gene2Phenotype is available at https://www.ebi.ac.uk/gene2phenotype/.
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Journal articleBalakrishnan ID, Heymans ABM, Claggett B, et al., 2026, , Circ Heart Fail
BACKGROUND: Atrial fibrillation (AF) is the most common arrhythmia in dilated cardiomyopathy (DCM) and is associated with adverse outcomes. However, the genetic determinants of AF risk and its prognostic significance across genotyped DCM subtypes remain unknown. METHODS: In this observational cohort study, we analyzed 3117 genotyped patients with DCM from the SHaRe (Sarcomeric Human Cardiomyopathy Registry). AF prevalence, incidence, and clinical characteristics were assessed by genotype. Patients were classified as genotype-positive [G(+)] if they had a pathogenic or likely pathogenic variant in a DCM-associated gene, and genotype-negative [G(-)] if genetic testing was negative. Factors associated with incident AF were evaluated using Cox regression. AF was modeled as a time-dependent variable to evaluate associations with clinical outcomes. RESULTS: Among 3117 genotyped patients with DCM (mean age, 48±15 years; 39% were female; and 35% were G[+]), 12.3% (n=384) had prevalent AF. Of 2491 patients without prevalent AF and with follow-up, 312 (12.5%) developed AF during a median of 4.5 years (interquartile range, 1.6-9.0). Among 2851 patients with follow-up, cumulative AF prevalence was 23.6%. LMNA had the highest AF incidence (7.6/100 patient-years) and cumulative AF prevalence (56.7%) and was the only genotype independently associated with incident AF compared with that in G(-) patients (hazard ratio, 5.52 [95% CI, 3.84-7.95]; P<0.001). TTN had an AF incidence of 2.1 per 100 patient-years and cumulative AF prevalence of 24.4%, comparable to that in G(-) patients. Older age, male sex, and prior heart failure hospitalization were also independently associated with incident AF. AF was independently associated with a higher risk of the composite clinical outcome (hazard ratio, 1.58 [95% CI, 1.29-1.94]; P<0.001), including heart failure, ventricular arrhythmias, and all-cause mortality. CONCLUSIONS: In this large genotyped DCM cohort, AF burden and incident
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Journal articleMazzarotto F, Ware J, 2026,
An updated evidence assessment of the genetic causes of dilated cardiomyopathy
, Circulation, ISSN: 0009-7322Background: Evidence of the diverse genetic architecture of dilated cardiomyopathy (DCM) continues to emerge and requires reassessment of the clinical relevance of implicated disease genes. Building on the 2019-2020 Clinical Genome Resource (ClinGen) evaluation, the DCM Gene Curation Expert Panel (GCEP) reconvened in 2024-2025 to conduct a reassessment of genes in DCM.Methods: The ClinGen semi-quantitative clinical validity classification framework was applied with specifications to DCM to classify genes into categories based upon strength of published evidence for a DCM phenotype. Previously curated genes were reassessed and newly reported gene-disease-mode of inheritance (MOI) relationships, termed “curations,” were evaluated.Results: Sixty-eight genes were evaluated, inclusive of 72 unique gene-disease-MOI relationships across 51 previously evaluated and 17 newly assessed genes. Thirty-five curations were classified as high evidence (16 Definitive, 10 Strong, 9 Moderate), increasing by 16 from the prior assessment. Nine newly assessed genes were classified as high evidence, including BAG5, FLII, LMOD2, MYLK3, MYZAP, NRAP, PPA2, PPP1R13L, and RPL3L. Twelve genes (11 newly appraised) were rated as high evidence with an autosomal recessive (AR) MOI. Five re-evaluated genes from 2019-2020 had clinically significant changes in classification. Except for JPH2, for which curation was modified to separate autosomal dominant (-AD) and -AR MOI curations, clinically significant changes involved upgrades from low to high evidence categories (PLEKHM2, PRDM16, TBX20, TNNI3K), demonstrating the robustness of the ClinGen gene curation process over time. An additional 29 gene-disease-MOI curations were classified as Limited, including six newly evaluated genes and one new MOI for a previously evaluated gene, MYBPC3-AR; four were classified as No Known Disease Relationship, and four remained Disputed. Four previously evaluated genes were curated for both AD and AR MOIs
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Journal articleRodero C, Curran L, Lanyon CW, et al., 2026, , J Mol Cell Cardiol, Vol: 218, Pages: 137-150
Hypertrophic cardiomyopathy (HCM) is a condition characterized by variable patterns of myocardial hypertrophy. Progressive functional remodeling of material properties contributes to symptoms, disease progression, and variability in treatment response. However, it is not clear how these properties interact to determine cardiac performance and response to treatment. We quantified how cardiac anatomy variability, functional remodeling, and pharmacological treatment influence the relative importance of biophysical mechanisms that govern cardiac function. We built five four-chamber electromechanical heart models representing anatomical clusters. We performed global sensitivity analyses on 46 parameters across 32 outputs. We repeated this process 18 times to model different types of functional remodeling and two times to model mavacamten and aficamten. Across all representative HCM phenotypes, sensitivity profiles were preserved. Within the parameter ranges examined, ventricular afterload explained the largest share of variance in hemodynamic outputs across anatomies (up to 69%). Functional remodeling led to shifts in parameter importance, mostly when ventricular stiffness was increased. The modeling of pharmacological treatments led to modest but targeted changes, with mavacamten and aficamten producing comparable effects, particularly for outputs related to arterial pressures. Across major anatomical phenotypes of hypertrophic cardiomyopathy, functional remodeling, rather than anatomy alone, reshaped the relative importance of cellular, myocardial, and loading-related parameters, with the largest shifts under increased ventricular stiffness and under aficamten in obstructive physiology. These hypothesis-generating results suggest that the integration of biomarkers reflecting ventricular-arterial coupling, myocardial stiffness, and contractile state may help anticipate symptoms and treatment response in HCM.
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Journal articleLuo Y, Ferreira PF, Wen K, et al., 2026, , Magn Reson Med, Vol: 96, Pages: 1097-1110
PURPOSE: Slice interleaving, a limited phase encode (PE) field of view (FOV), and effective fat suppression are vital for efficient cardiac diffusion tensor imaging (cDTI) with minimal artifacts. This study aimed to optimize reduced FOV and fat suppression methods for interleaved multislice cDTI to improve signal-to-noise ratio (SNR) and minimize artifacts. METHODS: Two-slice motion compensated spin echo datasets from 20 healthy volunteers were acquired. Four reduced PE FOV sequences were evaluated: 2DRF pulse; applying either 180 ° or 90 ° pulses in PE direction; and the proposed flip-back sequence with a nonselective 180 ° pulse after readout to restore inverted magnetization. Four fat suppression techniques were implemented: no fat suppression (standard); fat saturation; binomial water excitation and spectral attenuated inversion recovery (SPAIR). RESULTS: The proposed flip-back sequence with SPAIR achieved the highest median SNR, and its SNR values are significantly higher ( p < 0.01 ) than 2DRF with SPAIR as current state-of-the-art. SPAIR and water excitation demonstrated comparable performance when combined with the flip-back sequence, and both yielded superior image quality than with no suppression or fat saturation. SPAIR showed robust fat suppression across most subjects, whilst water excitation exhibited advantages in some subjects with a high body mass index. CONCLUSION: The proposed flip-back sequence with SPAIR enables efficient interleaved multislice imaging with reduced PE FOV and effective fat suppression, facilitating clinical translation of in vivo cDTI.
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Journal articleShun-Shin M, Whinnett Z, 2026, , Lancet
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Journal articleRowin EJ, Maron BJ, Siontis KC, et al., 2026, , Circulation
BACKGROUND: Implanted cardioverter-defibrillators (ICDs) have been used in patients with hypertrophic cardiomyopathy (HCM) to prevent sudden death, and have proven lifesaving for many patients. However, experience with ICD therapy has largely been derived from relatively small HCM cohorts confined to specific countries or regions of the world. Therefore, we sought to determine the effectiveness of ICDs in preventing sudden death due to life-threatening ventricular arrhythmias in a large international multicenter HCM population. METHODS: Databases from 25 HCM centers (8 in the United States, 9 in Europe, 4 in Asia, and 1 each in Australia, Africa, Mexico, and South America) were retrospectively interrogated to identify consecutive patients with HCM with ICDs (1992 to 2024) followed for 7±6 years (up to 32 years) for clinical outcomes. RESULTS: A total of 3387 patients were identified (63% men). They had a mean left ventricular thickness of 22±7 mm. The participants had received ICDs at a mean age of 47±17 years. Over follow-up, 550 patients (16%) experienced ≥1 appropriate ICD therapy (2.6%/y), including 86 of the 247 implanted for secondary prevention (35% [6.4%/y]) and 464 of the 3140 implanted for primary prevention (15% [2.2%/y]). Appropriate therapy occurred in the 464 primary prevention patients at a mean age of 49±17 years, with a median time to first appropriate therapy of 4 years after ICD implantation; 16% of these received their first appropriate therapy ≥10 years after implantation, and 47% experienced multiple interventions. Independent predictors of appropriate ICD therapy included unexplained syncope, left ventricular apical aneurysms, left ventricular systolic dysfunction, and nonsustained ventricular tachycardia on ambulatory monitoring. Of the 3140 primary prevention patients, 2946 survived (94%) and 194 died (6%) (0.8%/y), including 68 due to HCM (0.3%/y), predominantly of end-stage heart failure (n=43) or stroke (
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Journal articleVinther M, Philbert BT, Svendsen JH, et al., 2026, , JACC Clin Electrophysiol
BACKGROUND: Cardiac resynchronization therapy (CRT) in patients with symptomatic heart failure and left bundle branch block (LBBB) can be achieved with biventricular pacing (BIV-CRT) or conduction system pacing (CSP-CRT). OBJECTIVES: The present study examined if CSP-CRT was feasible and noninferior to BIV-CRT. METHODS: A total of 150 patients with symptomatic heart failure, left ventricular ejection fraction (LVEF) ≤35%, and LBBB (Strauss criteria) were included. Patients were randomized 1:2 to either BiV-CRT or CSP-CRT (HIS-CRT or LBB-CRT) and followed for 6 months. The primary endpoint was the relative change in left ventricular end-systolic volume (LVESV). Two patients withdrew their consent before implant. RESULTS: At implantation, 15 patients (15 %) crossed over from the CSP-CRT group to the BiV-CRT group and 1 patient crossed over from BiV-CRT to the CSP-CRT group. Accordingly, 85 patients (57 %) were treated with CSP-CRT (26 His-CRT, 59 patients LBB-CRT) and 63 patients (43 %) with BiV-CRT. For the primary endpoint, intention-to-treat 6-month follow-up LVESV decreased by 35% ± 22% with CSP-CRT vs 34% ± 22% with BiV-CRT (between-group differences 0.9%, 95% CI: -6.0% to 7.8%; P < 0.01 for noninferiority, P = 0.80 for superiority). Furthermore, LVEF increased by 14% ± 8% with CSP-CRT vs 14% ± 9% with BiV-CRT (P = NS). QRS duration shortening (-31 ± 22 ms vs -31 ± 21 ms), 6-min walking distance increase (37 ± 53 m vs 24 ± 48 m), Minnesota Living with Heart Failure score reduction (-16 ± 18 vs -13 ± 15), NYHA functional class improvement (-0.6 ± 0.6 vs -0.6 ± 0.7), and N-terminal pro-B-type natriuretic peptide reductions (-72 ± 152 pmol/l vs -110 ± 116 pmol/l) were similar between groups. CONCLUSIONS: In heart failure patients with LBBB, CSP-CRT was noninferior to BiV-CRT in reducing LVESV and both treatment modalities provided similar and excellent improvement
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Journal articleSamways JW, Ali N, Arnold AD, et al., 2026, , Pacing Clin Electrophysiol
BACKGROUND: Conduction system pacing (CSP) is an emerging alternative modality of cardiac resynchronization therapy (CRT). However, not all patients obtain electrical resynchronization with CSP, there is a clinical need for reliable non-invasive predictors of response. We aimed to assess the ability of several non-invasive modalities to predict electrical resynchronization with CSP-CRT. METHODS: Patients with standard heart failure CRT indications (excluding right-bundle branch block) underwent CSP-CRT using His-bundle and left-bundle branch pacing. Electrical resynchronization was defined as a >10 ms reduction in left ventricular activation time or conversion to a physiological left ventricular activation pattern on non-invasive multi-electrode mapping. We assessed whether 12-lead ECG morphology, vector electrocardiogram (VCG) derived QRS area, Ultra High Frequency (UHF)-ECG parameters or MRI scar burden predicted electrical resynchronization. RESULTS: Thirty four patients were analyzed (mean age 69±10 years; 82% male; LVEF 30±6%; QRS duration 161±23 ms; 32% ischemic cardiomyopathy). Electrical resynchronization was achieved in 24/34 (71%; 95%CI 53-85). Strauss criteria positivity on 12-lead ECG yielded a positive predictive value (PPV) of 83% (95%CI 61-95%) and negative predictive value (NPV) of 55% (95%CI 23-83%). VCG QRS area >100µVs demonstrated PPV 100% (95% CI 81-100%) and NPV 73% (95%CI 85-100%). UHF-ECG e-DYS >50 ms gave PPV 93% (95%CI 66-100%) and NPV 47% (23%-72%); >60 ms gave PPV 90% (95%CI 66-100%) and NPV 38% (95%CI 18-62%). MRI scar burden <15% resulted in PPV 88% (95%CI 64-99%) and NPV 56% (95%CI 21-86%). Lines of propagation discontinuity on multi-electrode mapping showed PPV 100% (95%CI 85-100%) and NPV 83% (95%CI 52-98%). CONCLUSIONS: Multiple non-invasive markers, including QRS morphology, VCG QRS area, UHF-ECG e-DYS, MRI scar burden showed potential to identify patients who are likely
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Journal articleNikolaev VO, Gorelik J, 2026, , Cardiovasc Res, Vol: 122, Pages: 1415-1416
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Journal articleHou Y, Singal S, Swiatlowska P, et al., 2026, , Current Issues in Molecular Biology, Vol: 48, ISSN: 1467-3037
Cardiovascular diseases (CVDs) remain a leading cause of mortality worldwide, and ageing is strongly associated with progressive arterial stiffening. Age-related alterations in extracellular matrix (ECM) mechanics influence vascular smooth muscle cell (VSMC) behaviour, while sympathetic innervation represents an additional regulator of vascular homeostasis. However, how neural signalling interacts with ageing-associated mechanical conditions to regulate VSMC behaviour remains unclear. In this study, an in vitro sympathetic neuron–VSMC co-culture model was established to investigate neuro-mechanical regulation. Primary rat sympathetic neurons and A7r5 VSMCs were cultured on glass or polydimethylsiloxane (PDMS) substrates with defined stiffness (20 and 130 kPa), representing healthy and ageing-associated stiffened arterial environments, respectively. VSMC behaviour was assessed through analysis of cell area, proliferation, migration, cellular Young’s modulus (YM), and DNA damage marker γH2AX. Sympathetic neuronal co-culture was associated with reduced VSMC spreading and decreased γH2AX levels. Under the conditions tested, neural signalling exerted limited effects on cell proliferation and migration. In contrast, increased substrate stiffness promoted cell proliferation and elevated YM. Both neuronal input and substrate stiffness were associated with increased cellular YM. Together, these findings indicate that neural and mechanical cues may jointly influence VSMC behaviour within ageing-associated mechanical environments. This co-culture system provides a controllable platform for studying neuro-mechanical interactions in vascular biology.
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Journal articleEllard S, Hanson H, Cassidy E-J, et al., 2026, , J Med Genet
BACKGROUND: Genomic testing will occasionally identify a highly actionable genetic variant or other finding that is not related to the reason for testing. Such incidental findings may be relevant to the patient undergoing testing or to their family members. METHODS: This guidance on managing incidental findings was developed by the British Society for Genetic Medicine to support clinicians requesting genomic tests and clinical scientists working in genomic laboratories within the National Health Service. RESULTS: Clinicians should include the possibility of incidental findings with a patient/parent(s) in discussions around genomic testing. Decisions regarding the reporting of a genetic variant unrelated to the referral reason will depend on clinical actionability, penetrance and the variant classification. Pathogenic variants may be reported if there is evidence of high penetrance and available treatment or surveillance that is likely to improve clinical outcome. Testing using large next generation sequencing gene panels and genome-wide array analysis increases the likelihood of revealing heterozygous carrier status for autosomal recessive disorders unrelated to the reason for testing. Reporting incidental heterozygous carrier status for autosomal recessive conditions is not recommended. CONCLUSION: This guidance provides a framework for the reporting of incidental findings with case examples and a cancer susceptibility gene list. Decision-making in accordance with guidelines will achieve greater consistency than case by case decisions. This guidance may be of use to healthcare professionals in other publicly funded healthcare systems with evolving genomic testing services.
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Journal articleRaman B, Prasad SK, 2026, , Circulation, Vol: 154, Pages: 512-516
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Journal articleRajendra S, Salmasi Y, Raj B, et al., 2026, , Interdiscip Cardiovasc Thorac Surg, Vol: 41
OBJECTIVES: Right ventricular failure (RVF) remains a frequent complication following left ventricular assist device (LVAD) implantation. Conventional risk scores rely on preoperative data acquired under stable conditions, which may overlook early signs of RV decompensation that emerge under perioperative stress. This study evaluates whether perioperative haemodynamic markers prior to cardiopulmonary bypass (CPB) improve RVF prediction compared to preoperative assessment obtained by right heart catheterization (RHC), echocardiographic parameters, and scoring systems such as the European Registry for Patients with Mechanical Circulatory Support (EUROMACS) RHF score. METHODS: We conducted a retrospective single-centre study of 203 LVAD patients (2013-2023). The primary outcome was RVF. Preoperative data included clinical variables, echocardiography, and RHC. Perioperative data included vasoactive-inotropic score (VIS), pulmonary artery (PA) catheter, and arterial-line monitoring between induction and start of CPB. Two multivariable models were developed using least absolute shrinkage-and-selection operator (LASSO) logistic regression: (1) Preoperative model; (2) Pre-CPB model. Model performance was assessed using area under the curve (AUC) and compared against EUROMACS-RHF using DeLong tests. RESULTS: Thirty-six patients (17.7%) developed RVF. No preoperative RHC-derived parameter independently predicted RVF. The Preoperative model achieved moderate discrimination (AUC: 0.747). Incorporating intraoperative mean arterial pressure (MAP), pulmonary artery pulsatility index (PAPi), and maximum VIS yielded a Pre-CPB model with strong discrimination (AUC: 0.834). The Pre-CPB model significantly outperformed both EUROMACS-RHF (P = 0.0299) and the Preoperative model (P = 0.049), with no significant difference between our Preoperative model and EUROMACS-RHF (P = 0.222). CONCLUSIONS: Perioperative markers prior to CPB significantly outp
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Journal articleOng AQC, Ang C-S, Bojic I, et al., 2026, , EClinicalMedicine, Vol: 98, ISSN: 2589-5370
Background: Artificial intelligence (AI) holds potential to transform cardiovascular care, but evidence on its effectiveness in clinical practice remains inconsistent. We aimed to synthesise evidence from randomised controlled trials (RCTs) on the effectiveness of AI-enabled cardiovascular care, summarise the trial design and characteristics of AI systems, and evaluate methodological quality and reporting transparency.Methods: In this systematic review and meta-analysis, we searched Embase, MEDLINE, Scopus, Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov for RCTs that evaluated effectiveness of AI interventions in cardiovascular care, published in English from database inception to July 07, 2025. The search was updated on April 28, 2026. We followed Cochrane guidance for study selection and data extraction. Risk of bias was assessed using Cochrane’s Risk of Bias tools and reporting transparency using CONSORT-AI checklist. We calculated summary effects using inverse-variance-weighted random-effects meta-analyses and assessed the certainty of evidence using GRADE. Between-study heterogeneity was quantified using χ² (Cochran’s Q) test and I² statistic. Publication bias was not assessed due to small number of studies. This study was registered with PROSPERO (CRD420251090250).Findings: Of 12,217 records identified, 31 RCTs from 13 regions (n=1,685,717 patients) were included in the systematic review, and 11 of these (n=1,614,689) in the meta-analysis. Most RCTs were published after 2021 (90%), multicentre (58%), and had short follow-up duration (<12 months; 52%). Risk of bias was low in seven trials (23%), and overall reporting transparency was moderate. Twenty-two trials (71%) reported significant benefit of AI interventions on primary endpoints, mostly intermediate process measures, while nine trials (29%) found no significant effect. Compared with routine care, image-based AI-clinical decision support system had sig
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Journal articlePastika L, Patlatzoglou K, Sieliwonczyk E, et al., 2026, , Eur Heart J Digit Health, Vol: 7
AIMS: A significant proportion of type 2 diabetes cases remain undiagnosed despite screening advances, carrying substantial cardiometabolic risk. Artificial intelligence-enhanced electrocardiography (AI-ECG) detects subtle ECG changes in subclinical disease, potentially enabling opportunistic screening. METHODS AND RESULTS: We developed AI-ECG Risk Estimator for Diabetes Mellitus (AIRE-DM), a convolutional neural network with discrete-time survival loss, for diagnosis of prevalent and prediction of incident type 2 diabetes. It was trained on 1 163 401 ECGs from 189 537 individuals from Beth Israel Deaconess Medical Center (BIDMC) and externally validated in UK Biobank (UKB; n = 65 606) and ELSA-Brasil (n = 13 739). AI-ECG Risk Estimator for Diabetes Mellitus demonstrated moderate discrimination for prevalent type 2 diabetes (area under the receiver operating characteristic curve: BIDMC 0.724, UKB 0.733, ELSA-Brasil 0.706) and incident type 2 diabetes (C-index: BIDMC 0.667, UKB 0.688, ELSA-Brasil 0.625). The highest AIRE-DM risk quartile had elevated incident diabetes risk vs. the lowest (hazard ratio: BIDMC 4.75, UKB 7.52, ELSA-Brasil 3.96). AI-ECG Risk Estimator for Diabetes Mellitus was non-inferior to the American Diabetes Association Diabetes Risk Test in BIDMC, with improved predictive accuracy when combined. In normoglycaemic patients, AIRE-DM was superior to glycated haemoglobin (HbA1c) for predicting incident diabetes in BIDMC and non-inferior in ELSA-Brasil. The highest risk quartile reached 5% cumulative type 2 diabetes mellitus incidence 5.4 years (BIDMC) and 4.8 years (ELSA-Brasil) earlier than the lowest risk quartile, after adjusting for HbA1c, age, and sex. Phenome- and genome-wide association studies revealed biologically plausible associations with glucose regulation, cardiac morphology, diastolic dysfunction, arterial stiffness, and lipid metabolism. CONCLUSION: AI-ECG Risk Estimator for Diabetes Mellitus detects prevalent type 2 diabetes and predi
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Journal articleBoichenko V, Frolova S, Voellenkle C, et al., 2026, , Biomed Pharmacother, Vol: 201
Liver and cardiac fibrosis are critical drivers of chronic organ dysfunction, characterised by fibroblast activation, excessive extracellular matrix deposition, and inflammation. While these fibrotic processes are initiated by distinct triggers and monitored by organ-specific biomarkers, emerging evidence reveals both shared and unique regulatory networks, particularly involving non-coding RNAs (ncRNAs). This review focuses on the roles of microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), such as miR-21, miR-22, miR-29, miR-34a, miR-122, miR-133a, miR-210, miR-214, H19, MALAT1, MEG3, NEAT1, and circHIPK3, in modulating key fibrotic pathways including TGF-β/SMAD signalling, oxidative stress, and extracellular matrix remodelling in both hepatic and cardiac tissues. Some ncRNAs exhibit convergent regulatory functions across both organs, while others demonstrate divergent or context-dependent effects within and between tissues. Furthermore, circulating ncRNAs, potentially transferred via extracellular vesicles (EVs), hold potential as minimally invasive biomarkers for early detection of combined cardio-hepatic fibrosis, as exemplified in conditions like Fontan circulation, though extensive validation in large, prospective cohorts is essential. This article summarises established clinical biomarkers, discusses the ncRNA-mediated mechanisms operating in liver and heart fibrosis, distinguishing shared, divergent, and mixed evidence, and explores their translational potential in diagnostics and experimental therapeutics. Finally, it addresses remaining challenges and outlines future directions, emphasising multi-omic integration, longitudinal ncRNA profiling, and mechanistic validation to advance precision management of fibrotic diseases.
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