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Journal articleNg FS, Shah A, Casadei B, 2026,
Interpreting AI-Enhanced ECG Performance in High-Risk, Resource-Limited Settings.
, JAMA Cardiol, Vol: 11 -
Journal articleCraig NJ, Loganath K, Everett RJ, et al., 2026,
Myocardial Fibrosis and Early Intervention in Asymptomatic Patients With Severe Aortic Stenosis: Insights From the EVOLVED Randomized Clinical Trial.
, JAMA Cardiol, Vol: 11, Pages: 599-605IMPORTANCE: Myocardial fibrosis burden has been associated with adverse clinical outcomes in symptomatic patients with aortic stenosis. OBJECTIVE: To determine whether midwall myocardial fibrosis burden is associated with adverse clinical outcomes in asymptomatic patients and whether those with more fibrosis derive greater benefit from early intervention. DESIGN, SETTING, AND PARTICIPANTS: This post hoc analysis of a randomized clinical trial was conducted between August 2017 and October 2022. The trial took place at 24 cardiac centers across the United Kingdom and Australia. Participants included asymptomatic patients with severe aortic stenosis and midwall fibrosis on cardiac magnetic resonance. These data were analyzed from October 2024 through June 2025. INTERVENTION: Early intervention with transcatheter or surgical aortic valve replacement. MAIN OUTCOMES AND MEASURES: Primary outcome was all-cause death or unplanned aortic stenosis-related hospitalization. Secondary outcomes included the individual components of the primary outcome. RESULTS: In 224 trial participants (mean [SD] age, 73 [9] years; 63 women and 161 men, and mean [SD] aortic valve peak velocity 4.3 [0.5] m per second) with a median follow-up of 42 months, fibrosis burden (per 1% increase) was associated with an increase in the primary end point (hazard ratio [HR], 1.23; 95% CI, 1.08-1.37) and its component of unplanned aortic stenosis-related hospitalizations (HR, 1.22; 95% CI, 1.03-1.40) but not all-cause death (HR, 1.17; 95% CI, 0.98-1.35). There were no interactions between randomization arm and the midwall fibrosis burden for the primary (P for interaction = .39) or secondary end points. In patients with high fibrosis burden above the median, the primary end point occurred in 12 of 59 (20%) of those randomized to early intervention and 17 of 53 (32%) of those randomized to guideline-directed conservative management (HR, 0.62; 95% CI, 0.29-1.28). For the individual components, al
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Journal articleKorstanje R, Strong R, Salmon AB, et al., 2026,
Astaxanthin, meclizine, mitoglitazone, pioglitazone, alpha-ketoglutarate, mifepristone, methotrexate, and atorvastatin-telmisartan do not increase lifespan in UM-HET3 mice.
, Geroscience, Vol: 48, Pages: 3821-3830The Interventions Testing Program (ITP) evaluated eleven compounds in genetically heterogeneous UM-HET3 mice to assess their potential to extend lifespan. These interventions included both novel agents and previously tested compounds administered at novel doses or starting ages. Despite prior evidence suggesting lifespan benefits of these proposed interventions in other models or under different conditions, none of the tested compounds significantly increased lifespan in male or female mice. Notably, astaxanthin, mitoglitazone, and meclizine-previously associated with lifespan extension in the ITP-showed no benefit when administered at different doses or starting at later ages. In females, astaxanthin, late-start mitoglitazone, and pioglitazone were associated with significantly reduced lifespan when pooling the data from all three sites. However, site-specific analysis revealed unusually long lifespans in control females at The Jackson Laboratory, prompting reanalysis using data from the other two sites and only showed a negative effect for mitoglitazone and pioglitazone. This study underscores the importance of rigorous, multi-site testing and highlights the challenges of translating promising initial findings into consistent lifespan benefits at other doses or with alternate starting ages. These results suggest that timing and dosage are critical variables in aging intervention studies and reinforce the need for cautious interpretation of single-site or single-cohort findings.
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Journal articleNakhare S, Kelshiker MA, Young H, et al., 2026,
Targeted screening for heart failure in primary care: evidence, challenges and a pathway-first approach to implementation.
, Expert Rev Cardiovasc Ther, Vol: 24, Pages: 513-520INTRODUCTION: Heart failure remains a leading cause of morbidity and mortality, yet diagnosis continues to occur late in routine practice, frequently during emergency hospitalization. Primary care is well positioned to detect heart failure earlier, but indiscriminate screening approaches have not delivered timely diagnosis at scale. This has prompted growing interest in targeted screening strategies while raising important practical implementation challenges. AREAS COVERED: This Special Report synthesizes the evidence and operational pathways underpinning screening for heart failure in primary care. Heart failure is a heterogeneous umbrella diagnosis, with important implications for how screening pathways are designed and scaled across its subtypes. Evidence from existing screening pathways and implementation studies is considered, from established biomarkers to newer diagnostic approaches, including machine learning-enabled tools and risk prediction models. A systematic search of PubMedMEDLINE, EMBASE, and the Cochrane Library was conducted using key terms including 'heart failure,' 'screening,' 'primary care,' and 'artificial intelligence,' encompassing publications up to January 2026. EXPERT OPINION: Implementation of any innovative technology in healthcare relies on effective pathway redesign as the primary determinant of impact. Progress will depend on targeted, risk-based screening pathways evaluated through pragmatic, implementation-aware trials to determine whether screening improves outcomes, for whom, and under what conditions.
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Journal articlede Villiers C, Ormondroyd E, Thomson K, et al., 2026,
Hypertrophic cardiomyopathy caused by filamin-C variants has restrictive and extracardiac features and a distinctive ECG.
, Heart Rhythm, Vol: 23, Pages: 1289-1299BACKGROUND: Filamin-C (FLNC) gene variants are associated with cardiac and skeletal muscle diseases including a clear role of loss-of-function variants in dilated cardiomyopathy. OBJECTIVE: This study aimed to assess the contribution of rare FLNC variants to hypertrophic cardiomyopathy (HCM)/restrictive cardiomyopathy (RCM). METHODS: Family-based studies in 2 specialist services and statistical modeling of rare FLNC missense variants were conducted, using a cohort of 3289 sarcomere-negative HCM cases and 122,348 genome aggregation database controls. RESULTS: Clinical evaluation of patients with HCM/RCM and a rare FLNC variant identified a distinct electrocardiographic (ECG) repolarization phenotype in 37% (19 of 51 individuals, from 12 families), which was observed in only 1.0% of a control HCM cohort (2 of 197). FLNC variant carriers with the characteristic ECG had smaller left ventricular cavity size, lower contractility, and more severe diastolic dysfunction and were more likely to have a restrictive phenotype. Heart failure death, transplant, or cardiac arrest occurred in at least 1 individual in 7 of the 12 families (58%) in the "ECG-positive" group, and musculoskeletal abnormalities were present in 4 families (33%). 5 of 12 variants (41.7%) in the "ECG-positive" group cosegregated, and 2 were apparently de novo. 11 variants were missense, and 1 splice site. Rare FLNC missense variant burden indicated a low case excess among all HCM cases (etiologic fraction, 0.45; 95% confidence interval, 0.36-0.54), but in "ECG-positive" cases the etiologic fraction was substantially higher (0.98; 95% confidence interval, 0.97-0.99). CONCLUSION: Pathogenic FLNC variants in patients with HCM/RCM are nontruncating and cause a discrete phenotype comprising a characteristic ECG, hypertrophic and restrictive features without hypercontractility, and extracardiac abnormalities.
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Journal articleStroeks SLVM, Bart NK, Rossano J, et al., 2026,
Sex and Age Specific Genetic Risk Across the Dilated and Arrhythmogenic Cardiomyopathy Spectrum
, JACC, Vol: 87, Pages: 3573-3588, ISSN: 0735-1097 -
Journal articleChan JH, Grace C, Mazidi M, et al., 2026,
Biobank-Scale Plasma Proteomics Identifies Novel Biomarkers in Hypertrophic Cardiomyopathy.
, Circ Genom Precis Med, Vol: 19BACKGROUND: Hypertrophic cardiomyopathy (HCM) is characterized by substantial heterogeneity in both clinical phenotype and risk of adverse outcomes, including heart failure and sudden cardiac death. This highlights the need for robust biomarkers for risk stratification, and while previous studies have identified the role of select plasma proteins, comprehensive large-scale proteomic analyses have been limited in HCM. METHODS: We performed a case-control analysis of 2922 plasma proteins in 49 588 UK Biobank participants (100 HCM cases) to identify proteins associated with HCM. External replication analyses were performed in the deCODE Genetics Icelandic study (51 cases/38 904 controls) and All of Us (546 cases/41 049 controls) data sets. Associations with adverse clinical outcomes and cardiac endophenotypes of disease severity were further identified, and causal relationships were evaluated using Mendelian randomization. Relative biomarker importance was also assessed by joint modeling via machine learning. RESULTS: We identified novel associations of ANGPT2 (angiopoietin-2) and LTBP2 (latent transforming growth factor-beta binding protein 2) with HCM, with both also showing prognostic utility for heart failure-related outcomes in HCM cases. We also confirmed the associations of established biomarkers (eg, NT-proBNP [N-terminal pro-B-type natriuretic peptide], troponins I and T) with HCM cases, cardiac imaging markers of disease severity, and adverse outcomes. Mendelian randomization analyses supported a causal effect of HCM on increasing NT-proBNP and troponin T levels. CONCLUSIONS: This biobank-scale plasma proteomic study in HCM identified ANGPT2 and LTBP2 as novel HCM biomarkers with potential diagnostic and prognostic utility. These findings highlight the potential for plasma proteomics to improve risk prediction and provide insight into HCM pathobiology.
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Journal articleHe Y, Bae JSH, Nowak E, et al., 2026,
Rational discovery of therapeutic PAK1 allosteric activators
, Cell, Vol: 189, Pages: 3444-3464.e28, ISSN: 0092-8674Although kinase activators hold significant therapeutic promise, their development remains challenging and rarely achieved. Here, we report the discovery of direct small-molecule activators of p21-activated kinase-1 (PAK1), a key regulator of cardiac homeostasis, using a rational peptide-guided strategy. Targeting PAK1 autoinhibitory regulation, we identified a previously unrecognized autoinhibition-release site between the autoregulatory region and the kinase domain. Subsequent high-throughput screening and medicinal chemistry optimization yielded selective allosteric activators that enhance PAK1 activity with micromolar potency and isoform selectivity. Structural and mechanistic analyses indicate that these activators disrupt autoinhibitory regulation and promote local and global conformational transitions to the active state. Enhanced PAK1 signaling was confirmed in cardiac cells, and in vivo studies demonstrated therapeutic efficacy in both inherited and acquired cardiac hypertrophy. Collectively, these findings establish rational modulation of kinase autoinhibitory regulation as a potential strategy for the broader discovery of kinase activators, a largely unexplored area of therapeutic development.
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Journal articleTaylor DJ, Yones E, Newman T, et al., 2026,
Coronary Microvascular Resistance as a Predictor of the Placebo-Controlled Response to Percutaneous Coronary Intervention: Microvascular-Stratified Analysis of ORBITA.
, JACC Cardiovasc Interv, Vol: 19, Pages: 1259-1270BACKGROUND: The first placebo-controlled trial of percutaneous coronary intervention (PCI), ORBITA (Objective Randomised Blinded Investigation With Optimal Medical Therapy of Angioplasty in Stable Angina; NCT02062593), showed minimal symptom benefit with PCI. No placebo-controlled data describing the relationship between microvascular resistance (MVR) and PCI exist. The authors hypothesized that patients with low MVR would derive the greatest benefit from PCI. OBJECTIVES: The aims of this study were to compute MVR in patients recruited for ORBITA and to evaluate interactions with prespecified endpoints. METHODS: Hyperemic MVR was calculated using computational fluid dynamics (CFD) and compared against placebo-controlled changes in treadmill exercise time, patient-reported symptoms, physician-assessed symptoms, and dobutamine stress echocardiography scores at 6-week follow-up. RESULTS: MVRCFD was computed for 131 patients (66 undergoing PCI and 65 placebo). Median MVRCFD was 1.38 mm Hg · min/mL (Q1-Q3: 0.89-2.09 mm Hg · min/mL). Baseline exercise time correlated with MVRCFD (ordinal correlation coefficient = 0.20; 95% credible interval [CrI]: 0.18-0.22). For patients with low (20th centile) MVRCFD, PCI increased exercise time by 48 seconds vs placebo (95% CrI: 6-92 seconds; Pr = 98.5%). Exercise time did not improve for patients with high (80th centile) MVRCFD (16 seconds; 95% CrI: -29 to 61 seconds; probability of significant difference [Pr] = 75.2%), but evidence for an interaction was modest (Printeraction = 83.1%). Low MVRCFD was also associated with a placebo-controlled benefit of PCI for likelihood of complete freedom from angina (Pr = 98.8%) and improvements in angina frequency (Pr = 97.8%) and stress echocardiography scores (Pr = 99.9%). CONCLUSIONS: The placebo-controlled benefit of PCI was greater in patients with lower MVRCFD, but interactions with symptom-based endpoints were modest. For patients with severe single-vessel disease taking opti
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Journal articleSoattin L, Topal L, Tikhomirov R, et al., 2026,
Endurance exercise remodels pulmonary vein sleeve myocytes and promotes a proarrhythmic atrial substrate.
, Eur Heart JBACKGROUND AND AIMS: The risk of atrial fibrillation (AF) is higher in endurance athletes. Pulmonary vein isolation (PVI) is effective in this group, implicating pulmonary vein (PV) remodelling, but underlying mechanisms are unclear. This study investigated if endurance training remodels PV sleeves and the PV-left atrial (LA) junction to promote PV triggers and a permissive peri-antral substrate for AF. METHODS: In canine and murine endurance-running models, in vivo PV-LA mapping, ex vivo PV electrophysiology, intracellular action potential (AP) profiling with machine learning classification, histology, bulk RNA-seq, and subcellular-resolution spatial transcriptomics of PV-LA tissue were performed. These findings were incorporated into biophysically detailed computer models of human PV cardiomyocytes and a 3D human LA. RESULTS: Training produced an athlete's heart phenotype and increased AF inducibility. In vivo, trained animals showed PV-LA conduction slowing and increased rotational activity. Ex vivo, trained PVs showed enhanced β-adrenergically evoked firing, prolonged burst activity, and a higher proportion of pacemaker-like APs. Spatial transcriptomics revealed discrete PV myocyte subpopulations with training upregulated Hcn4, Cacna1d, and Cacna1g (enhancing automaticity), downregulated Scn5a and Gja1 (slowing conduction), and enriched profibrotic/inflammatory signalling (Tnfα, Il6) alongside fibroblast expansion and extracellular matrix deposition. In silico, these changes reproduced faster spontaneous PV firing and sustained re-entry. CONCLUSIONS: Endurance training drives coupled electrical, structural, and inflammatory PV-LA remodelling that provides both trigger and substrate for AF. These data support why PV-targeted strategies can be effective in athletic AF and nominate modifiable pathways including HCN4-linked automaticity and TNFα-associated signalling.
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Journal articleOwais A, Chen H, Farooq H, et al., 2026,
Gene-gene interactions between a LMNA variant and common polymorphisms drive early-onset atrial fibrillation.
, Nat Commun, Vol: 17Atrial fibrillation (AF), the most common sustained arrhythmia, has a complex genetic basis; however, the molecular mechanisms linking rare and common variants remain poorly understood. Polygenic risk score (PRS) analysis in the UK Biobank and All of Us cohorts reveals that carriers of protein-altering LMNA variants (PAVs) have a significantly higher risk of incident AF than predicted by PRS alone, supporting an additive effect of common polymorphisms and LMNA variants. Induced pluripotent stem cell derived atrial cardiomyocytes (iPSC-aCMs) from individuals carrying the pathogenic missense variant p.S143P in LMNA exhibit widespread disruption of chromatin architecture and perturbation of atrial gene regulatory networks, particularly at loci harboring AF-associated variants and transcription factors essential for atrial rhythm control and contractility. Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-based epigenetic editing validates the function of several AF-associated regulatory elements and their downstream targets. Notably, reduced accessibility at an intronic SCN10A enhancer harboring the AF-associated SNP rs6801957 is associated with reduced sodium current in p.S143P iPSC-aCMs. These findings are reproduced in iPSC-aCMs derived from an additional individual carrying a distinct pathogenic LMNA variant, supporting a broader mechanism in which rare LMNA variants and common polymorphisms converge on shared regulatory networks to influence AF susceptibility and highlighting the value of integrating both in arrhythmia risk assessment.
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Journal articlePaul S, Munoz C, Ferreira P, et al., 2026,
Motion compensated spin echo cardiac diffusion tensor imaging in multiple cardiac phases using an ultrahigh gradient strength scanner
, Journal of Cardiovascular Magnetic Resonance, Vol: 28, ISSN: 1097-6647BackgroundCardiac diffusion tensor imaging (cDTI) has traditionally relied on inefficient stimulated echo techniques to robustly assess microstructural changes over the cardiac cycle. Ultrahigh gradient strength systems (>80mT/m) allow shorter motion compensated diffusion encoding. This study compares the ability of high and ultrahigh strength gradient systems to provide systolic and diastolic motion compensated spin echo (MCSE) cDTI.MethodsSecond order MCSE sequences were developed for a research-only Siemens 3T Connectom (300mT/m maximum gradient amplitude per axis) and breath hold cDTI was acquired at peak systole and end diastole. Acquisitions used the maximum achievable gradient strength (GUH, 116mT/m) and also limited to typical high gradient strengths (GH, 66mT/m based on 80mT/m maximum allowable), giving TE=48ms and 58ms respectively. Data were acquired at 2.8x2.8x8mm3, b=500s/mm2 (8 averages) and b=150s/mm2 (2 averages) in 6 encoding directions.Results22 healthy subjects were recruited. 20/21 and 21/22 systolic acquisitions at GUH and GH respectively met the >50% criteria of the circumferential myocardium showing the expected transmural variation in helix angle. For GUH and GH (16/20) 80% and (16/22) 73% of diastolic acquisitions were successful respectively. SNR was increased using GUH compared to GH (median [IQR]: 112.9 [3.8] vs. 9.6 [2.9], p=0.0002 diastole, 15.6 [5.9] vs. 12.5 [6.7], p=0.006 systole). Using GUH fractional anisotropy was lower in systole (0.349 [0.040] vs. 0.373 [0.019], p=0.002) and GUH transmural helix angle gradient (HAG) was steeper in diastole (-0.70 [0.17] vs. -0.55 [0.12] ˚/%, p=0.04). At both GUH and GH, sheetlet angle (|E2A|) was higher in systole than in diastole (30.7 [7.3] vs. 21.3 [6.7]˚ p=10-4 and 32.6 [10.9] vs. 26.0 [7.4]˚, p=0.03 respectively). Differences in HAG between phases were only apparent with GH (-0.88 [0.23] vs. -0.55 [0.15], p=10-4) and differences in the mean diffusivity only with GUH (1.64 [0.11] vs
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Journal articleNg FS, Khattak GR, Patlatzoglou K, 2026,
Artificial intelligence-enhanced electrocardiograms: building on solid foundations.
, Eur Heart J, Vol: 47, Pages: 2187-2189 -
Journal articlePrzybylski R, Norrish G, Claggett B, et al., 2026,
The Natural History of Massive Left Ventricular Hypertrophy in Pediatric Hypertrophic Cardiomyopathy: A Multiregistry Analysis.
, Circulation, Vol: 153, Pages: 1463-1476BACKGROUND: Massive left ventricular hypertrophy (LVH) is a risk factor for sudden cardiac death in children with hypertrophic cardiomyopathy (HCM), but little is understood about its natural history. METHODS: Patients with pediatric-onset HCM identified from 2 registries (SHaRe [Sarcomeric Human Cardiomyopathy Registry] and IPHCC [International Paediatric Hypertrophic Cardiomyopathy Consortium]) with or without massive LVH were compared. Massive LVH was defined as absolute maximal left ventricular wall thickness (MLVWT) ≥30 mm or MLVWT z score ≥+20 at <18 years of age. Data from SHaRe and IPHCC include encounters from January 1960 through March 2024 and January 1970 through March 2024, respectively. Demographic, clinical, and serial MLVWT data were collected. Composite outcomes included major ventricular arrhythmia event (sudden cardiac death, aborted sudden cardiac death, or appropriate implantable cardioverter defibrillator therapy); heart failure (HF) event (left ventricular ejection fraction <50%, New York Heart Association class III or IV, transplant, or HF-related death); major adverse cardiac event (stroke or any major ventricular arrhythmia or HF outcome aside from left ventricular ejection fraction <50%); and HCM-related mortality (sudden cardiac death or HF-related death). Time-to-event analyses were performed using Cox proportional hazards models. RESULTS: We identified 587 patients (54 female [30%]). In 186 children with massive LVH, age at diagnosis was younger (median, 9.2 years [interquartile range, 2.1-13.1 years]) versus 13.6 years (9.7-15.5 years; P<0.001) and sarcomeric genetic variants more prevalent (72% versus 61%; P=0.034), as was HCM-related mortality (unadjusted hazard ratio, 3.3 [95% CI,1.2-9.7]; P=0.026), major adverse cardiac events (hazard ratio, 2.6 [1.7-3.9]; P<0.001), major ventricular arrhythmia (hazard ratio, 3.1 [1.8-5.2]; P<0.001), and HF (hazard ratio, 1.9 [1.1-3.1]; P=0.013). These associations remained
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Journal articleBenfield N, Thami PK, Ware J, et al., 2026,
GWAS reveals common SLX4 variants associated with telomere length and hypertension in individuals of African ancestry.
, Genes Genomics, Vol: 48, Pages: 673-682BACKGROUND: Cardiovascular disease (CVD) and its risk factors are highly prevalent in the UK, with incidence differing by ethnicity. Black individuals have an increased prevalence of heart failure, stroke and hypertension compared to White individuals. Telomere length has been associated with many age-related conditions, with shorter telomeres associated with increased CVD risk. However, Black individuals have longer telomeres on average compared to White individuals, which should be protective against CVDs. The increased incidence of CVD in this population indicates a paradoxical association. OBJECTIVES: To investigate the relationship between telomere length and cardiovascular disease risk across ethnic groups and to identify genetic variants that may explain observed differences. METHODS: Using the UK Biobank cohort, we assessed telomere length in Black and White populations and performed GWAS analysis to identify ethnicity-specific variants associated with telomere length. RESULTS: We report that Black individuals had significantly longer telomeres than White individuals (0.9035 vs 0.8301, p < 0.0001). Contrary to published reports, Black individuals showed lower incidence of most CVD subtypes compared to White individuals. However, hypertension was more prevalent in Black individuals despite longer telomeres. GWAS analysis identified 12 ethnicity-specific variants at genome-wide significance associated with longer telomeres in Black populations. Notably, 3 variants in SLX4 were significantly more common in Black individuals and associated with both longer telomere length and hypertension risk. High BMI and lower household income were found to influence hypertension risk, overriding the protective effect of longer telomeres in Black populations. CONCLUSIONS: The increased rate of hypertension in Black populations, as well as longer telomere length, may be influenced by common genetic variants. The protective effect of longer telomeres against CV
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Journal articleNaidoo P, Fernandes P, Dadashi Serej N, et al., 2026,
Robust fine-grained echocardiographic view classification with supervised contrastive learning.
, Med Image Anal, Vol: 110Accurate classification of echocardiographic views is fundamental for automated cardiac analysis. However, clinical practice relies on a large, heterogeneous set of fine-grained acquisitions that introduce substantial inter-observer variability. Existing studies have primarily focused on limited view sets, often collapsing specialised views into broad categories, which limits their clinical relevance. We address this limitation by introducing TTE47, the first publicly available benchmark comprising 47 clinically meaningful views annotated independently by three experts. This dataset enables the rigorous quantification of inter-observer agreement and establishes a foundation for reproducible, clinically relevant evaluation. To tackle the dual challenges of subtle inter-class distinctions and structured label variability, we propose a novel supervised contrastive learning framework incorporating a tailored loss function. Our method outperforms cross-entropy and standard supervised contrastive baselines, achieving leading performance among evaluated methods on TTE47 and surpassing prior work on TMED-2 without dataset-specific pretraining, using a model pretrained on TTE47. Beyond accuracy, we introduce clustering-based metrics, Detection Rate and Label Recovery Precision, that measure semantic coherence and the model's ability to resist annotation variability. Results show that the learned feature space aligns more strongly with underlying anatomical structure than with any single annotator's style, enabling resilience to label shifts and maintaining robustness comparable to human-level disagreement. By integrating multi-expert evaluation, robust representation learning, and interpretable feature-space analysis, this work establishes a scalable and clinically relevant framework for fine-grained echo view classification. Our findings highlight the potential of contrastive pretraining to standardise interpretation, mitigate subjectivity, and enhance the reliability of AI
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Journal articlePreston AJ, Blackman J, Krahn AD, et al., 2026,
Pace and Ablate or Pace Then Ablate: Defining the Risk of Concomitant AV Node Ablation and Pacemaker Implantation Using a Probability Based Approach.
, Circ Arrhythm Electrophysiol, Vol: 19 -
Journal articleWaks JW, Poulin M-F, Tung P, et al., 2026,
Peak QRS/T ratio and the spatial ventricular gradient differentiate acute vs chronic left bundle branch block after transcatheter aortic valve replacement.
, Heart Rhythm O2, Vol: 7, Pages: 928-937BACKGROUND: Differentiating chronic from acute left bundle branch block (LBBB) is useful in various cardiac disorders. Peak QRS/T ratio, a measure of cardiac memory, can differentiate chronic from acute LBBB with high sensitivity and specificity, but its utility in post-transcatheter aortic valve replacement (TAVR) patients with LBBB is unclear. OBJECTIVE: This study aimed to validate the QRS/T ratio for differentiating chronic/acute LBBB in post-TAVR patients and assess whether the spatial ventricular gradient (SVG), which integrates 3-dimensional depolarization/repolarization throughout the cardiac cycle, could also distinguish chronic from acute LBBB. METHODS: This was a post hoc analysis of a prospective, observational, single-center TAVR study. After TAVR, patients were classified as acute (new <24 hours) or chronic/preexisting LBBB. Electrocardiograms were transformed into vectorcardiograms, and peak QRS/T ratio and SVG were calculated. Sensitivity, specificity, and area under the receiver-operating curve (AUROC) assessed how QRS/T ratio and SVG differentiated chronic from acute LBBB. RESULTS: Of 409 patients, 21 had preexisting, and 53 had acute/new LBBB. Patients with chronic LBBB had a higher peak QRS/T ratio than patients with acute LBBB (median 3.8 vs 2.2; P < .0001). 3-dimensional SVG vectors significantly differed between chronic and acute LBBB (joint P < .0001), due to differences in the anterior/posterior (Z) direction, (SVGz): median 43.4 vs -14.2 mV·ms, P < .0001, for chronic vs acute LBBB, respectively. A peak QRS/T ratio of ≥2.7 and an SVGz of ≥15 mV·ms had 100% sensitivity, 98.1% specificity, and an AUROC of 0.991 for chronic LBBB. Over long-term follow-up, patients transitioned from acute to chronic LBBB vectorcardiographic phenotype. CONCLUSION: Peak QRS/T ratio and SVG differentiate chronic from acute LBBB in post-TAVR patients with 100% sensitivity, 98% specificity, and an AUROC of 0.99.
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Journal articleHabibi H, Dimopoulos K, Constantine A, et al., 2026,
Listening to learn: translating qualitative insights from adults with congenital heart disease and heart failure into patient-centered care.
, Eur Heart J Qual Care Clin Outcomes, Vol: 12, Pages: 336-341AIMS: Adults with congenital heart disease and heart failure (HF) face lifelong, complex challenges. Despite improved survival, current care models often overlook their emotional, social, and long-term planning needs. Existing health-related quality of life (HRQoL) tools frequently miss key domains relevant to adult congenital heart disease (ACHD) patients, such as psychological fatigue, family dependence, and unmet support needs. Standard metrics like NYHA class and LVEF offer limited insight into their lived psychosocial burden. To explore the lived experiences of ACHD patients with HF (ACHD-HF) and identify domains to inform development of patient-centered HRQoL tools and improvements in shared decision-making and care delivery. METHODS AND RESULTS: Three focus groups (n = 22) and cognitive interviews (n = 12) were conducted with ACHD-HF patients at a UK specialist center. Data were analysed using template analysis, guided by predefined domains (physical, psychological, social, and long-term planning) and emergent themes. Five themes reflected unmet psychosocial and care needs: (i) mental exhaustion and cognitive fatigue, (ii) feeling misunderstood and emotionally invisible, (iii) the burden of lifelong family dependence, (iv) challenges with relationships, intimacy, and identity, and (v) uncertainty around end-of-life planning. Participants voiced the need for more meaningful communication, integrated psychological support, and structured opportunities to engage in care decisions. CONCLUSION: Patient narratives provide critical insight into care quality. Incorporating underrepresented psychosocial domains into HRQoL assessment and service planning can promote more responsive, equitable, and emotionally informed ACHD-HF care.
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Journal articleKoeckerling D, Reddy RK, Howard JP, et al., 2026,
Long-Term Mortality After PCI or CABG for Left Main Stem Disease: Updated Meta-Analysis of Randomized Trials Using Reconstructed Individual-Participant Survival Data.
, J Am Coll Cardiol, Vol: 87, Pages: 2180-2183
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