Heart Rhythm

Background Accurate assessment of the QT interval is challenging in the presence of QRS prolongation, such as during ventricular pacing or bundle branch block. Current correction methods are heterogeneous and lack consensus. To evaluate the relationship between QRS duration and QT interval during ventricular pacing and to develop a practical correction method for QT assessment. Methods In this prospective single-centre study, 94 patients undergoing electrophysiology study for supraventricular tachycardia were included. Standardised pacing was performed at the same cycle length from the right ventricular (RV) apex, high output and low output pacing from His catheter, and coronary sinus (reference). QRS and QT intervals were measured from 12-lead ECGs. Changes in QT (QT) and QRS duration (QRS) were analysed using linear regression and mixed-effects modelling. QT correction formulas of the form QT corrected = QT N x QRS were evaluated using Bland-Altman analysis across multiple coefficients. Results A significant positive correlation between QRS and QT was observed across all pacing sites (r = 0.52-0.74, p < 0.001). In mixed-effects modelling, QRS was a strong independent predictor of QT (0.59, p < 0.001), with no significant interaction between pacing site and QRS, supporting a consistent relationship across pacing locations. Bland-Altman analysis demonstrated that correction coefficients of 0.65-0.70 minimised systematic bias compared with lower coefficients, with similar precision across models (SD 16 ms) and no evidence of proportional bias. A coefficient of 0.65 provided the most balanced performance between bias and variability. Conclusion QT prolongation during ventricular pacing is primarily driven by QRS widening and follows a consistent linear relationship across pacing sites. A simple correction using QT corrected = QT 0.65 x (QRS 100 ms) provides a practical and accurate method for QT assessment, with potential clinical applicability in patients with conduction abnormalities or ventricular pacing.

Background Substrate mapping using multielectrode catheters is increasingly used for post-myocardial infarction (MI) ventricular tachycardia (VT) avoiding repeated VT induction and mapping during VT. However, these catheters may mechanically induce ventricular arrhythmias with hemodynamic compromise. This study compares pro-arrhythmogenicity between single-tip and multi-spline catheters during functional substrate mapping. Methods Thirty post-MI patients (age 68{+/-}8 years, 97% male, LVEF 40% [IQR 33-46]) referred for VT ablation at two centers (2021-2024) underwent endocardial mapping during baseline rhythm in random order with both a multi-spline catheter (Octaray, n=4; Pentaray, n=26) and a single-tip QDOT catheter. The protocol was prematurely terminated if (i) two mechanically induced VTs required ECV, (ii) recurrent ATP-treated mechanical VTs caused hemodynamic compromise, or (iii) excessive mechanically induced ectopy impaired catheter contact. Mapping time, point density, and mechanically induced arrhythmias were assessed. Results Multi-spline catheters enabled faster mapping (26{+/-}9 vs 60{+/-}16 minutes, p<0.001) with more acquired points (p<0.001). VTs were more frequently mechanically induced with multi-spline catheters (median 2 [IQR 1-4] vs 0 [0-3], p<0.05) and these VTs were faster (304ms, IQR 292-320] vs 373ms, IQR [316-405], p=0.01) and degenerated more often into VF (3 vs. 0). Overall, 17 patients (57%) experienced at least one mechanically induced VT; seven (23%) required cardioversion, and mapping was prematurely terminated in eight (27%), all while using multi-spline catheters. Conclusion Multi-spline catheters allow rapid substrate mapping but with substantial risk of mechanically induced arrhythmias, requiring premature termination of substrate mapping because of safety concerns. Their use in post-MI VT ablation warrants careful risk?benefit assessment.

Background. Durable mitral isthmus (MI) block remains challenging in persistent atrial fibrillation (PeAF) ablation. Recent epicardial vein of Marshall (VoM) recordings have shown incomplete MI transmurality and time-dependent conduction recovery after pulsed field ablation (PFA). Whether systematic VoM ethanol infusion (VoM-EI) followed by focal PFA provides stable acute MI block remains unknown. **Objectives.** To assess the incidence, timing, and procedural implications of early MI conduction recovery after systematic VoM-EI followed by focal Sphere-9 PFA. Methods.In this prospective single-center study, 55 consecutive patients undergoing first ablation for symptomatic PeAF with planned MI ablation were screened. VoM-EI was systematically attempted before left atrial access and successfully performed in 51 (92.7%), who constituted the study cohort. Pulmonary vein isolation, roof-line, and MI ablation were performed with the Sphere-9? lattice-tip catheter. After bidirectional MI block, conduction was systematically reassessed during a standardized 30-minute waiting period. Results.Mean age was 70.3 {+/-} 8.2 years, and 36 patients (70.6%) were men. Initial bidirectional MI block was achieved in 50/51 patients (98.0%). During the waiting period, conduction recovered in 9/50 (18.0%; 95% CI, 9.8%-30.8%), at a median of 16 minutes (IQR, 10-20; range, 8?23). Six of 9 patients with recovery (66.7%) required targeted coronary sinus (CS) ablation. Block was restored in all 9, yielding a final block rate of 50/51 (98.0%). Median procedure duration was 82 minutes (IQR, 73-95), with no major complications. Conclusions. Immediate bidirectional MI block was not synonymous with stable block. Despite systematic VoM-EI followed by focal Sphere-9 PFA, conduction recovered in approximately one in five patients, including beyond 20 minutes, and two thirds required targeted CS ablation. These findings support standardized 30-minute reassessment and targeted CS interrogation rather than reliance on immediate block. Chronic invasive remapping is required to determine whether this strategy improves long-term MI block durability.

Background: Vagally mediated syncope and functional bradyarrhythmias can cause recurrent symptoms, injury and a need for permanent pacing, yet standard therapies do not address the underlying autonomic reflex. Cardioneuroablation (CNA) targets this mechanism, but adoption has been limited by uncertainty about patient selection, procedural endpoints and durable outcomes. Methods: We studied 95 consecutive patients with vagally mediated syncope (n=78) or functional bradyarrhythmia (n=17) who underwent CNA at a single center by a single lead operator under a uniform, prospectively maintained protocol. Extracardiac vagal stimulation (ECVS) was performed before and after ablation to confirm vagally mediated sinus or atrioventricular (AV) nodal responses and to verify their attenuation. Outcomes through 1 year included clinical recurrence, quality of life, pacing burden and pacemaker extraction. Results: Before ablation, ECVS provoked sinus pauses in 95.8% of patients and AV block in 91.6%; after ablation, sinus pauses were abolished in every patient and residual AV block was present in 4.2%. One-year freedom from recurrent syncope and from bradyarrhythmia-related events was 93.8% and 94.1%. Syncope burden fell from a median of 2.7 episodes per year to none, and disease-specific quality of life improved substantially (P<0.001). Among patients with pre-existing devices, atrial pacing burden fell from a median of 22% to 0%. There were no strokes, deaths or myocardial infarctions. Conclusions: In this single-center cohort, physiology-guided CNA was associated with durable symptom control, improved quality of life and reduced pacing across vagally mediated bradyarrhythmia syndromes. Multicenter controlled studies are needed to confirm these findings.

Background: Short and long sleep duration have been linked to atrial fibrillation (AF), but their influence on arrhythmia recurrence after catheter ablation is uncertain. We evaluated the association between nocturnal sleep duration and the risk of recurrent arrhythmias in patients undergoing catheter ablation for AF in the PREDIMAR trial. Methods: The PREDIMAR study is a multicentre, randomized, controlled, single-blind trial evaluating a Mediterranean diet enriched with extra-virgin olive oil for preventing arrhythmia recurrence after catheter ablation for AF. Nocturnal sleep duration was categorized as adequate (6?8 h/day) or inadequate (<6 h/day or >8 h/day). Multivariable Cox regression models estimated the association between sleep duration and the risk of recurrent atrial flutter (AFL) or AF. Results: Among 720 participants, we observed 226 incident cases of AF relapse and 107 cases of AFL. Inadequate nocturnal sleep duration was associated with a significantly higher risk of AFL recurrence compared with adequate sleep (adjusted HR = 1.87; 95% CI 1.18?2.96). No significant association was observed for AF recurrence (HR = 0.99; 95% CI 0.70?1.41). The association with AFL recurrence was particularly evident in patients with persistent AF at baseline before ablation (adjusted HR = 3.42; 95% CI 1.47?7.97), whereas no significant relationship was observed in those with baseline paroxysmal AF. Conclusions: Inadequate nocturnal sleep duration (<6 h/day or >8 h/day) may increase the risk of AFL recurrence following AF ablation. These findings highlight the relevance of sleep habits as a modifiable behavioural factor potentially influencing post-ablation outcomes.

Background: Pulsed-field ablation (PFA) systems increasingly provide impedance-based contact indicators, such as tissue proximity indication (TPI), derived from local impedance changes relative to a blood-pool baseline. These indicators are largely binary and do not quantify post-application catheter?tissue energy coupling. We evaluated Bipolar Local Impedance Delta (BiLID), the peri-application bipolar local impedance drop, as a complementary impedance-based index of delivered energy coupling. Methods: We retrospectively analyzed 1,556 VARIPULSE applications in 23 patients undergoing pulmonary vein isolation. BiLID was derived from 29,822 paired pre-/post-ablation impedance measurements obtained from numeric local impedance readouts displayed by the mapping system, without proprietary data export or waveform estimation. Reproducibility was assessed by intraclass correlation. Associations with TPI status, vein anatomy, application order, and peak creatine kinase-MB (CK-MB) were examined using linear mixed-effects models with within-patient clustering and exploratory patient-level analyses. Results: BiLID showed excellent interobserver reproducibility and increased stepwise with the number of TPI-positive electrodes per pair (0?2; P < 0.0001), while varying widely among TPI-positive signals. BiLID differed by electrode position and was lower during right than left pulmonary vein ablation (both P < 0.0001). Total BiLID correlated with peak CK-MB (r = 0.71; 95% CI, 0.42?0.87; P = 0.0001), whereas application count (r = 0.16, P = 0.4711) and TPI-positive signals (r = 0.26, P = 0.2334) did not. Lower CK-MB elevation was associated with larger left atrial volume index, female sex, and heart failure, suggesting substrate-modulated biomarker release. Conclusions: BiLID is a reproducible, continuous index of catheter?tissue energy coupling that complements pre-delivery binary contact indicators by quantifying the response after PFA delivery. It captures graded contact quality and anatomical heterogeneity and may inform individualized, coupling-guided PFA titration.

Background: Iatrogenic atrial septal defect (iASD) is a known consequence of transseptal catheterization. Left atrial intracardiac echocardiography (LA ICE) requires additional septal instrumentation, yet data on persistent iASD after pulsed field ablation (PFA) with an LA ICE workflow remain limited. We evaluated the incidence, predictors, and one-year clinical significance of persistent iASD in this setting. Methods: Consecutive patients undergoing PFA for atrial fibrillation with LA ICE were prospectively evaluated with transthoracic echocardiography before ablation and at one year, including systematic agitated saline contrast. Persistent iASD was defined as residual interatrial shunting on color Doppler at follow-up, classified as small (<3 mm), moderate (3-5 mm), or large (>5 mm). Groups were compared by t-test and chi-square test. Results: Among 850 patients, persistent iASD was identified in 153 (18.0%) at one year; 97 (63.4%) were small and 56 (36.6%) moderate, with no large defects. All shunts were left-to-right. No stroke or transient ischemic attack, paradoxical embolism, hypoxemia, right-heart enlargement, or septal closure occurred. Persistent iASD was associated with female sex (64.7% vs 48.1%), longer septal dwell time (52{+/-}12 vs 31{+/-}11 min), higher left atrial pressure (28{+/-}4 vs 12{+/-}3 mmHg), lower LVEF (32{+/-}11% vs 54{+/-}14%), and larger-caliber sheaths ([&ge;]17 Fr; 80.4% vs 48.2%; all p<0.001). Conclusions: Persistent iASD following PFA with LA ICE occurs in approximately one in five patients but is predominantly small, exclusively left-to-right, and clinically benign at one year. Persistence is associated with mechanical and hemodynamic factors, particularly sheath caliber, rather than the ablation energy source.

BackgroundEmerging evidence in humans has linked Xp22.31 genetic deletions to an increased risk of stress-induced arrhythmias, and association analysis across Xp22.31 has shown enrichment for atrial fibrillation genetic risk variants around STS (steroid sulfatase). MethodsWe compared heart rhythm in homozygous STS-knockout (STS-KO) adult mice (n=19) to wildtype (WT) mice (n=11) under baseline (Tyrodes solution), and {beta}-adrenergic stimulation (stress), conditions using ex vivo perfused-heart electrocardiography (ECG). Ventricular ectopic beats (VEBs) were manually-identified, and rhythm abnormalities were quantified using a semi-automated approach. ResultsAt baseline, the groups displayed comparable sinus cycle length and ECG intervals; all WT hearts showed stable sinus rhythm, whereas [~]30% of STS-KO hearts developed spontaneous VEBs. WT hearts typically maintained steady rhythm under {beta}-adrenergic stimulation; in contrast, [~]60% of STS-KO hearts displayed VEBs. Under baseline and stimulated conditions the QRS interval was greater during VEBs than normal beats in STS-KO hearts, consistent with a ventricular origin. We identified a higher frequency of any abnormal beats in STS-KO hearts than in WT hearts under baseline (1.9{+/-}0.7% vs. 0.3{+/-}0.1%, p=0.038) and stimulated (5.3{+/-}2.2% vs. 0.5{+/-}0.3%, p=0.047) conditions. Under stimulated conditions, abnormal beats only occurred singly in WT hearts, whereas in STS-KO hearts, [~]50% of the time they occurred in runs of two or more. ConclusionSTS deficiency in mice predisposes to arrhythmias, and the STS-KO mouse represents a tractable model for mechanistic investigation. These data support the contention that STS activity influences arrhythmic vulnerability in humans and that STS should be considered for inclusion in arrhythmia-related gene panels.

Introduction. Hypertrophic cardiomyopathy (HCM) is characterized by clinical and genetic heterogeneity. Age of manifestation, clinical and anatomical phenotypes of HCM vary significantly. This study discusses genetic causes and reconstructive surgery results for patients with particular intracardiac phenotype - diffused generalized HCM (DG-HCM). Methods: personal and familial medical history, general examination, 12-lead resting ECG, 24-hour ECG Holter monitoring, transthoracic and transesophageal EchoCG, cardiac MRI with gadolinium enhancement. A ten-gene panel was sequenced by IonTorrent PGM. Mutational screening in patients with suspected multisystemic diseases was performed by Sanger sequencing. Results: 170 patients with obstructive HCM (oHCM) requesting genetic counseling and surgical correction of HCM were evaluated. We distinguished particular DG-HCM subtype of oHCM (diffuse hypertrophy of IVS, LV free walls, papillary muscles displaced towards the LV apex) in 34 patients; 31 out of 34 underwent open heart reconstructive surgery. Patients with DG-HCM were younger at the time of surgery, had higher risk of SCD, and connective tissue dysplasia of the mitral valve. Hemodynamics normalization was observed in 1, 3, and 5 years after surgery. Eighteen ICDs were implanted; five patients experienced appropriate shocks. The genetic spectrum was enriched up to 30% by multisystem disorders. Mutations in "sarcomeric" genes were detected in 15%. Conclusion: Intracardiac phenotype of HCM may correlate with genetic cause and long-term prognosis. DG-HCM phenotype accounts for 20% oHCM patients and indications for open-heart surgery. Extended myectomy with parietal resection of papillary muscles and correction of mitral valve insufficiency provides long-term benefits for DG-HCM patients. Multisystem disorders in patients with DG-HCM should be of special attention. Study was supported by research project FURG-2024-0004.

Background and Aims: Machine learning has shown potential in predicting ablation targets for ventricular tachycardia (VT) in an animal model. This study progresses to externally validating deep learning approaches for human data. Methods: The development and external validation dataset included 21 and 13 patients, respectively, with structural VT undergoing catheter ablation. In the development datasets, electrophysiological studies were conducted using the AdvisorTM HD grid (EnsiteTM X), while both CARTO and Ensite Precision were used in the validation dataset. In each patient, VT ablation targets were defined as mapping points within 8 mm of VT isthmuses. Three advanced machine learning models were trained using cardiac mapping data acquired in both omnipolar and unipolar configurations during sinus rhythm and ventricular pacing. Discrimination was evaluated using nested leave-one-out cross-validation at patient level. Results: Overall, graph convolutional networks (GCNs), which integrate intracardiac signal waveforms with three-dimensional electroanatomical geometries, achieved the highest performance, with optimal results obtained from unipolar electrograms acquired in sinus rhythm (median AUC 0.793, sensitivity 83.6%, specificity 69.0%). This may be partly explained by the inclusion of repolarization dynamics in unipolar electrograms and the higher point density of sinus rhythm maps. Comparable performance was observed in the external dataset. Conclusion: This study demonstrates that graph convolutional networks applied to sinus rhythm EGM waveforms collected during substrate mapping can localise critical components of VT re-entry circuits. This approach has potential to provide fast and accurate ablation guidance without the need to induce and map VT, improving safety and efficacy of VT catheter ablation.

Background: Three pulsed-field ablation (PFA) systems are FDA-approved for atrial fibrillation (AF), yet whether their safety profiles differ from each other and from radiofrequency (RF) ablation has not been systematically characterized using real-world adverse event data. We compared platform-specific complication profiles across three FDA-approved PFA systems and contemporary RF catheters in MAUDE. Methods: We analyzed 2,262 manually adjudicated MAUDE adverse event reports (760 PFA, 1,502 RF) through July 2025. Neurologic events underwent independent adjudication into five tiers by three auditors. Disproportionality was assessed using Reporting Odds Ratios (ROR) with Benjamini-Hochberg (BH) correction. Results: Pooled PFA had significantly lower BH-adjusted ROR for tamponade (0.52, 95% CI 0.41-0.67) and esophageal injury (0.09, 0.01-0.66), consistent with a tissue-selective reporting profile across platforms. Platform-level analysis, however, revealed substantial heterogeneity: the stroke signal was driven by Varipulse (ROR 16.41, 8.61-31.28) and was not observed with Farapulse (ROR 1.26, NS). Pooled PFA had higher ROR for imaging-confirmed stroke (3.84, 2.27-6.49) and arrhythmia (2.57, 1.91-3.45). Coronary vasospasm (24 vs. 0 events) and hemolysis (15 vs. 1 events) were PFA-specific. Composite serious adverse events were similar. In a pre-specified extension period analysis (August-December 2025), the pooled PFA stroke signal attenuated to non-significance (ROR 1.60, 0.89-2.85), consistent with notoriety bias following the FDA Safety Communication. Conclusions: PFA adverse-event reporting shows substantial platform heterogeneity across approved systems. Varipulse was associated with a disproportionate neurologic reporting signal, while all PFA platforms show tissue-selective reporting patterns relative to RF. These findings support platform-aware clinical decision-making and post-market surveillance.

Background: Characterizing cardiac activation by its site of origin, propagation, and conduction velocity underlies arrhythmia diagnosis and management, but invasive electrophysiology (EP) mapping requires vascular access, fluoroscopy, and sedation. Magnetocardiography (MCG) enables contactless mapping, and recent solid-state sensors remove the cost, cryogenic, and shielding barriers of legacy systems. We assessed the feasibility of a novel solid-state MCG system for noninvasive arrhythmia site-of-origin (SOO) localization and activation reconstruction, benchmarked against electrocardiographic imaging (ECGi). Methods: In nine swine implanted with right atrial and right ventricular pacing leads, we recorded MCG and ECGi simultaneously during atrial and ventricular pacing. Invasive epicardial contact EP mapping provided the activation-time reference and MRI-derived lead-tip location the SOO reference. Local activation time (LAT), conduction velocity (CV), and SOO were compared on a co-registered chamber mesh. SOO error was the Euclidean distance to the MRI lead tip; LAT and CV agreement with EP were quantified by Pearson r and compared using Wilcoxon signed-rank tests. Results: Across 17 datasets (8 atrial, 9 ventricular), median SOO error was lower for MCG than ECGi in the atrium (19.6 vs 31.2 mm; p=0.023) and ventricle (12.0 vs 26.1 mm; p=0.074). LAT agreement with EP was comparable between modalities and higher in the ventricle (MCG r=0.63; ECGi r=0.68) compared with the atrium (MCG r=0.40; ECGi r=0.53), each correlating with invasive EP mapping above chance. CV agreement was modest and numerically higher for MCG in the ventricle. Conclusions: Solid-state MCG was feasible for noninvasive site-of-origin localization and activation mapping, with accuracy comparable to ECGi, motivating larger prospective studies to define its clinical role in noninvasive mapping.

Background: Digoxin use after the Norwood procedure has been associated with improved interstage survival in hypoplastic left heart syndrome and related conditions. Whether this benefit translates into improved longer-term outcomes through staged palliation remains unknown. We aimed to determine the association of digoxin use at Norwood discharge with transplant-free survival and Fontan completion. Methods: We conducted a retrospective cohort study using the Pediatric Heart Network (PHN) Single Ventricle Reconstruction trial public dataset, including 549 infants enrolled at 15 North American centers between 2005 and 2008. Competing risk analysis was used to evaluate Fontan completion and Cox regression to assess death or transplantation within 6 years after the Norwood procedure. Mixed-effects models compared pre-Fontan hemodynamic and echocardiographic right ventricular indices between patients treated with and without digoxin after accounting for center clustering and adjustment for sex, shunt type, heart failure medications at Norwood discharge, and census block poverty level. Results: The 6-year cumulative incidence of Fontan completion was higher among patients discharged on digoxin than among those not receiving digoxin (82% vs 71%; p = 0.013). Competing-risk analysis accounting for death and transplant demonstrated a greater likelihood of Fontan completion among digoxin users (aHR 1.31; 95%CI 1.09-1.58; p = 0.005), without significant difference in the hazard of death or transplant (aHR 0.78; 95%CI 0.53-1.15; p = 0.208). No significant differences in pre-Fontan hemodynamic or echocardiographic indices were observed between groups. Initiation of digoxin post Stage II procedure was not associated with improved survival or likelihood to complete Fontan. Conclusion: Digoxin use at the time of Norwood discharge was associated with a 30% greater likelihood of Fontan completion by 6 years, without accompanying improvement in transplant-free survival. These findings extend prior observations of improved interstage outcomes associated with digoxin use and suggest that treatment may facilitate progression through staged palliation.

Genetic testing for cardiomyopathy and arrhythmia (CM/ARRH) provides diagnostic information and informs screening for at-risk relatives. Clinical guidelines recommend genetic testing for these conditions; however, data on how genetic test results influence clinical management recommendations are limited. Here, we determined the frequency of cardiologist-recommended management changes for patients following CM/ARRH genetic testing. This was a retrospective cross-sectional study of patients referred for multigene panel testing between April 2016 and April 2024. Genetically-experienced cardiologists at multicenter academic clinical practices were recruited for participation to complete surveys indicating clinical decision making on patients who had genetic testing. Cases for review were randomly selected to have both positive and non-positive results. Among 249 patients (138 positive, 111 non-positive), 136 (54.6%) received clinical management recommendations for their own or their at-risk relatives? care. Of these, 75 (55.1%) received recommendations for the patient?s own care, most frequently additional diagnostic tests/procedures (n=33). Compared to non-positive results, patients with positive results were more likely to receive recommendations for their own management (66/138, 47.8% vs 9/111, 8.1%; P<0.00001). Patients with positive results in arrhythmogenic cardiomyopathy genes had 263% higher odds of recommended management changes compared to those with TTN (OR=3.63, CI:1.40-9.84, P=0.009). The results from CM/ARRH genetic testing on affected patients influenced cardiologists? medical decision making and management recommendations. Additional research is needed to evaluate how genetic testing for CM/ARRH impact health outcomes.

Background: Postoperative atrial fibrillation (POAF) is a frequent complication following coronary artery bypass grafting (CABG) and is associated with increased acute morbidity and resource utilization. However, its independent role in driving post-discharge adverse events in contemporary practice remains debated. Objective: To evaluate the association between POAF and short-term outcomes after CABG, and to utilize empirical Bayesian risk updating to stratify 90-day post-discharge vulnerabilities. Methods: A retrospective cohort analysis of 4,684 adult patients who underwent isolated CABG in Florida between January 1, 2021, and June 30, 2024, was conducted, excluding those with documented preoperative AFib. We employed multivariable negative binomial and logistic regression models to assess length of stay (LOS), discharge disposition, 90-day readmission, and 90-day composite complications. Additionally, a Bayesian Beta-Binomial conjugate model with an objective Jeffreys Prior was utilized to estimate the posterior probabilities of adverse outcomes across key clinical phenotypes. Results: POAF occurred in 355 patients (7.58%). Multivariable analysis demonstrated a 30% relative increase in expected LOS (IRR 1.30, 95% CI [1.23 - 1.36], P < .001) and 33% higher odds of facility discharge (OR 1.33, 95% CI [1.03 - 1.72], P = .030) for patients with POAF. However, POAF was not independently associated with 90-day readmission (OR 1.25, P = .063) or composite complications (OR 1.20, P = .118). Chronic heart failure (CHF) emerged as the dominant predictor. Bayesian risk updating revealed that while the baseline posterior probability for a 90-day complication was 27.2%, the synergistic presence of both POAF and CHF radically shifted this posterior risk to 42.6% (Probability of Direction > 0.999 vs. baseline). Conclusions: POAF prolongs hospitalization and drives non-home discharges, but it does not independently dictate 90-day morbidity. Bayesian stratification demonstrates that post-discharge outcomes are predominantly driven by underlying chronic conditions. Effective reduction of readmissions requires robust transition-of-care frameworks, empowering primary care clinicians to aggressively optimize heart failure and metabolic disease rather than focusing solely on the acute surgical arrhythmic event.

Ambulatory blood pressure monitoring (ABPM) is recommended for confirming hypertension and assessing out-of-office blood pressure (BP). However, patient burden and device tolerability may limit broader implementation. We compared participant experience with a traditional oscillometric ABPM device and a compact cuff-integrated ABPM. The PRO-BP Study was a pilot randomized crossover study of 20 adults in New York City. Participants completed two 24-hour ABPM periods over 7 days using the SpaceLabs 90227 and SOMNOmedics ABPM Pro devices. After each period, participants rated comfort, pain, sleep interference, embarrassment, noise, skin irritation, and interference with daytime activities. Both devices achieved guideline-based recording-quality thresholds. Compared with SpaceLabs, ABPM Pro was associated with greater comfort (median 7.0 [IQR, 5.0-8.5] vs 3.5 [IQR, 2.0-6.5]; P=0.004), less pain (1.5 [0-3.5] vs 5.0 [0.5-7.0]; P=0.003), and less embarrassment (0.5 [0-3.5] vs 3.0 [0-6.0]; P=0.01). Other experience ratings did not differ significantly. Participant experience should be considered alongside recording quality when evaluating validated ambulatory BP monitoring technologies.

Background: A growing burden of cardiovascular risk factors has raised cardiovascular disease-related mortality in Sub-Saharan Africa (SSA), driving higher prevalence of heart failure with reduced ejection fraction (HFrEF) and its complication with atrial fibrillation (AF). No prospective study has examined AF's clinical impact on HFrEF in SSA. Aim: To determine AF prevalence in HFrEF, describe HFrEF-AF clinical characteristics, and determine AF's impact on mortality. Methods: In this prospective observational study at a tertiary hospital in Johannesburg, 136 HFrEF patients were enrolled and categorised as HFrEF- SR (sinus rhythm) or HFrEF-AF. Baseline clinical characteristics and biochemistry were recorded. Comprehensive echocardiography including left atrial strain by 2D speckle-tracking was performed. Median follow-up was 30.6 months. Results: AF was present in 28 patients (21%). The mean age was 58.7 {+/-} 14.9 years (52.9% male) and differed between groups (p < 0.001). Hypertensive heart disease was the leading cause of HFrEF (36%). Compared with SR, HFrEF-AF patients had poorer health status (KCCQ 27 [16-43] vs 45 [32-60], p < 0.001) and lower left atrial strain (26.2 {+/-} 11.3%, p < 0.001). Guideline-directed medical therapy was suboptimal in the AF group: anticoagulation use was higher than SR (60% vs 9.5%, p < 0.001) but overall inadequate; HFrEF-AF patients received lower median doses of carvedilol (15.6 mg vs 25 mg, p = 0.002) and enalapril (10 mg vs 20 mg, p = 0.004), and fewer received spironolactone (50% vs 75.3%, p = 0.013). Survival was significantly lower in HFrEF-AF (0.41 [0.22-0.61]) versus SR (0.73 [0.61-0.82], p < 0.001). Independent predictors of mortality included prior stroke, lower TAPSE and KCCQ, and higher E/e' and heart rate. Conclusion: AF is common among HFrEF patients in this SSA cohort (though lower than in high-income countries) and associates with worse clinical status, suboptimal therapy, and higher mortality.

Background: Obstructive hypertrophic cardiomyopathy (oHCM) causes substantial symptom burden and impaired functional capacity. Mavacamten has emerged as a targeted pharmacologic treatment, whereas alcohol septal ablation (ASA) is an established septal reduction therapy (SRT). Direct comparative real-world data remain limited. Methods: In this propensity-controlled observational study, longitudinal registry data from Heidelberg University Hospital were analyzed. Consecutive adults with oHCM, NYHA class ?II symptoms, and a maximum LVOT gradient ?50 mmHg treated with mavacamten or ASA were included. The cohort comprised 107 ASA- and 113 mavacamten-treated patients. Follow-up was performed at 6 and 12 months. The primary endpoint was a composite adverse clinical outcome including cardiovascular death, heart failure hospitalization, SRT, heart transplantation, ventricular assist device implantation, permanent pacemaker implantation for third-degree atrioventricular block, or decline in left ventricular ejection fraction to <40%. Results: Both treatments showed significant improvement in NYHA class and LVOT gradient reduction over 12 months. Mean LVOT gradient decreased from 100.3 to 44.2 mmHg after ASA and from 85.7 to 18.4 mmHg with mavacamten at 12 months (both p<0.001). Between-group differences were not significant at 6 months, whereas residual LVOT gradient was lower with mavacamten at 12 months (p=0.004). NT-proBNP declined in both groups and was lower with mavacamten at both follow-up visits (both p<0.001). Third-degree atrioventricular block occurred more frequently after ASA (6.5% vs 0%, p=0.002). The composite endpoint occurred in 13 ASA- (12.1%) and 4 mavacamten-treated patients (3.5%) (p=0.003), with higher 1-year event-free survival in the mavacamten group (HR 0.19; 95%-CI 0.06-0.60; p=0.001). Conclusions: In this real-world comparative study, both ASA and mavacamten improved symptoms and LVOT obstruction in oHCM. Mavacamten was associated with a more favorable short-term hemodynamic and safety profile at 12 months.

Background Postoperative atrial fibrillation (POAF) is a common complication of cardiac surgery with POAF susceptibility thought to be primarily the result of pre-existing structural atrial disease, specifically fibrosis. We tested this hypothesis directly by combining preoperative imaging of atrial fibrosis with continuous physiological monitoring before POAF onset. Methods This prospective single center study (2023?2025) comprised 6,697 adults without prior atrial fibrillation (AF) undergoing elective cardiac surgery. Subjects were enrolled into three prespecified, non-overlapping cohorts: a mechanistic imaging cohort (n=52) to test whether preoperative atrial fibroblast activation predicts POAF; a physiological monitoring cohort (n=3,183) to characterize peri-event autonomic dynamics via time-resolved HRV analysis; and an independent prospective observability cohort (n=3,451) for validation. The prespecified primary analyses assessed time-domain and frequency-domain HRV across six consecutive 10-minute intervals during the 60 minutes preceding POAF onset. Generalized estimating equations models were applied. Results Preoperative atrial fibroblast activation did not differ significantly between patients with (n=22) or without POAF (n=52). By contrast, in a physiological monitoring cohort (n=3,183), time-resolved heart rate variability analysis revealed progressive autonomic destabilization beginning approximately 20 minutes before POAF onset, with significant divergence in heart-rate-corrected SDNN in the final 10-minute pre-event interval (marginal mean difference 0.0139, 95% CI 0.0113?0.0164; P<0.001; Cohen's d=0.728). This signal was independently validated in a prospective observability cohort (n=3,451), achieving fragment-level sensitivity of 69.6% and specificity of 97.5% at the 10-minute horizon. Conclusions POAF is more closely associated with immediately preceding detectable autonomic destabilization than with preoperative structural substrate. These findings challenge the hypothesis that POAF susceptibility is structurally determined(structural-determinism) and reframe this frequent complication as a dynamic, state-dependent process that may be a target for active prevention.

After myocardial infarction (MI), pathological autonomic remodeling, including vagal dysfunction and sympathoexcitation, occurs and predisposes to ventricular arrhythmias (VT/VF). The underlying factors that drive this remodeling, including the observed neuroinflammation and glial activation, remain unknown. We hypothesized that sympathetic nociceptive afferents underlie this remodeling post-MI. Epidural resiniferatoxin (RTX, to ablate sympathetic cardiac afferent neurons) vs. saline was administered in pigs prior to MI and autonomic and electrophysiological effects assessed four to six weeks post-infarction. Acute effects of afferent ablation after chronic MI were also assessed in a separate group of animals. Baroreflex sensitivity and vagal tone, as measured by parasympathetic neuronal activity and cardiac nociceptive responses, were improved in infarcted animals which received epidural RTX prior to MI. These animals also demonstrated reduced spinal cord inflammation and glial activation, downregulation of circulating stress and inflammatory pathways, and stabilization of electrophysiological parameters, with reduced VT/VF-inducibility. Epidural RTX after chronic MI also acutely restored vagal function and decreased VT/VF. These data suggest that cardiac spinal nociceptive afferents directly contribute to VT/VF susceptibility and MI-induced autonomic remodeling, including oxidative stress, inflammation, glial activation, and reduced vagal function, providing novel insights into the causal role of these afferents in driving sympathovagal imbalance after MI.