Initiation Of Atrial Fibrillation Research Articles

Effectiveness, utilisation and cost associated with implantable loop recorders versus external monitors after ischaemic or cryptogenic stroke

ObjectiveImplantable loop recorders (ILRs) are increasingly used for long-term rhythm monitoring after ischaemic and cryptogenic stroke, with the goal of detecting atrial fibrillation (AF) and subsequent initiation of oral anticoagulation...

Aproximación práctica para la caracterización de la miocardiopatía auricular en pacientes con fibrilación auricular

Atrial fibrillation (AF) causes progressive structural and electrical changes in the atria that can be summarized within the general concept of atrial remodeling. In parallel, other clinical characteristics and comorbidities may also affect atrial tissue properties and make the atria susceptible to AF initiation and its long-term persistence. Overall, pathological atrial changes lead to atrial cardiomyopathy with important implications for rhythm control. Although there is general agreement on the role of the atrial substrate for successful rhythm control in AF, the current classification oversimplifies clinical management. The classification uses temporal criteria and does not establish a well-defined strategy to characterize the individual-specific degree of atrial cardiomyopathy. Better characterization of atrial cardiomyopathy may improve the decision-making process on the most appropriate therapeutic option. We review current scientific evidence and propose a practical characterization of the atrial substrate based on 3 evaluation steps starting with a clinical evaluation (step 1), then assess outpatient complementary data (step 2), and finally include information from advanced diagnostic tools (step 3). The information from each of the steps or a combination thereof can be used to classify AF patients in 4 stages of atrial cardiomyopathy, which we also use to estimate the success on effective rhythm control.

Electrophysiology and 3D-imaging reveal properties of human intracardiac neurons and increased excitability with atrial fibrillation.

Altered autonomic input to the heart plays a major role in atrial fibrillation (AF). Autonomic neurons termed ganglionated plexi (GP) are clustered on the heart surface to provide the last point of neural control of cardiac function. To date the properties of GP neurons in humans are unknown. Here we have addressed this knowledge gap in human GP neuron structure and physiology in patients with and without AF. Human right atrial GP neurons embedded in epicardial adipose tissue were excised during open heart surgery performed on both non-AF and AF patients and then characterised physiologically by whole cell patch clamp techniques. Structural analysis was also performed after fixation at both the single cell and at the entire GP levels via three-dimensional confocal imaging. Human GP neurons were found to exhibit unique properties and structural complexity with branched neurite outgrowth. Significant differences in excitability were revealed between AF and non-AF GP neurons as measured by lower current to induce action potential firing, a reduced occurrence of low action potential firing rates, decreased accommodation and increased synaptic density. Visualisation of entire GPs showed almost all neurons are cholinergic with a small proportion of noradrenergic and dual phenotype neurons. Phenotypic distribution differences occurred with AF including decreased cholinergic and dual phenotype neurons, and increased noradrenergic neurons. These data show both functional and structural differences occur between GP neurons from patients with and without AF, highlighting that cellular plasticity occurs in neural input to the heart that could alter autonomic influence on atrial function. KEY POINTS: The autonomic nervous system plays a critical role in regulating heart rhythm and the initiation of AF; however, the structural and functional properties of human autonomic neurons in the autonomic ganglionated plexi (GP) remain unknown. Here we perform the first whole cell patch clamp electrophysiological and large tissue confocal imaging analysis of these neurons from patients with and without AF. Our data show human GP neurons are functionally and structurally complex. Measurements of action potential kinetics show higher excitability in GP neurons from AF patients as measured by lower current to induce action potential firing, reduced low firing action potential rates, and decreased action potential accommodation. Confocal imaging shows increased synaptic density and noradrenergic phenotypes in patients with AF. Both functional and structural differences occur in GP neurons from patients with AF that could alter autonomic influence on atrial rhythm.

Vein of Marshall Ethanol Infusion for AF Ablation; A Review.

The outcomes of persistent atrial fibrillation (AF) ablation are modest with various adjunctive strategies beyond pulmonary vein isolation (PVI) yielding largely disappointing results in randomised controlled trials. Linear ablation is a commonly employed adjunct strategy but is limited by difficulty in achieving durable bidirectional block, particularly at the mitral isthmus. Epicardial connections play a role in AF initiation and perpetuation. The ligament of Marshall has been implicated as a source of AF triggers and is known to harbour sympathetic and parasympathetic nerve fibres that contribute to AF perpetuation. Ethanol infusion into the Vein of Marshall, a remnant of the superior vena cava and key component of the ligament of Marshall, may eliminate these AF triggers and can facilitate the ease of obtaining durable mitral isthmus block. While early trials have demonstrated the potential of Vein of Marshall 'ethanolisation' to reduce arrhythmia recurrence after persistent AF ablation, further randomised trials are needed to fully determine the potential long-term outcome benefits afforded by this technique.

Risk of atrial fibrillation development in adolescent patients with inflammatory bowel disease.

There is increasing evidence linking chronic inflammation to the initiation and continuation of atrial fibrillation (AF). Inflammatory bowel diseases (IBD), namely (Crohn's disease (CD) and ulcerative colitis (UC), are chronic systemic inflammatory disorders with both intestinal and extra-intestinal manifestations. Atrial electromechanical delay (EMD) has been known as an early marker of AF. The objective of this study was to evaluate the atrial electromechanical properties in children and adolescents with IBD during remission. One hundred IBD patients aged 12-17 years (50 with CD and 50 with UC) in remission state and 100 healthy controls were recruited for the study. Atrial electromechanical properties were measured using transthoracic echocardiography, tissue Doppler imaging, and simultaneous surface ECG recording. Interatrial EMD, left intra-atrial, and right intra-atrial EMD were calculated. IBD patients in remission state have significantly prolonged left and right intra-atrial EMD and interatrial EMD compared to healthy controls (P = 0.03, P = 0.02, and P = 0.01 respectively). No statistical difference was observed between CD and UC in terms of inter- and intra-atrial EMDs. Conclusion:Atrial EMD is increased in pediatric patients with IBD indicating the increased risk of AF development. Measurement of atrial EMD parameters might be used to predict the risk of the development of AF in pediatric patients with IBD. What is Known: • There is increasing evidence linking chronic inflammation to the initiation and continuation of atrial fibrillation (AF). • Inflammatory bowel diseases are chronic systemic inflammatory disorders with both intestinal and extra-intestinal manifestations. • Atrial electromechanical delay (EMD) has been reported as an early marker of AF. What is New: • Atrial EMD is increased in pediatric patients with IBD indicating the increased risk of AF development. • Measurement of atrial EMD parameters might be used to predict the risk of the development of AF in pediatric patients with IBD.

Atrial fibrillation initiation and organization in a mechanistic model of atrial remodeling and calcium homeostatic regulation

Atrial fibrillation initiation and organization in a mechanistic model of atrial remodeling and calcium homeostatic regulation

Practical approach for atrial cardiomyopathy characterization in patients with atrial fibrillation

Atrial fibrillation (AF) causes progressive structural and electrical changes in the atria that can be summarized within the general concept of atrial remodeling. In parallel, other clinical characteristics and comorbidities may also affect atrial tissue properties and make the atria susceptible to AF initiation and its long-term persistence. Overall, pathological atrial changes lead to atrial cardiomyopathy with important implications for rhythm control. Although there is general agreement on the role of the atrial substrate for successful rhythm control in AF, the current classification oversimplifies clinical management. The classification uses temporal criteria and does not establish a well-defined strategy to characterize the individual-specific degree of atrial cardiomyopathy. Better characterization of atrial cardiomyopathy may improve the decision-making process on the most appropriate therapeutic option. We review current scientific evidence and propose a practical characterization of the atrial substrate based on 3 evaluation steps starting with a clinical evaluation (step 1), then assess outpatient complementary data (step 2), and finally include information from advanced diagnostic tools (step 3). The information from each of the steps or a combination thereof can be used to classify AF patients in 4 stages of atrial cardiomyopathy, which we also use to estimate the success on effective rhythm control.

Exploring the Intricate Interplay Between Obesity and Atrial Fibrillation: Mechanisms, Management, and Clinical Implications.

Atrial fibrillation (AF) stands as a prevalent and escalating cardiac arrhythmia in the United States, with obesity emerging as a prominent modifiable risk factor. This article explores the intricate relationship between obesity and AF, delving into the multifaceted pathophysiological mechanisms linking the 2 conditions. Various factors, such as autonomic dysfunction, left atrial stretch, inflammation, and hormonal imbalances, contribute to the initiation and perpetuation of AF in obese individuals. The Atrial Fibrillation Better Care pathway, emphasizing lifestyle modifications and weight loss strategies, emerges as a practical guideline for managing AF in obesity. This comprehensive review underscores the critical role of obesity as a significant modifiable risk factor for AF, urging a proactive approach to its management. Implementing the Atrial Fibrillation Better Care approach, focusing on encouraging physical activity, promoting healthy dietary habits, and raising awareness about the risks associated with obesity prove essential in preventing and mitigating the burden of AF in the obese population.

Structural and electro-anatomical characterization of the equine pulmonary veins: implications for atrial fibrillation

Introduction/objectivesSpontaneous pulmonary vein (PV) activity triggers atrial fibrillation (AF) in humans. Although AF frequently occurs in horses, the origin remains unknown. This study investigated the structural and electro-anatomical properties of equine PVs to determine the potential presence of an arrhythmogenic substrate. Animals, materials and methodsEndocardial three-dimensional electro-anatomical mapping (EnSite Precision) using high-density (HD) catheters was performed in 13 sedated horses in sinus rhythm. Left atrium (LA) access was obtained retrogradely through the carotid artery. Post-mortem, tissue was harvested from the LA, right atrium (RA), and PVs for histological characterization and quantification of ion channel expression using immunohistochemical analysis. ResultsGeometry, activation maps, and voltage maps of the PVs were created and a median of four ostia were identified. Areas of reduced conduction were found at the veno-atrial junction. The mean myocardial sleeve length varied from 28 ± 13 to 49 ± 22 mm. The PV voltage was 1.2 ± 1.4 mV and lower than the LA (3.4 ± 0.9 mV, P < 0.001). The fibrosis percentage was higher in PV myocardium (26.1 ± 6.6%) than LA (14.5 ± 5.0%, P = 0.003). L-type calcium channel (CaV1.2) expression was higher in PVs than LA (P = 0.001). T-type calcium channels (CaV3.3), connexin-43, ryanodine receptor-2, and small conductance calcium-activated potassium channel-3 was expressed in PVs. ConclusionsThe veno-atrial junction had lower voltages, increased structural heterogeneity and areas of slower conduction. Myocardial sleeves had variable lengths, and a different ion channel expression compared to the atria. Heterogeneous properties of the PVs interacting with the adjacent LA likely provide the milieu for re-entry and AF initiation.

Anticoagulation-Associated Bleeding in Patients Screened for Atrial Fibrillation versus Usual Care-A Post Hoc Analysis from the LOOP Study.

Background Atrial fibrillation (AF) prevalence is rising; however, data on the bleeding risks associated with the detection of subclinical AF are needed. Objective Our objective was to determine the bleeding increment associated with implantable loop recorder (ILR) screening for subclinical AF and subsequent anticoagulation initiation compared with usual care. Methods This post hoc study utilized LOOP trial data from 6,004 elderly patients with stroke risks randomized to either ILR ( n = 1,503) or usual care ( n = 4,503). The mean follow-up time was 64.5 months, and none were lost to follow-up. The primary exposure was the initiation of oral anticoagulation, and the main outcome was the risk of major bleeding events following initiation of oral anticoagulants (OACs), determined by time-dependent cox regression. Second, we investigated antithrombotic prescription patterns and major bleeding events after antiplatelet treatment and in subgroups. Results OAC was initiated in 1,019 participants with a mean age (years) of 78.8 (± 4.67) in control versus 77.0 (± 4.84) in ILR, p < 0.0001. Altogether did 202 participants end or pause OAC treatment. Among AF patients (n = 910) had 40 (28%) completely ended OAC and 105 (72%) temporarily paused OAC during follow-up. Major bleeding events totaled 221 (3.7%). Forty-seven major bleeding events followed an OAC initiation in 1,019 participants (4.6%); 26 versus 21 events in the control and ILR groups, respectively. The hazard ratio (HR) for major bleeding after OAC initiation compared with before initiation was 2.08 (1.50-2.90) p < 0.0001 overall, 2.81 (1.82-4.34) p < 0.0001 for control and 1.32 (0.78-2.23) p = 0.31 for the ILR group ( p = 0.07 for interaction). Antiplatelet treatment resulted in an overall adjusted HR of 1.3 (0.96-1.75) p = 0.09. For OAC users aged ≥75 years in the ILR group, the rate of major bleeding was 1.73 (0.92-2.96) compared with 0.84 (0.36-1.66) for an age <75 years, and the rate of the corresponding control subgroup aged ≥75 years was 2.20 (1.23-3.63) compared with 1.64 (0.82-2.93) for an age <75 years. Conclusion The individual risk of major bleeding increased twofold after initiation of oral anticoagulation for all patients in this study. However, the patients screened for subclinical AF did not have a higher bleeding risk after initiation of anticoagulation compared with those in usual care. Trial Registration: The LOOP study is registered at ClinicalTrials.gov, identifier: NCT020364 50.

Developing Pharmacological Therapies for Atrial Fibrillation Targeting Mitochondrial Dysfunction and Oxidative Stress: A Scoping Review.

Atrial fibrillation (AF) is a cardiac arrhythmia caused by electrophysiological anomalies in the atrial tissue, tissue degradation, structural abnormalities, and comorbidities. A direct relationship exists between AF and altered mitochondrial activity resulting from membrane potential loss, contractile dysfunction, or decreased ATP levels. This review aimed to elucidate the role of mitochondrial oxidative mechanisms in AF pathophysiology, the impact of mitochondrial oxidative stress on AF initiation and perpetuation, and current therapies. This review followed the Preferred Reporting Items for Systematic Reviews and the Meta-Analysis Extension for Scoping Reviews. PubMed, Excerpta Medica Database, and Scopus were explored until June 2023 using "MESH terms". Bibliographic references to relevant papers were also included. Oxidative stress is an imbalance that causes cellular damage from excessive oxidation, resulting in conditions such as AF. An imbalance in reactive oxygen species production and elimination can cause mitochondrial damage, cellular apoptosis, and cardiovascular diseases. Oxidative stress and inflammation are intrinsically linked, and inflammatory pathways are highly correlated with the occurrence of AF. AF is an intricate cardiac condition that requires innovative therapeutic approaches. The involvement of mitochondrial oxidative stress in the pathophysiology of AF introduces novel strategies for clinical treatment.

Ubiquitin-specific protease 38 promotes inflammatory atrial fibrillation induced by pressure overload.

Atrial structural and electrical remodelling is a major reason for the initiation and perpetuation of atrial fibrillation (AF). Ubiquitin-specific protease 38 (USP38) is a deubiquitinating enzyme, but its function in the heart remains unknown. The aim of this study was to investigate the effect of USP38 in pressure overload-induced AF. Cardiac-specific knockout USP38 and cardiac-specific transgenic USP38 mice and their corresponding control mice were used in this study. After 4 weeks with or without aortic banding (AB) surgery, atrial echocardiography, atrial histology, electrophysiological study, and molecular analysis were assessed. Ubiquitin-specific protease 38 knockout mice showed a remarkable improvement in vulnerability to AF, atrial weight and diameter, atrial fibrosis, and calcium-handling protein expression after AB surgery. Conversely, USP38 overexpression further increased susceptibility to AF by exacerbating atrial structural and electrical remodelling. Mechanistically, USP38 interacted with and deubiquitinated nuclear factor-kappa B (NF-κB), and USP38 overexpression increased the level of p-NF-κB in vivo and in vitro, accompanied by the upregulation of NOD-like receptor protein 3 (NLRP3) and inflammatory cytokines, suggesting that USP38 contributes to adverse effects by driving NF-κB/NLRP3-mediated inflammatory responses. Overall, our study indicates that USP38 promotes pressure overload-induced AF through targeting NF-κB/NLRP3-mediated inflammatory responses.

Successful caudal vena cava and pulmonary vein isolation in healthy horses using 3D electro-anatomical mapping and a contact force-guided ablation system.

Recently, treatment of equine atrial tachycardia by three-dimensional electro-anatomical mapping (3D EAM) and radiofrequency catheter ablation (RFCA) has been described. Myocardial sleeves in the caudal vena cava and pulmonary veins are a potential trigger for initiation and perpetuation of atrial tachycardia and atrial fibrillation in the horse. Isolation of these myocardial sleeves by RFCA may be an effective treatment for these arrhythmias. To describe the feasibility of 3D EAM and RFCA to isolate caudal vena cava and pulmonary veins in adult horses using 3D mapping and a contact force (CF)-guided ablation system. In vivo experiments. 3D EAM and RFCA was performed in five horses without cardiovascular disease under general anaesthesia, using the CF-guided system CARTO®3. Point-by-point RFCA aimed for isolation of caudal vena cava and pulmonary veins. Radiofrequency energy was delivered in power-controlled mode with a target power of 45 W, CF between 10 and 15 g and 30 mL/min irrigation rate, until an ablation-index of 450-500 was reached. In the right atrium, myocardial sleeves of the caudal vena cava were isolated (n = 5). In the left atrium, isolation of ostium II (n = 3), ostium III (n = 1) and ostium I, II and III en bloc (n = 1) was performed. Successful isolation was confirmed by entrance and exit block. Horses were euthanised at the end of the procedure, so long term effects such as potential reconnection of isolated veins could not be studied. This is the first description of 3D EAM and RFCA with CARTO®3 in horses, thereby showing the technical feasibility and successful caudal vena cava and pulmonary vein isolation. CF measurement allowed monitoring of catheter-tissue contact, resulting in efficient acute lesion creation as confirmed by entrance and exit block. This is a promising treatment for cardiac arrhythmias in horses.

PITX2 gain-of-function mutation associated with atrial fibrillation alters mitochondrial activity in human iPSC atrial-like cardiomyocytes.

Atrial fibrillation (AF) is the most common cardiac arrhythmia worldwide; however, the underlying causes of AF initiation are still poorly understood, particularly because currently available models do not allow in distinguishing the initial causes from maladaptive remodeling that induces and perpetuates AF. Lately, the genetic background has been proven to be important in the AF onset. iPSC-derived cardiomyocytes, being patient- and mutation-specific, may help solve this diatribe by showing the initial cell-autonomous changes underlying the development of the disease. Transcription factor paired-like homeodomain 2 (PITX2) has been identified as a key regulator of atrial development/differentiation, and the PITX2 genomic locus has the highest association with paroxysmal AF. PITX2 influences mitochondrial activity, and alterations in either its expression or function have been widely associated with AF. In this work, we investigate the activity of mitochondria in iPSC-derived atrial cardiomyocytes (aCMs) obtained from a young patient (24 years old) with paroxysmal AF, carrying a gain-of-function mutation in PITX2 (rs138163892) and from its isogenic control (CTRL) in which the heterozygous point mutation has been reverted to WT. PITX2 aCMs show a higher mitochondrial content, increased mitochondrial activity, and superoxide production under basal conditions when compared to CTRL aCMs. However, increasing mitochondrial workload by FCCP or β-adrenergic stimulation allows us to unmask mitochondrial defects in PITX2 aCMs, which are incapable of responding efficiently to the higher energy demand, determining ATP deficiency.

AF in the AFternoon: The circadian pattern of incident atrial fibrillation in a loop recorder population

Abstract Introduction Loop recorders have provided the opportunity to systematically screen individuals for arrhythmias, and in doing so provide new appreciated mechanistic insights to arrhythmia pathophysiology. Atrial fibrillation (AF) is a complex arrhythmia with a multitude of precipitants and substrates. Previous studies looking at the circadian rhythm of AF, have required patient symptoms to define onset. All studies on the circadian rhythm of AF suggest that AF does not occur randomly. It has been suggested that the circadian variation in autonomic function may provide an underlying substrate for AF initiation. This is the largest study to utilise loop recorder detected AF to explore the circadian pattern of AF. Purpose We sought to ascertain how the detection of incident AF varied throughout the day, in patients monitored with a loop recorder Methods This was a single-centre retrospective observational study. Consecutive adult patients referred for ILR implantation between March 2009 and November 2019, without prevalent AF or atrial flutter, were included. Demographic and anthropometric data was identified from the individuals medical notes. The time of incident AF episodes was identified from loop recorder reports. Results A total of 1168 AF episodes of any duration were identified by the ILR, of which onset time was available for 1118 episodes. Onset of AF episodes in our data for the entire population demonstrated a monophasic distribution (figure 1a). The OR for developing AF between 13.00-14.59 compared to 03.00-04.59 was 4.89 (95% CI 3.47-6.90). Amongst the ESUS population time of onset distribution showed multiple daytime peaks (figure 1b). The OR for developing AF between 10.00-11.59 compared to 03.00-04.59 was 4.39 (95% CI 2.68-7.20). Amongst the non- ESUS population time of onset distribution (figure 1c) shows a monophasic pattern with the peak at time blocks 12.00-14.59. The OR for developing AF between 13.00-14.59 compared to 02.00-03.59 was 6.75 (95% CI 4.17-10.93). Conclusion(s) Our study demonstrated that there is a diurnal variation for incident AF detection using a loop recorder. There is a general propensity for episodes to occur in the afternoon, with a nadir at night. This is in contrast to previous reports which have suggested that the nocturnal and morning peaks are more apparent. Moreover, different cohorts appear to show different temporal patterns, with ESUS patients having multiple time peaks, whereas the non-stroke cohort had a solitary peak period. Understanding the diurnal variation of AF may help to shed more light on the complex pathogenesis of AF, and whether different AF phenotypes are associated with stroke risk. Moreover, the finding of a day-time propensity for AF, adds weight to the utilisation of consumer facing non-invasive monitoring tools during the day for AF identification in high-risk populations.

Characterization of unipolar electrogram morphology: a novel tool for quantifying conduction inhomogeneity.

Areas of conduction inhomogeneity (CI) during sinus rhythm may facilitate the initiation and perpetuation of atrial fibrillation (AF). Currently, no tool is available to quantify the severity of CI. Our aim is to develop and validate a novel tool using unipolar electrograms (EGMs) only to quantify the severity of CI in the atria. Epicardial mapping of the right atrium (RA) and left atrium, including Bachmann's bundle, was performed in 235 patients undergoing coronary artery bypass grafting surgery. Conduction inhomogeneity was defined as the amount of conduction block. Electrograms were classified as single, short, long double (LDP), and fractionated potentials (FPs), and the fractionation duration of non-single potentials was measured. The proportion of low-voltage areas (LVAs, <1 mV) was calculated. Increased CI was associated with decreased potential voltages and increased LVAs, LDPs, and FPs. The Electrical Fingerprint Score consisting of RA EGM features, including LVAs and LDPs, was most accurate in predicting CI severity. The RA Electrical Fingerprint Score demonstrated the highest correlation with the amount of CI in both atria (r = 0.70, P < 0.001). The Electrical Fingerprint Score is a novel tool to quantify the severity of CI using only unipolar EGM characteristics recorded. This tool can be used to stage the degree of conduction abnormalities without constructing spatial activation patterns, potentially enabling early identification of patients at high risk of post-operative AF or selection of the appropriate ablation approach in addition to pulmonary vein isolation at the electrophysiology laboratory.

Box Lesion Isolation of the Left Atrial Posterior Wall with Radiofrequency Ablation Restricted in Predetermined Lines for the Treatment of Persistent Atrial Fibrillation: The Prognostic Role of Acute Interventional Outcome and Trigger Identification.

The left atrial posterior wall (PW) is known to be a critical substrate for the initiation and perpetuation of atrial fibrillation (AF) and has been explored as a target for catheter ablation, particularly in persistent AF (PerAF). In this retrospective study, we investigate the clinical outcome of patients with PerAF who underwent PW isolation (PWI) restricted in predetermined lines in addition to pulmonary vein isolation (PVI). One hundred consecutive patients (64 ± 9.1 years, 66% male, 20% with previous PVI ablation) underwent PWI in a box lesion setting for PerAF lasting >3 months (34% long-standing PerAF). PW triggers were defined as either foci from the PW that repeatedly induced AF or as isolated AF or atrial tachycardia (AT) within the PW. After a mean follow-up period of 25.6 ± 6.7 months, 61% of the patients remained in sinus rhythm after the last procedure. In 79 patients, the PW was successfully isolated, while, in 21 patients, complete isolation was not possible due to failure in completion of the roof line (n = 16), the floor line (n = 7), or both (n = 2). Patients with incomplete isolation had similar AF/AT recurrence rates compared to those with complete PWI. In 12 patients, PW triggers were identified, and PWI in these patients was shown to have a significantly better prognosis in terms of sinus rhythm maintenance (P = .031). Failure of complete PWI does not predispose a patient to an inferior outcome nor is it responsible for iatrogenic ATs. The presence of AF triggers within the PW leads to a particularly favorable result after box lesion isolation.

Haemodynamic changes after atrial fibrillation initiation in patients eligible for catheter ablation: a randomized controlled study.

Atrial fibrillation (AF) haemodynamics is less well studied due to challenges explained by the nature of AF. Until now, no randomized data are available. This study evaluates haemodynamic variables after AF induction in a randomized setting. Forty-two patients with AF who had been referred for ablation to the University Hospital, Linköping, Sweden, and had no arrhythmias during the 4-day screening period were randomized to AF induction vs. control (2:1). Atrial fibrillation was induced by burst pacing after baseline intracardiac pressure measurements. Pressure changes in the right and left atrium (RA and LA), right ventricle (RV), and systolic and diastolic blood pressures (SBP and DBP) were evaluated 30 min after AF induction compared with the control group. A total of 11 women and 31 men (median age 60) with similar baseline characteristics were included (intervention n = 27, control group n = 15). After 30 min in AF, the RV end-diastolic pressure (RVEDP) and RV systolic pressure (RVSP) significantly reduced compared with baseline and between randomization groups (RVEDP: P = 0.016; RVSP: P = 0.001). Atrial fibrillation induction increased DBP in the intervention group compared with the control group (P = 0.02), unlike reactions in SBP (P = 0.178). Right atrium and LA mean pressure (RAm and LAm) responses did not differ significantly between the groups (RAm: P = 0.307; LAm: P = 0.784). Induced AF increased DBP and decreased RVEDP and RVSP. Our results allow us to understand some paroxysmal AF haemodynamics, which provides a haemodynamic rationale to support rhythm regulatory strategies to improve symptoms and outcomes. No NCT01553045. https://clinicaltrials.gov/ct2/show/NCT01553045?term=NCT01553045&rank=1.

NADPH Oxidases and Oxidative Stress in the Pathogenesis of Atrial Fibrillation.

Atrial fibrillation (AF) is the most common type of cardiac arrhythmia and its prevalence increases with age. The irregular and rapid contraction of the atria can lead to ineffective blood pumping, local blood stasis, blood clots, ischemic stroke, and heart failure. NADPH oxidases (NOX) and mitochondria are the main sources of reactive oxygen species in the heart, and dysregulated activation of NOX and mitochondrial dysfunction are associated with AF pathogenesis. NOX- and mitochondria-derived oxidative stress contribute to the onset of paroxysmal AF by inducing electrophysiological changes in atrial myocytes and structural remodeling in the atria. Because high atrial activity causes cardiac myocytes to expend extremely high energy to maintain excitation-contraction coupling during persistent AF, mitochondria, the primary energy source, undergo metabolic stress, affecting their morphology, Ca2+ handling, and ATP generation. In this review, we discuss the role of oxidative stress in activating AF-triggered activities, regulating intracellular Ca2+ handling, and functional and anatomical reentry mechanisms, all of which are associated with AF initiation, perpetuation, and progression. Changes in the extracellular matrix, inflammation, ion channel expression and function, myofibril structure, and mitochondrial function occur during the early transitional stages of AF, opening a window of opportunity to target NOX and mitochondria-derived oxidative stress using isoform-specific NOX inhibitors and mitochondrial ROS scavengers, as well as drugs that improve mitochondrial dynamics and metabolism to treat persistent AF and its transition to permanent AF.

Inflammatory Markers as Predictors of Atrial Fibrillation Recurrence: Exploring the C-Reactive Protein to Albumin Ratio in Cryoablation Patients.

Atrial fibrillation (AF) is a common cardiac rhythm disorder associated with hemodynamic disruptions and thromboembolic events. While antiarrhythmic drugs are often recommended as the initial treatment, catheter ablation has emerged as a viable alternative. However, the recurrence of AF following ablation remains a challenge, and there is growing interest in exploring inflammatory markers as predictors of recurrence. This retrospective, cross-sectional analysis included 249 patients who underwent cryoablation for paroxysmal AF. The relationship between the 'C-reactive protein (CRP) to albumin ratio (CAR)' and AF recurrence was examined. Two hundred and forty-nine patients with paroxysmal non-valvular atrial fibrillation were included. They were divided into two groups: those without recurrence (Group 1) and those with recurrence (Group 2). Significant differences were observed in age (57.2 ± 9.9 vs. 62.5 ± 8.4, p = 0.001) and left atrial size (4.0 ± 0.5 vs. 4.2 ± 0.7, p = 0.001) between the two groups. In blood parameters, significant differences were found in CRP (5.2 ± 1.3 vs. 9.4 ± 2.8, p < 0.001) and neutrophil counts (5.1 ± 2.2 vs. 6.7 ± 3.6, p = 0.001). In univariate regression analysis, age (OR: 1.058, CI: 1.024-1.093, p = 0.001), WBC count (OR: 1.201, CI: 1.092-1.322, p < 0.001), neutrophil count (OR: 1.239, CI: 1.114-1.378, p = 0.001), CAR (OR: 1.409, CI: 1.183-1.678, p < 0.001), and left atrial diameter (OR: 0.968, CI: 0.948-0.989, p = 0.002) showed significant associations with AF recurrence. Inflammation plays a crucial role in the initiation and progression of AF. This study demonstrated that along with age, the CAR can serve as an independent predictor of AF recurrence following cryoablation.