Conduction Disorders during Sinus Rhythm in Relation to Atrial Fibrillation Persistence.
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ABSTRACT:
SUBMITTER: van der Does WFB
PROVIDER: S-EPMC8269325 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Valvular heart disease (VHD) is a common risk factor for atrial fibrillation (AF). Conduction abnormalities (CA) during sinus rhythm (SR) across Bachmann's bundle (BB) are associated with AF development. The study goal is to compare electrophysiological characteristics across BB during SR between patients with ischemic (IHD) and/or VHD either with or without ischemic heart disease ((I)VHD), with/without AF history using high-resolution intraoperative epicardial mapping. In total, 304 patients (IHD: n = 193, (I)VHD: n = 111) were mapped; 40 patients (13%) had a history of AF. In 116 patients (38%) there was a mid-entry site with a trend towards more mid-entry sites in patients with (I)VHD vs. IHD (p = 0.061), whereas patients with AF had significant more mid-entry sites than without AF (p = 0.007). CA were present in 251 (95%) patients without AF compared to 39 (98%) with AF. The amount of CA was comparable in patients with IHD and (I)VHD (p > 0.05); AF history was positively associated with the amount of CA (p < 0.05). Receiver operating characteristic (ROC) curve showed 85.0% sensitivity and 86.4% specificity for cut-off values of CA lines of respectively ? 6 mm and ? 26 mm. Patients without a mid-entry site or long CA lines (? 12 mm) were unlikely to have AF (sensitivity 90%, p = 0.002). There are no significant differences in entry-sites of wavefronts and long lines of CA between patients with IHD compared to (I)VHD. However, patients with AF have more wavefronts entering in the middle of BB and a higher incidence of long CA lines compared to patients without a history of AF. Moreover, in case of absence of a mid-entry site or long line of CA, patients most likely have no history of AF.
| S-EPMC7355925 | biostudies-literature
Project description:Echocardiography is the basic imaging technique used to determine the odds of maintaining sinus rhythm (SR) following direct current cardioversion (DCCV) for persistent atrial fibrillation (AF). However, most studies are focused on the echocardiographic parameters obtained during SR resulting from successful DCCV. The aim of this study was to assess the value of the echocardiographic parameters measured before DCCV for the prognosis of SR maintenance after DCCV. The study included 146 patients with persistent AF who underwent DCCV. Clinical and echocardiographic data were collected directly before DCCV and, for patients with SR, one month, six months, and 12 months after DCCV. We found that left atrial emptying fraction (LAEF) assessed during atrial fibrillation was significantly larger in the group with SR maintenance after 12 months than in the group with AF recurrence (30.8±8.3 vs. 24.6±10.4%; p<0.001). In multivariable logistic regression analysis with a model containing echocardiographic parameters, LAEF (OR 1.053; 95% CI 1.011-1.096; p = 0.013) and the E/e'mean ratio (OR 0.883; 95% CI 0.788-0.990; p = 0.033) were independent predictors of SR maintenance. Analyzing a model including clinical and echocardiographic variables, only LAEF (OR 1.046; 95% CI 1-1.095; p = 0.049) and beta-blockers used before DCCV (OR 14.694; 95% CI 1.622-133.139; p = 0.017) were independent predictors of SR maintenance after 12 months. Our results indicate that LAEF measured during AF is a significant predictor of SR maintenance in the 12 months following DCCV due to persistent AF. Our findings confirm the recently raised hypothesis about the superiority of echocardiographic parameters assessing mechanical remodeling over parameters assessing structural remodeling of left atrium in predicting sinus rhythm maintenance after electrical cardioversion.
| S-EPMC7446797 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-04-30 | GSE226284 | GEO
Project description:Understanding atrial fibrillation (AF) requires integrated understanding of ionic currents and Ca2+ transport in remodeled human atrium, but appropriate models are limited.To study AF, we developed a new human atrial action potential (AP) model, derived from atrial experimental results and our human ventricular myocyte model.Atria versus ventricles have lower I(K1), resulting in more depolarized resting membrane potential (?7 mV). We used higher I(to,fast) density in atrium, removed I(to,slow), and included an atrial-specific I(Kur). I(NCX) and I(NaK) densities were reduced in atrial versus ventricular myocytes according to experimental results. SERCA function was altered to reproduce human atrial myocyte Ca2+ transients. To simulate chronic AF, we reduced I(CaL), I(to), I(Kur) and SERCA, and increased I(K1),I(Ks) and I(NCX). We also investigated the link between Kv1.5 channelopathy, [Ca2+]i, and AF. The sinus rhythm model showed a typical human atrial AP morphology. Consistent with experiments, the model showed shorter APs and reduced AP duration shortening at increasing pacing frequencies in AF or when I(CaL) was partially blocked, suggesting a crucial role of Ca2+ and Na+ in this effect. This also explained blunted Ca2+ transient and rate-adaptation of [Ca2+]i and [Na+]i in chronic AF. Moreover, increasing [Na+]i and altered I(NaK) and I(NCX) causes rate-dependent atrial AP shortening. Blocking I(Kur) to mimic Kv1.5 loss-of-function increased [Ca2+]i and caused early afterdepolarizations under adrenergic stress, as observed experimentally.Our study provides a novel tool and insights into ionic bases of atrioventricular AP differences, and shows how Na+ and Ca2+ homeostases critically mediate abnormal repolarization in AF.
| S-EPMC3208665 | biostudies-literature
Project description:GSE2240 contains two different experimental subsets: 1) Comparison of atrial and ventricular gene expression (atrial tissue of patients with sinus rhythm vs. human left ventricular non-failing myocardium) The purpose of our investigation was to identify the transcriptional basis for ultrastructural and functional specialization of human atria and ventricles. Using exploratory microarray analysis (Affymetrix U133A+B), we detected 11,740 transcripts expressed in human heart, representing the most comprehensive report of the human myocardial transcriptome to date. Variation in gene expression between atria and ventricles accounted for the largest differences in this data set, as 3.300 and 2.974 transcripts showed higher expression in atria and ventricles, respectively. Functional classification based on Gene Ontology identified chamber-specific patterns of gene expression and provided molecular insights into the regional specialization of cardiomyocytes, correlating important functional pathways to transcriptional activity: Ventricular myocytes preferentially express genes satisfying contractile and energetic requirements, while atrial myocytes exhibit specific transcriptional activities related to neurohumoral function. In addition, several pro-fibrotic and apoptotic pathways were concentrated in atrial myocardium, substantiating the higher susceptibility of atria to programmed cell death and extracellular matrix remodelling observed in human and experimental animal models of heart failure. Differences in transcriptional profiles of atrial and ventricular myocardium thus provide molecular insights into myocardial cell diversity and distinct region-specific adaptations to physiological and pathophysiological conditions (Barth AS et al., Eur J Physiol, 2005). 2) Comparison of atrial gene expression in patients with permanent atrial fibrillation and sinus rhythm. Atrial fibrillation is associated with increased expression of ventricular myosin isoforms in atrial myocardium, regarded as part of a dedifferentiation process. Whether re-expression of ventricular isoforms in atrial fibrillation is restricted to transcripts encoding for contractile proteins is unknown. Therefore, this study compares atrial mRNA expression in patients with permanent atrial fibrillation to atrial mRNA expression of patients with sinus rhythm as well as to ventricular gene expression using Affymetrix U133 arrays. In atrial myocardium, we identified 1.434 genes deregulated in atrial fibrillation, the majority of which, including key elements of calcium-dependent signaling pathways, displayed down-regulation. Functional classification based on Gene Ontology provided the specific gene sets of the interdependent processes of structural, contractile and electrophysiological remodeling. In addition, we demonstrate for the first time a prominent up-regulation of transcripts involved in metabolic activities, suggesting an adaptive response to an increased metabolic demand in fibrillating atrial myocardium. Ventricular-predominant genes were five times more likely to be up-regulated in atrial fibrillation (174 genes up-regulated, 35 genes down-regulated), while atrial-specific transcripts were predominantly down-regulated (56 genes up-regulated, 564 genes down-regulated). Overall, in atrial myocardium, functional classes of genes characteristic of ventricular myocardium were found to be up-regulated (e.g. metabolic processes) while functional classes predominantly expressed in atrial myocardium were down-regulated in atrial fibrillation (e.g. signal transduction and cell communication). Therefore, dedifferentiation with adoption of a ventricular-like signature is a general feature of the fibrillating atrium, uncovering the transcriptional response pattern in pmAF (Barth AS et al., Circ Res, 2005). Keywords = human myocardium Keywords = atrial fibrillation Keywords = sinus rhythm Keywords = left ventricular gene expression Keywords: other
2005-05-13 | GSE2240 | GEO
Project description:IntroductionAtrial fibrillation (AF) is associated with an increased risk of stroke, often caused by thrombi that form in the left atrium (LA), and especially in the left atrial appendage (LAA). The underlying mechanism is not fully understood but is thought to be related to stagnant blood flow, which might be present despite sinus rhythm. However, measuring blood flow and stasis in the LAA is challenging due to its small size and low velocities. We aimed to compare the blood flow and stasis in the left atrium of paroxysmal AF patients with controls using computational fluid dynamics (CFD) simulations.MethodsThe CFD simulations were based on time-resolved computed tomography including the patient-specific cardiac motion. The pipeline allowed for analysis of 21 patients with paroxysmal AF and 8 controls. Stasis was estimated by computing the blood residence time.Results and discussionResidence time was elevated in the AF group (p < 0.001). Linear regression analysis revealed that stasis was strongest associated with LA ejection ratio (p < 0.001, R2 = 0.68) and the ratio of LA volume and left ventricular stroke volume (p < 0.001, R2 = 0.81). Stroke risk due to LA thrombi could already be elevated in AF patients during sinus rhythm. In the future, patient specific CFD simulations may add to the assessment of this risk and support diagnosis and treatment.
| S-EPMC10463733 | biostudies-literature
Project description:Atrial fibrillation (AF) is the most prevalent arrhythmia and is associated with increased morbidity and mortality. Its early detection is challenging because of the low detection yield of conventional methods. We aimed to develop a deep learning-based algorithm to identify AF during normal sinus rhythm (NSR) using 12-lead electrocardiogram (ECG) findings. We developed a new deep neural network to detect subtle differences in paroxysmal AF (PAF) during NSR using digital data from standard 12-lead ECGs. Raw digital data of 2,412 12-lead ECGs were analyzed. The artificial intelligence (AI) model showed that the optimal interval to detect subtle changes in PAF was within 0.24 s before the QRS complex in the 12-lead ECG. We allocated the enrolled ECGs to the training, internal validation, and testing datasets in a 7:1:2 ratio. Regarding AF identification, the AI-based algorithm showed the following values in the internal and external validation datasets: area under the receiver operating characteristic curve, 0.79 and 0.75; recall, 82% and 77%; specificity, 78% and 72%; F1 score, 75% and 74%; and overall accuracy, 72.8% and 71.2%, respectively. The deep learning-based algorithm using 12-lead ECG demonstrated high accuracy for detecting AF during NSR.
| S-EPMC8211689 | biostudies-literature
Project description:Studies have suggested that patients with atrial fibrillation (AF) have impairment in the baroreflex. It is not clear whether these findings are the result of the associated comorbid conditions or the arrhythmia itself. We hypothesized that AF is associated with impairment in baroreflex function and that the arrhythmia itself is a contributing factor.Twenty-four patients with persistent AF referred for cardioversion were enrolled. A second group of patients with no history of AF matched for age and left ventricular ejection fraction was identified and served as the control group. In the AF group, baroreflex gain (BRG) was measured on the day of cardioversion (Day 1) and again at 30 days post-cardioversion (Day 30) in patients who remained in sinus rhythm (SR). The clinical characteristics of patients with AF were not different than those of the control group. The mean BRG in the AF group on Day 1 was significantly lower than the mean BRG of the control group (5.2±3.6 versus 10.8±5.5 ms/mm Hg, P<0.05). Ten patients experienced AF recurrence before the 30-day follow-up and 14 patients remained in SR. In the group that remained in SR, BRG increased from 4.1±3.7 ms/mm Hg on Day 1 to 7.0±6.0 ms/mm Hg on Day 30 (P<0.01).We have shown that AF is associated with impairment of the baroreflex and that restoration of SR improves BRG. Our data suggest that AF might be a contributing factor to the observed impairment in BRG and that restoring SR might help improve baroreflex function.
| S-EPMC4802450 | biostudies-other
Project description:BackgroundUltra high-density mapping systems allow for comparison of atrial electroanatomical maps in unprecedented detail. Atrial scar determined by voltages and surface area between atria, rhythm and atrial fibrillation (AF) types was assessed.MethodsLeft (LA) and right atrial (RA) maps were created using Rhythmia HDx in patients listed for ablation for paroxysmal (PAF, sinus rhythm (SR) maps only) or persistent AF (PeAF, AF and SR maps). Electrograms on corresponding SR/AF maps were paired for direct comparison. Percentage surface area of scar was assigned low- (LVM, ≤ 0.05 mV), intermediate- (IVM, 0.05-0.5 mV) or normal voltage myocardium, (NVM, > 0.5 mV).ResultsThirty-eight patients were recruited generating 96 maps using 913,480 electrograms. Paired SR-AF bipolar electrograms showed fair correlation in LA (Spearman's ρ = 0.32) and weak correlation in RA (ρ = 0.19) and were significantly higher in SR in both (LA: 0.61 mV (0.20-1.67) vs 0.31 mV (0.10-0.74), RA: 0.68 mV (0.19-1.88) vs 0.47 mV (0.14-1.07), p < 0.0005 both). Voltages were significantly higher in patients with PAF over PeAF, (LA: 1.13 mV (0.39-2.93) vs 0.52 mV (0.16-1.49); RA: 0.93 mV (0.24-2.46) vs 0.57 mV (0.17-1.69)). Minimal differences were seen in electrogram voltages between atria. Significantly more IVM/LVM surface areas were seen in AF over SR (LA only, p < 0005), and PeAF over PAF (LA: p = 0.01, RA: p = 0.04). There was minimal difference between atria within patients.ConclusionsUltra high-density mapping shows paired electrograms correlate poorly between SR and AF. SR electrograms are typically (but not always) larger than those in AF. Patients with PeAF have a lower global electrogram voltage than those with PAF. Electrogram voltages are similar between atria within individual patients.
| S-EPMC11016007 | biostudies-literature
Project description:Slowly inactivating Na+ channels conducting "late" Na+ current (INa,late) contribute to ventricular arrhythmogenesis under pathological conditions. INa,late was also reported to play a role in chronic atrial fibrillation (AF). The objective of this study was to investigate INa,late in human right atrial cardiomyocytes as a putative drug target for treatment of AF. To activate Na+ channels, cardiomyocytes from transgenic mice which exhibit INa,late (?KPQ), and right atrial cardiomyocytes from patients in sinus rhythm (SR) and AF were voltage clamped at room temperature by 250-ms long test pulses to -30 mV from a holding potential of -80 mV with a 100-ms pre-pulse to -110 mV (protocol I). INa,late at -30 mV was not discernible as deviation from the extrapolated straight line IV-curve between -110 mV and -80 mV in human atrial cells. Therefore, tetrodotoxin (TTX, 10 ?M) was used to define persistent inward current after 250 ms at -30 mV as INa,late. TTX-sensitive current was 0.27±0.06 pA/pF in ventricular cardiomyocytes from ?KPQ mice, and amounted to 0.04±0.01 pA/pF and 0.09±0.02 pA/pF in SR and AF human atrial cardiomyocytes, respectively. With protocol II (holding potential -120 mV, pre-pulse to -80 mV) TTX-sensitive INa,late was always larger than with protocol I. Ranolazine (30 ?M) reduced INa,late by 0.02±0.02 pA/pF in SR and 0.09±0.02 pA/pF in AF cells. At physiological temperature (37°C), however, INa,late became insignificant. Plateau phase and upstroke velocity of action potentials (APs) recorded with sharp microelectrodes in intact human trabeculae were more sensitive to ranolazine in AF than in SR preparations. Sodium channel subunits expression measured with qPCR was high for SCN5A with no difference between SR and AF. Expression of SCN8A and SCN10A was low in general, and lower in AF than in SR. In conclusion, We confirm for the first time a TTX-sensitive current (INa,late) in right atrial cardiomyocytes from SR and AF patients at room temperature, but not at physiological temperature. While our study provides evidence for the presence of INa,late in human atria, the potential of such current as a target for the treatment of AF remains to be demonstrated.
| S-EPMC4485891 | biostudies-literature