Non-invasive Characterization of Human AV-Nodal Conduction Delay and Refractory Period During Atrial Fibrillation
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SUBMITTER: Karlsson M
PROVIDER: S-EPMC8584495 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Atrial fibrillation (AF) resumes within 90 s in 27% of patients after sinus rhythm (SR) restoration. The aim of this study is to compare conduction heterogeneity during the supervulnerable period immediately after electrical cardioversion (ECV) with long-term SR in patients with AF. Epicardial mapping of both atria was performed during SR and premature atrial extrasystoles in patients in the ECV (N = 17, age: 73 ± 7 years) and control group (N = 17, age: 71 ± 6 years). Inter-electrode conduction times were used to identify areas of conduction delay (CD) (conduction times 7-11 ms) and conduction block (CB) (conduction times ≥ 12 ms). For all atrial regions, prevalences and length of longest CB and continuous CDCB lines, magnitude of conduction disorders, conduction velocity, biatrial activation time, and voltages did not differ between the ECV and control group during both SR and premature atrial extrasystoles (p ≥ 0.05). Hence, our data suggest that there may be no difference in biatrial conduction characteristics between the supervulnerable period after ECV and long-term SR in AF patients. The supervulnerable period after AF termination is not determined by conduction heterogeneity during SR and PACs. It is unknown to what extent intra-atrial conduction is impaired during the supervulnerable period immediately after ECV and whether different right and left atrial regions are equally affected. This high-resolution epicardial mapping study (upper left panel) of both atria shows that during SR the prevalences and length of longest CB and cCDCB lines (upper middle panel), magnitude of conduction disorders, CV and TAT (lower left panel), and voltages did not differ between the ECV and control group. Likewise, these parameters were comparable during PACs between the ECV and control group (lower left panel). †Non-normally distributed. cm/s = centimeters per second; mm = millimeter; ms = millisecond; AF = atrial fibrillation; AT = activation time; BB = Bachmann's bundle; cCDCB = continuous lines of conduction delay and block; CB = conduction block; CD = conduction delay; CT = conduction time; CV = conduction velocity; ECV = electrical cardioversion; LA = left atrium; LAT = local activation times; PAC = premature atrial complexes; PVA = pulmonary vein area; RA = right atrium; SR = sinus rhythm; TAT = total activation time.
| S-EPMC9988743 | biostudies-literature
Project description:PurposePR interval prolongation > 200 ms resulting in the diagnosis of first-degree atrioventricular block (AVB1) is caused by a delay in the AV nodal/His conduction and/or the right intra-atrial conduction (RIAC). The aim of the study was to assess the prevalence of AVB1 due to RIAC delay (AVB1 with normal AH and HV) in patients with atrial fibrillation (AF) and atrial flutter (AFlu).MethodsWe included 1067 consecutive patients (33% female, age 63 ± 13 years) referred for catheter ablation of AF (AF-group) (453 patients), AF and AFlu (136 patients), AFlu (292 patients), and AVNRT/AVRT (186 patients). AH-, HV-, PR-interval, and P-wave duration were measured on the 12-lead ECG and the intracardiac electrograms in sinus rhythm. RIAC delay was defined as a prolonged PR interval > 200 ms with normal AH and HV intervals.ResultsThe prevalence of AVB1 is higher in patients with AFlu (41%) and AF (21%) and patients with both arrhythmias (30%) as compared with a reference group (8%) of patients with AVNRT/AVRT. AVB1 was due to RIAC delay in 42 of 67 patients (63%) in the AF-group, in 37 of 96 patients (39%) in the AFlu-group, and in 17 of 36 patients (47%) in the AF/AFlu group, respectively. AV nodal conduction delay was more common in AFlu patients compared with AF patients.ConclusionRIAC delay is a common underlying cause of AVB1 in patients with AF and AFlu. These findings may impact the prescription of antiarrhythmic and AV-nodal blocking drugs.
| S-EPMC8324594 | biostudies-literature
Project description:ObjectivesThis study sought to characterize direction-dependent and coupling interval-dependent changes in left atrial conduction and electrogram morphology in uniformly classified patients with paroxysmal atrial fibrillation (AF) and normal bipolar voltage mapping.BackgroundAlthough AF classifications are based on arrhythmia duration, the clinical course, and treatment response vary between patients within these groups. Electrophysiological mechanisms responsible for this variability are incompletely described.MethodsIntracardiac contact mapping during incremental atrial pacing was used to characterize atrial conduction, activation dispersion, and electrogram morphology in 15 consecutive paroxysmal AF patients undergoing first-time pulmonary vein isolation. Outcome measures were vulnerability to AF induction at electrophysiology study and 2-year follow-up for arrhythmia recurrence.ResultsConduction delay showed a bimodal distribution, occurring at either long (high right atrium pacing: 326 ± 13 ms; coronary sinus pacing: 319 ± 16 ms) or short (high right atrium pacing: 275 ± 11 ms; coronary sinus pacing: 271 ± 11 ms) extrastimulus coupling intervals. Arrhythmia recurrence was found only in patients with conduction delay at long extrastimulus coupling intervals, and patients with inducible AF were characterized by increased activation dispersion (activation dispersion time: 168 ± 29 ms vs. 136 ± 11 ms). Electrogram voltage and duration varied throughout the left atrium, between patients, and with pacing site but were not correlated with AF vulnerability or arrhythmia recurrence.ConclusionsWithin the single clinical entity of paroxysmal AF, incremental atrial pacing identified a spectrum of activation patterns correlating with AF vulnerability and arrhythmia recurrence. In contrast, electrogram morphology (characterized by electrogram voltage and duration) was highly variable and not associated with AF vulnerability or recurrence. An improved understanding of the electrical phenotype in AF could lead to improved mechanistic classifications.
| S-EPMC5612260 | biostudies-literature
Project description:BACKGROUND:We aimed to elucidate the long-term prognosis of nonspecific intraventricular conduction delay (NIVCD) in patients with structurally normal heart. METHODS:We included 107,838 patients (age, 52.1?±?15.5 years; men, 46.8%) who underwent electrocardiography in outpatient clinics or medical checkup (unmatched cohort). NIVCD was defined as QRS duration ?110?ms without meeting the criteria for bundle branch block. Patients with structurally normal heart and sinus rhythm were assigned to the NIVCD and normal QRS groups according to propensity score with matching variables of age, sex, hypertension, and diabetes (matched cohort 1), and additional PR interval (matched cohort 2). Baseline characteristics, electrocardiographic parameters, and clinical outcomes were compared in the unmatched cohort and the matched cohort. RESULTS:In the unmatched cohort, the frequencies of male sex and preexisting atrial fibrillation were significantly higher in the NIVCD group than in the normal QRS group. In matched cohort 1 (n?=?690), the NIVCD group exhibited significant slower sinus rate and longer PR interval than the normal QRS group. In matched cohort 2 (n?=?598), the cumulative incidence of atrial fibrillation was significantly higher in the NIVCD group than in the normal QRS group during a follow-up period of 8.8?±?2.9 years. NIVCD significantly increased the risk for AF (hazard ratio, 2.571; 95% confidence interval, 1.074-6.156; p?=?0.034). CONCLUSIONS:It is suggested that NIVCD may be associated with future occurrence of atrial fibrillation in patients with structurally normal heart and sinus rhythm.
| S-EPMC7190503 | biostudies-literature
Project description:Background and objective: Prevalence of atrial fibrillation is higher in hemodialysis patients as compared to the general population. Atrial electromechanical delay is known as a significant predictor of atrial fibrillation. In this study, we aimed to reveal the relationship between atrial electromechanical delay and attacks of atrial fibrillation. Materials and methods: The study included 77 hemodialysis patients over 18 years of age giving written consent to participate in the study. The patients were divided into two groups based on the results of 24-h Holter Electrocardiogram (Holter ECG) as the ones having attacks of atrial fibrillation and the others without any attack of atrial fibrillation. Standard echocardiographic measurements were taken from all patients. Additionally, atrial conduction times were measured by tissue Doppler technique and atrial electromechanical delays were calculated. Results: Intra- and interatrial electromechanical delay were found as significantly lengthened in the group of patients with attacks of atrial fibrillation (p = 0.03 and p < 0.001 respectively). The optimal cut-off time for interatrial electromechanical delay to predict atrial fibrillation was >21 ms with a specificity of 79.3% and a sensitivity of 73.7% (area under the curve 0.820; 95% confidence interval (CI), 0.716?0.898). In the multivariate logistic regression model, interatrial electromechanical delay (odds ratio = 1.230; 95% CI, 1.104?1.370; p < 0.001) and hypertension (odds ratio = 4.525; 95% CI, 1.042?19.651; p = 0.044) were also associated with atrial fibrillation after adjustment for variables found to be statistically significant in univariate analysis and correlated with interatrial electromechanical delay. Conclusions: Interatrial electromechanical delay is independently related with the attacks of atrial fibrillation detected on Holter ECG records in hemodialysis patients.
| S-EPMC6174336 | biostudies-other
Project description:Previous studies have shown an association between elevated atrial NADPH-dependent oxidative stress and decreased plasma apelin in patients with atrial fibrillation (AF), though the basis for this relationship is unclear. In the current study, RT-PCR and immunofluorescence studies of human right atrial appendages (RAAs) showed expression of the apelin receptor, APJ, and reduced apelin content in the atria, but not in plasma, of patients with AF versus normal sinus rhythm. Disruption of the apelin gene in mice increased (2.4-fold) NADPH-stimulated superoxide levels and slowed atrial conduction velocities in optical mapping of a Langendorff-perfused isolated heart model, suggesting that apelin levels may influence AF vulnerability. Indeed, in mice with increased AF vulnerability (induced by chronic intense exercise), apelin administration reduced the incidence and duration of induced atrial arrhythmias in association with prolonged atrial refractory periods. Moreover, apelin decreased AF induction in isolated atria from exercised mice while accelerating conduction velocity and increasing action potential durations. At the cellular level, these changes were associated with increased atrial cardiomyocyte sodium currents. These findings support the conclusion that reduced atrial apelin is maladaptive in fibrillating human atrial myocardium and that increasing apelin bioavailability may be a worthwhile therapeutic strategy for treating and preventing AF.
| S-EPMC7526452 | biostudies-literature
Project description:Atrial fibrillation is a challenging pathologic process. There continues to be a great need for the development of a reproducible, durable cure when medical management has failed. An effective, minimally invasive, sternal-sparing intervention without the need for cardiopulmonary bypass is a promising treatment approach. In this article, we describe a hybrid technique being refined at our center that combines a thoracoscopic epicardial surgical approach with an endocardial catheter-based procedure. We also discuss our results and review the literature describing this unique treatment approach.
| S-EPMC4847967 | biostudies-other
Project description:Several lines of evidence have suggested that maintenance of atrial fibrillation (AF) depends on reentrant mechanisms. Maintenance of reentry necessitates a sufficiently short refractory period and/or delayed conduction, and AF has been associated with both alterations. Fibrosis, cellular dysfunction, and gap junction protein alterations occur in AF and cause conduction delay. We performed this study to test the hypothesis that gap junction protein overexpression would improve conduction and prevent AF.Thirty Yorkshire swine were randomized into 2 groups (sinus rhythm and AF), and each group into 3 subgroups: sham-operated control, gene therapy with adenovirus expressing connexin (Cx) 40, and gene therapy with adenovirus expressing Cx43 (n=5 per subgroup). All animals had epicardial gene painting; the AF group had burst atrial pacing. All animals underwent terminal study 7 days after gene transfer. Sinus rhythm animals had strong transgene expression but no atrial conduction changes. In AF animals, controls had reduced and lateralized Cx43 expression, and Cx43 gene transfer restored expression and cellular location to sinus rhythm control levels. In the AF group, both Cx40 and Cx43 gene transfer improved conduction and reduced AF relative to controls.Connexin gene therapy preserved atrial conduction and prevented AF.
| S-EPMC3260348 | biostudies-literature
Project description:BackgroundConduction velocity (CV) heterogeneity and myocardial fibrosis both promote re-entry, but the relationship between fibrosis as determined by left atrial (LA) late-gadolinium enhanced cardiac magnetic resonance imaging (LGE-CMRI) and CV remains uncertain.ObjectiveAlthough average CV has been shown to correlate with regional LGE-CMRI in patients with persistent AF, we test the hypothesis that a localized relationship exists to underpin LGE-CMRI as a minimally invasive tool to map myocardial conduction properties for risk stratification and treatment guidance.Method3D LA electroanatomic maps during LA pacing were acquired from eight patients with persistent AF following electrical cardioversion. Local CVs were computed using triads of concurrently acquired electrograms and were co-registered to allow correlation with LA wall intensities obtained from LGE-CMRI, quantified using normalized intensity (NI) and image intensity ratio (IIR). Association was evaluated using multilevel linear regression.ResultsAn association between CV and LGE-CMRI intensity was observed at scales comparable to the size of a mapping electrode: -0.11 m/s per unit increase in NI (P < 0.001) and -0.96 m/s per unit increase in IIR (P < 0.001). The magnitude of this change decreased with larger measurement area. Reproducibility of the association was observed with NI, but not with IIR.ConclusionAt clinically relevant spatial scales, comparable to area of a mapping catheter electrode, LGE-CMRI correlates with CV. Measurement scale is important in accurately quantifying the association of CV and LGE-CMRI intensity. Importantly, NI, but not IIR, accounts for changes in the dynamic range of CMRI and enables quantitative reproducibility of the association.
| S-EPMC7693630 | biostudies-literature
Project description:BackgroundControversy exists regarding how atrial activation mode and heart rate affect optimal atrioventricular (AV) delay in cardiac resynchronization therapy. We studied these questions using high-reproducibility hemodynamic and echocardiographic measurements.MethodsTwenty patients were hemodynamically optimized using noninvasive beat-to-beat blood pressure at rest (62 ± 11 beats/min), during exercise (80 ± 6 beats/min), and at three atrially paced rates: 5, 25, and 45 beats/min above rest, denoted as Apaced,r+5 , Apaced,r+25 , and Apaced,r+45 , respectively. Left atrial myocardial motion and transmitral flow were timed echocardiographically.ResultsDuring atrial sensing, raising heart rate shortened optimal AV delay by 25 ± 6 ms (P < 0.001). During atrial pacing, raising heart rate from Apaced,r+5 to Apaced,r+25 shortened it by 16 ± 6 ms; Apaced,r+45 shortened it 17 ± 6 ms further (P < 0.001). In comparison to atrial-sensed activation, atrial pacing lengthened optimal AV delay by 76 ± 6 ms (P < 0.0001) at rest, and at ?20 beats/min faster, by 85 ± 7 ms (P < 0.0001), 9 ± 4 ms more (P = 0.017). Mechanically, atrial pacing delayed left atrial contraction by 63 ± 5 ms at rest and by 73 ± 5 ms (i.e., by 10 ± 5 ms more, P < 0.05) at ?20 beats/min faster. Raising atrial rate by exercise advanced left atrial contraction by 7 ± 2 ms (P = 0.001). Raising it by atrial pacing did not (P = 0.2).ConclusionsHemodynamic optimal AV delay shortens with elevation of heart rate. It lengthens on switching from atrial-sensed to atrial-paced at the same rate, and echocardiography shows this sensed-paced difference in optima results from a sensed-paced difference in atrial electromechanical delay. The reason for the widening of the sensed-paced difference in AV optimum may be physiological stimuli (e.g., adrenergic drive) advancing left atrial contraction during exercise but not with fast atrial pacing.
| S-EPMC6099378 | biostudies-literature