REVIEW 3 major objections 5 minor 35 references
[Beat-to-beat AV nodal assessment] ECG-based beat-to-beat assessment of AV node conduction properties during AF
T0 review · 3 major / 5 minor · reviewed 2026-08-06 · deepseek-v4-flash
Pith's one-line read The paper claims that the AV node's fast- and slow-pathway refractory periods and conduction delays can be estimated from surface ECG one heartbeat at a time during atrial fibrillation, with the slow-pathway refractory period recovered…
desk verdict Genuine beat-to-beat AV-node estimation method with honest limitations, but the tilt-test validation is confounded by f-wave changes and the effect sizes sit below the estimator's noise floor; worth reviewing seriously. read the letter →
The pith
A machine-rendered reading of the paper's core claim, the machinery that carries it, and where it could break.
The reading
What carries the argument
The central object is the two-pathway AV node network model: each pathway has ten nodes plus a coupling node, incoming impulses are blocked if the preceding diastolic interval $\tilde t_i(n)$ is negative, and after each conducted impulse node $i$ updates its refractory period $R_i(n) = R_{\min} + \Delta R(1 - e^{-\tilde t_i(n)/\tau_R})$ and its conduction delay $D_i(n) = D_{\min} + \Delta D e^{-\tilde t_i(n)/\tau_D}$. This model is embedded in a particle filter, a sampling-based Bayesian filter whose particles are the twelve model parameters $\theta$; the filter simulates each candidate parameter's ventricular activation times, weights them against the observed RR series, resamples, and propagates with Gaussian noise. Impulses are propagated through the 21-node network with a modified Dijkstra algorithm, an event-based shortest-path routine. A forward filtering backward sampling smoother then draws $M = 20{,}000$ trajectories from the posterior, yielding beat-to-beat distributions of $\phi$. For ECG-only data, the atrial activation series are not known, so 40,000 parameter particles are copied 25 times and each copy is evaluated with a different Gaussian-random-walk atrial activation series derived from the f-wave frequency, which is the mechanism that lets the non-invasive version run.
What would settle it
Record simultaneous surface ECG and direct His-bundle or AV-node electrograms in patients during AF while performing a tilt or drug-induced sympathetic challenge; if the ECG-based beat-to-beat posterior distributions fail to cover the invasively measured refractory-period and conduction-delay changes in roughly 95% of beats, or fail to show the expected shortening under sympathetic stimulation, the claimed feasibility and uncertainty calibration would be refuted.
Extended reading notes
Core claim
The paper claims that AV nodal conduction properties, previously not assessable during atrial fibrillation, can be followed from beat to beat from non-invasive recordings. The authors posit that the AV node behaves as two converging pathways whose ten nodes each recover with an exponential time course set by the preceding diastolic interval, and that a particle filter over the model's twelve parameters, followed by forward filtering backward sampling, can turn an observed RR interval series into full posterior distributions for $\phi$. They report that the most probable estimates track simulated truth best for the slow-pathway refractory period (mean absolute error $67\pm10$ ms, about 6% of its simulated range), are largest for the slow-pathway conduction delay ($178\pm28$ ms, about 16%), and that one-minute averages cut the fast-pathway refractory-period error to about 92 ms. Comparing synchronized EGM and ECG estimates in five patients gave average agreement within 5% for all four properties, and in 21 tilt-test patients head-up tilt significantly decreased $R_{FP}$, $R_{SP}$, and $D_{FP}$, matching the expected effect of sympathetic activation. The conclusion is that beat-to-beat ECG-based estimation is feasible with different, quantifiable uncertainty levels per property.
Load-bearing premise
The whole validation rests on the assumption that a two-pathway network with ten nodes per pathway and exponential recovery dynamics is an adequate description of the real human AV node under atrial fibrillation; if that model is not faithful, the simulated ground truth used to measure accuracy is not the truth the method needs to estimate.
Editorial extensions
If this is right
- The slow-pathway refractory period can be tracked beat-to-beat from surface ECG alone: a mean absolute error of about 67 ms against simulated truth means changes of roughly that size or larger are resolvable at individual beats.
- Fast-pathway refractory period and the two conduction delays are not resolvable beat-to-beat from ECG; one-minute or phase averages are needed, with average errors of about 92 ms for $R_{FP}$ and 90 to 152 ms for the delays.
- Autonomic modulation of the AV node during AF is observable non-invasively at the group level: the tilt protocol shows the expected sympathetic shortening of $R_{FP}$, $R_{SP}$, and $D_{FP}$ from supine to head-up tilt.
- Because ECG-based estimates agree with EGM-based estimates within 5% on average, much of the information available from an intracardiac catheter near the AV node is preserved in the surface ECG.
- The reported 95% credibility regions cover the simulated ground truth in 93–99.8% of beats, so the uncertainty bounds produced by the method are conservative.
Reading between the lines
- If these results transfer to real physiology, beat-to-beat AV node monitoring offers an autonomic nervous system readout during AF, replacing heart rate variability where the sinus node signal is absent; one natural application is titrating rate-control drugs against each patient's AV node response.
- The strong asymmetry in identifiability—slow-pathway refractoriness reliably, fast-pathway refractoriness and both delays noisily—suggests that future clinical studies should choose endpoints accordingly, using $R_{SP}$ for beat-to-beat analyses and one-minute averages for the other properties.
- The largest source of uncertainty in the ECG version is the unobserved atrial activation timing; a model that jointly infers the atrial activation series and $\phi$ instead of sampling Gaussian random walks might substantially shrink the $D_{FP}$ and $D_{SP}$ errors.
- Because the simulated validation is generated from the same model used for estimation, independent invasive validation, such as direct His-bundle measurements during AF or a pharmacological autonomic challenge, would be the decisive next test of whether the estimated quantities correspond to real AV node physiology.
Signed reviews
Editorial analysis
A structured set of objections, weighed in public.
Referee Report
Summary. The manuscript proposes a framework for beat-to-beat estimation of four AV-nodal conduction properties (refractory periods R_FP and R_SP, conduction delays D_FP and D_SP) during atrial fibrillation, combining a two-pathway network model of the AV node (Eqs. 1-3) with a particle filter and forward-filtering backward-sampling smoother. Two variants are presented: EGM-PF, which uses intracardiac EGM-derived atrial activations, and ECG-PF, which synthesizes atrial activation series from f-wave characteristics. The method is evaluated in three steps: against simulated data generated from the same AV-node model, on five patients with synchronized EGM/ECG from the iafdb, and on 21 AF patients undergoing a tilt protocol. The paper reports large mean absolute errors in the simulation study and a statistically significant decrease in R_FP, R_SP, and D_FP from supine to head-up tilt, concluding that beat-to-beat estimation is feasible and agrees with expected autonomic modulation.
Significance. If the estimated quantities corresponded to true physiological AV-nodal properties, the work would be a useful advance: a non-invasive, beat-to-beat readout of AV-nodal modulation would enable new studies of autonomic control during AF and could inform individualized rate-control therapy. The paper's strengths include publicly available model code, a clinically relevant tilt-test dataset, transparent reporting of computational cost, and an honest limitations paragraph. However, the current evidence does not yet establish the physiological validity of the estimates: the simulation ground truth is generated from the same model that the estimator inverts, and the only external validation signal is smaller than the estimator's reported noise floor and is confounded by changes in atrial input. The significance of the contribution therefore depends on whether the manuscript is revised to either supply independent validation or substantially temper its claims.
major comments (3)
- [Section II-E and IV-A] The simulation-based accuracy evaluation is circular with respect to physiological validity. The ground truth phi*(k) is generated by running the same network model (Eqs. 1-3) with the same assumptions used in inference, so the reported l1 errors measure the estimator's ability to invert a known model under synthetic noise rather than its accuracy against true human AV-nodal behavior. The authors acknowledge this in Section IV-A ('only been validated using ground truth data generated from the same AV node model'), but the abstract and conclusion nonetheless present these error values as evidence that ECG-based beat-to-beat estimation is feasible. This is load-bearing: the central claim needs either an external reference (e.g., invasive measurements during a protocol with induced autonomic changes) or at least a model-misspecification sensitivity analysis showing that the estimator remains accurate when the simulated AV node differs from the assumed network structure.
- [Section III-C and Table III] The tilt-test result is confounded by atrial-input changes and lies below the estimator's reported noise floor. The ECG-PF does not measure atrial activations; it generates AA series from f-wave characteristics (Section II-B2), and head-up tilt is expected to change the atrial fibrillatory rate, as the authors themselves note for HDT based on reference [24]. A systematic shift in the generated AA input between supine and HUT could therefore produce the observed decreases in estimated phi even if the true AV-nodal properties were unchanged. Moreover, the mean HUT-vs-supine changes in Table III (-4.7 ms for R_FP, -21.6 ms for R_SP, -4.1 ms for D_FP, +2.0 ms for D_SP) are all smaller than the corresponding ECG-PF one-minute averaged errors in Table I (92.3, 23.6, 89.6, and 152 ms, respectively). The significant Wilcoxon results are thus not sufficient to establish that the estimates track AV-nodal modulation rather than systematic input-related bias. The authors should control for this confound, for example by including the f-wave frequency trend as a covariate, by fixing the input AA statistics across phases, or by validating against EGM-based estimates during tilt.
- [Abstract and Section IV] The abstract's claim that 'beat-to-beat estimation of AV nodal conduction properties during AF from ECG is feasible' is substantially stronger than the paper's own error analysis supports. Section IV states that variations smaller than 169 ms in R_FP, 178 ms in D_FP, and 178 ms in D_SP cannot be identified, and that only R_SP has a beat-to-beat error (67 ms, 6% relative) that may allow detection of typical beat-to-beat changes. The conclusion similarly narrows the feasible claim to 'capturing beat-to-beat changes in the refractory period of the SP.' The central claim should be rephrased to specify which properties are trackable and at what temporal resolution, and the abstract should not present the overall simulation errors as evidence of uniform feasibility.
minor comments (5)
- [Figure 3 caption] The caption lists 'RF P' for all four panels (a)-(d); the last three should be RSP, DFP, and DSP, respectively.
- [Section IV, paragraph on estimation accuracy] The sentence 'reducing its affect on the output' should read 'reducing its effect on the output.'
- [Figure 6 caption] The caption contains a typo: 'following five minues in HDT' should be 'five minutes.'
- [Section II-B2] The choices of the variance factor 4 in the AA-generation model and sigma_alpha = 4 sigma_f are described as empirical, but no sensitivity analysis is provided; the robustness of the ECG-PF estimates to these tuning parameters is therefore not established.
- [Throughout] The inconsistent spacing in 'A V node' (sometimes 'AV node') should be made uniform.
Circularity Check
No circular derivation: simulation validation is a self-consistency test, and the tilt test is independent external evidence, though confounded.
full rationale
The manuscript does not exhibit a circular derivation. The AV-node model (Eqs. 1–3) is stated explicitly, and the particle filter and smoothing algorithm (Algorithms 1–3) are standard Bayesian inference tools that do not receive the simulation ground truth. In the simulation study, ground-truth parameters are chosen, the forward model generates the RR series, and the estimator then attempts to recover the parameters from the observed RR and AA inputs; this is a conventional identifiability and accuracy test, not a renaming of fitted values as predictions. The paper's own limitation statement in Section IV-A ('The estimated AV node properties have only been validated using ground truth data generated from the same AV node model') correctly identifies the scope as external validity, not circularity: the estimator could fail even when the forward model is exactly correct, and here it does fail to various degrees. The tilt-test analysis uses independent patient data and an external physiological expectation (sympathetic activation shortens refractory periods and conduction delays), so it provides independent, although imperfect, evidence. The acknowledged confound that RR changes across tilt phases may reflect atrial-rate changes (Discussion) is a correctness and interpretation concern, not a circular step, because the estimator is not fitted to the tilt outcome and no output is defined in terms of the tilt label. The self-citations to the authors' prior model [15] are normal references to an explicitly re-stated modeling framework, not a load-bearing uniqueness theorem or a hidden ansatz imported by citation. No fitted parameter is relabeled as a prediction, and no equation reduces to its own input by construction. The reported uncertainties are large, but large error bars are a performance limitation, not evidence of circularity.
Assumptions & free parameters
free parameters (4)
- sigma_w (R-peak detection noise standard deviation) =
30 ms
- Propagation noise covariance Sigma =
Not specified in main text; see Supplementary S2
- AA series variance factor 4 =
4
- Mode histogram bin width =
5 ms
assumptions (6)
- domain assumption The AV node is represented as two pathways, each of 10 nodes plus a coupling node, with no other conduction routes (Eqs. 1-3).
- domain assumption Refractory period and conduction delay for each node obey exponential recovery and dependence on diastolic interval (Eqs. 1-3).
- domain assumption For ECG-only analysis, atrial activation time series can be approximated by a Gaussian random walk with mean drawn from inverse f-wave frequency and variance depending on signal quality.
- domain assumption Model parameters theta are fixed between heartbeats and evolve as a random walk with covariance Sigma.
- domain assumption Head-up tilt increases sympathetic activity and decreases AV nodal refractory periods and conduction delays.
- ad hoc to paper The simulation setup (50 parameter trends generated from the model) produces realistic AA and RR series representative of human AF.
Cite this review
Pith. "Pith review of [Beat-to-beat AV nodal assessment] ECG-based beat-to-beat assessment of AV node conduction properties during AF." pith.science (2026). https://pith.science/paper/6BXOGMI2
@misc{pith2026250619427,
author = {Pith},
title = {Pith review of: [Beat-to-beat AV nodal assessment] ECG-based beat-to-beat assessment of AV node conduction properties during AF},
year = {2026},
howpublished = {\url{https://pith.science/paper/6BXOGMI2}},
note = {Machine review of arXiv:2506.19427}
}
abstract
The refractory period and conduction delay of the atrioventricular (AV) node play a crucial role in regulating the heart rate during atrial fibrillation (AF). Beat-to-beat variations in these properties are known to be induced by the autonomic nervous system (ANS) but have previously not been assessable during AF. Assessing these could provide novel information for improved diagnosis, prognosis, and treatment on an individual basis. To estimate AV nodal conduction properties with beat-to-beat resolution, we propose a methodology comprising a network model of the AV node, a particle filter, and a smoothing algorithm. The methodology was evaluated using simulated data and using synchronized electrogram (EGM) and ECG recordings from five patients in the intracardiac atrial fibrillation database. The methodology's ability to quantify ANS-induced changes in AV node conduction properties was evaluated by analyzing ECG data from 21 patients in AF undergoing a tilt test protocol. The estimated refractory period and conduction delay matched the simulated ground truth based on ECG recordings with a mean absolute error ($\pm$ std) of 169$\pm$14 ms for the refractory period in the fast pathway; 131$\pm$13 ms for the conduction delay in the fast pathway; 67$\pm$10 ms for the refractory period in the slow pathway; and 178$\pm$28 ms for the conduction delay in the slow pathway. These errors decreased when using simulated ground truth based on EGM recordings. Moreover, a decrease in conduction delay and refractory period in response to head-up tilt was seen during the tilt test protocol, as expected under sympathetic activation. These results suggest that beat-to-beat estimation of AV nodal conduction properties during AF from ECG is feasible, with different levels of uncertainty, and that the estimated properties agree with expected AV nodal modulation.
Figures
Figures from the paper (4 more)
Reference graph
Works this paper leans on
-
[24]
Autonomic influence on atrial fibrillatory process: head-up and head-down tilting,
S. ¨Ostenson, V . D. Corino, J. Carlsson, and P. G. Platonov, “Autonomic influence on atrial fibrillatory process: head-up and head-down tilting,” Annals of Noninvasive Electrocardiology, vol. 22, no. 2, p. e12405, 2017
work page 2017
-
[1]
Heart disease and stroke statistics-2019 update a report from the american heart association,
E. J. Benjamin, P. Muntner, A. Alonso, M. S. Bittencourt, C. W. Callaway, A. P. Carson, A. M. Chamberlain, A. R. Chang, S. Cheng, S. R. Das et al., “Heart disease and stroke statistics-2019 update a report from the american heart association,” Circulation, 2019
work page 2019
-
[2]
N. E. Andrew, A. G. Thrift, and D. A. Cadilhac, “The prevalence, impact and economic implications of atrial fibrillation in stroke: what progress has been made?” Neuroepidemiology, vol. 40, no. 4, pp. 227–239, 2013
work page 2013
-
[3]
G. Hindricks, T. Potpara, N. Dagres, E. Arbelo, J. J. Bax, C. Blomstr ¨om-Lundqvist, G. Boriani, M. Castella, G.-A. Dan, P. E. Dilaveris et al., “2020 ESC guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the european association of cardio- thoracic surgery (EACTS),” Am. J. Physiol. Heart Circ. Physiol., 2020
work page 2020
-
[4]
Rate-and rhythm- control therapies in patients with atrial fibrillation: a systematic review,
S. M. Al-Khatib, N. M. Allen LaPointe, R. Chatterjee, M. J. Crowley, M. E. Dupre, D. F. Kong, R. D. Lopes, T. J. Povsic, S. S. Raju, B. Shah et al., “Rate-and rhythm- control therapies in patients with atrial fibrillation: a systematic review,” Annals of internal medicine, vol. 160, no. 11, pp. 760–773, 2014
work page 2014
-
[5]
Anatomy and electrophysiology of the human av node,
T. Kurian, C. Ambrosi, W. Hucker, V . V . Fedorov, and I. R. Efimov, “Anatomy and electrophysiology of the human av node,” Pacing and clinical electrophysiology, vol. 33, no. 6, pp. 754–762, 2010
work page 2010
-
[6]
Role of the autonomic nervous system in modulating cardiac arrhythmias,
M. J. Shen and D. P. Zipes, “Role of the autonomic nervous system in modulating cardiac arrhythmias,” Circulation research, vol. 114, no. 6, pp. 1004–1021, 2014
work page 2014
-
[7]
An overview of heart rate variability metrics and norms,
F. Shaffer and J. P. Ginsberg, “An overview of heart rate variability metrics and norms,” Frontiers in public health, vol. 5, p. 290215, 2017
work page 2017
Show all 35 references
-
[8]
A mathematical model of human atrioventricular nodal function incorporating concealed conduction,
P. Jørgensen, C. Sch ¨afer, P. G. Guerra, M. Talajic, S. Nattel, and L. Glass, “A mathematical model of human atrioventricular nodal function incorporating concealed conduction,” Bull. Math. Biol., vol. 64, no. 6, pp. 1083– 1099, 2002
2002
-
[9]
Effects of antiarrhythmic drug therapy on atrioventricular nodal func- tion during atrial fibrillation in humans,
L. Mangin, A. Vinet, P. Pag ´e, and L. Glass, “Effects of antiarrhythmic drug therapy on atrioventricular nodal func- tion during atrial fibrillation in humans,” EP Europace, vol. 7, no. s2, pp. S71–S82, 2005
2005
-
[10]
One- dimensional mathematical model of the atrioventricular node including atrio-nodal, nodal, and nodal-his cells,
S. Inada, J. Hancox, H. Zhang, and M. Boyett, “One- dimensional mathematical model of the atrioventricular node including atrio-nodal, nodal, and nodal-his cells,” Biophysical journal, vol. 97, no. 8, pp. 2117–2127, 2009
2009
-
[11]
Functional mathematical model of dual pathway A V nodal conduction,
A. M. Climent, M. S. Guillem, Y . Zhang, J. Millet, and T. Mazgalev, “Functional mathematical model of dual pathway A V nodal conduction,” Am. J. Physiol. Heart Circ. Physiol., vol. 300, no. 4, pp. H1393–H1401, 2011
2011
-
[12]
Dynamics of av coupling during human atrial fibrillation: role of atrial rate,
M. Mas `e, M. Marini, M. Disertori, and F. Ravelli, “Dynamics of av coupling during human atrial fibrillation: role of atrial rate,” American Journal of Physiology-Heart and Circulatory Physiology, vol. 309, no. 1, pp. H198– H205, 2015
2015
-
[13]
A statistical atrioventricular node model accounting for pathway switching during atrial fibrillation,
M. Henriksson, V . D. Corino, L. S¨ornmo, and F. Sandberg, “A statistical atrioventricular node model accounting for pathway switching during atrial fibrillation,” IEEE Trans Biomed Eng, vol. 63, no. 9, pp. 1842–1849, 2015
2015
-
[14]
A compact multi-functional model of the rabbit atrioventricular node with dual pathways,
M. Ryzhii and E. Ryzhii, “A compact multi-functional model of the rabbit atrioventricular node with dual pathways,” Frontiers in Physiology, vol. 14, p. 353, 2023
2023
-
[15]
Non-invasive characterization of human A V-nodal conduction delay and refractory period during atrial fibrillation,
M. Karlsson, F. Sandberg, S. R. Ulimoen, and M. Wall- man, “Non-invasive characterization of human A V-nodal conduction delay and refractory period during atrial fibrillation,” Front. Physiol., p. 1849, 2021
2021
-
[16]
ECG based assessment of circadian variation in A V-nodal conduction during AF – influence of rate control drugs,
M. Karlsson, M. Wallman, P. G. Platonov, S. R. Ulimoen, and F. Sandberg, “ECG based assessment of circadian variation in A V-nodal conduction during AF – influence of rate control drugs,” Frontiers in Physiology, p. 2015, 2022
2015
-
[17]
Model-based estimation of av-nodal refractory period and conduction delay trends from ECG,
M. Karlsson, P. G. Platonov, S. R. Ulimoen, F. Sandberg, and M. Wallman, “Model-based estimation of av-nodal refractory period and conduction delay trends from ECG,” Frontiers in Physiology, vol. 14, p. 1287365, 2024
2024
-
[18]
Rate-related and autonomic effects on atrioventricular conduction assessed through beat-to-beat pr interval and cycle length variability,
C. T. Leffler, J. P. Saul, and R. J. Cohen, “Rate-related and autonomic effects on atrioventricular conduction assessed through beat-to-beat pr interval and cycle length variability,” Journal of cardiovascular electrophysiology, vol. 5, no. 1, pp. 2–15, 1994
1994
-
[19]
Atrial flutter and atrial tachycardia detection using bayesian approach with high resolution time–frequency spectrum from ECG recordings,
J. Lee, D. D. McManus, P. Bourrell, L. S ¨ornmo, and K. H. Chon, “Atrial flutter and atrial tachycardia detection using bayesian approach with high resolution time–frequency spectrum from ECG recordings,” Biomedical Signal Processing and Control, vol. 8, no. 6, pp. 992–999, 2013
2013
-
[20]
Particle filtering and sensor fusion for robust heart rate monitoring using wearable sen- sors,
V . Nathan and R. Jafari, “Particle filtering and sensor fusion for robust heart rate monitoring using wearable sen- sors,” IEEE journal of biomedical and health informatics, vol. 22, no. 6, pp. 1834–1846, 2017
2017
-
[21]
Automated annotation and quantitative description of ultrasound videos of the fetal heart,
C. P. Bridge, C. Ioannou, and J. A. Noble, “Automated annotation and quantitative description of ultrasound videos of the fetal heart,” Medical image analysis, vol. 36, pp. 147–161, 2017
2017
-
[22]
Chopin, O
N. Chopin, O. Papaspiliopoulos et al., An introduction to sequential Monte Carlo. Springer, 2020, vol. 4
2020
-
[23]
Physiobank, physiotoolkit, and physionet: Components of a new research resource for complex physiologic signals,
A. L. Goldberger, L. A. Amaral, L. Glass, J. M. Hausdorff, P. C. Ivanov, R. G. Mark, J. E. Mietus, G. B. Moody, C.- K. Peng, and H. E. Stanley, “Physiobank, physiotoolkit, and physionet: Components of a new research resource for complex physiologic signals,” Circulation [Onlin...
2000
-
[25]
Iterative method to detect atrial activations and measure cycle length from electrograms during atrial fibrillation,
J. Ng, V . Sehgal, J. K. Ng, D. Gordon, and J. J. Goldberger, “Iterative method to detect atrial activations and measure cycle length from electrograms during atrial fibrillation,” IEEE Transactions on Biomedical Engineering, vol. 61, no. 2, pp. 273–278, 2013
2013
-
[26]
Detection of atrial activity from high-voltage leads of implantable ventricular defibrillators using a cancellation technique,
S. Shkurovich, A. V . Sahakian, and S. Swiryn, “Detection of atrial activity from high-voltage leads of implantable ventricular defibrillators using a cancellation technique,” IEEE Transactions on Biomedical Engineering, vol. 45, no. 2, pp. 229–234, 1998
1998
-
[27]
A technique for measurement of the extent of spatial organization of atrial activation during atrial fibrillation in the intact human heart,
G. W. Botteron and J. M. Smith, “A technique for measurement of the extent of spatial organization of atrial activation during atrial fibrillation in the intact human heart,” IEEE transactions on biomedical engineering, vol. 42, no. 6, pp. 579–586, 1995
1995
-
[28]
Model-based assessment of f-wave signal quality in patients with atrial fibrillation,
M. Henriksson, A. Petr ˙enas, V . Marozas, F. Sandberg, and L. S ¨ornmo, “Model-based assessment of f-wave signal quality in patients with atrial fibrillation,” IEEE Transactions on Biomedical Engineering, vol. 65, no. 11, pp. 2600–2611, 2018
2018
-
[29]
A subspace projection approach to quantify respiratory variations in the f-wave frequency trend,
M. Abdollahpur, G. Engstr ¨om, P. G. Platonov, and F. Sandberg, “A subspace projection approach to quantify respiratory variations in the f-wave frequency trend,” Frontiers in Physiology, vol. 13, p. 976925, 2022
2022
-
[30]
Characterisation of human A V-nodal properties using a network model,
M. Wallman and F. Sandberg, “Characterisation of human A V-nodal properties using a network model,” Med Biol Eng, vol. 56, no. 2, pp. 247–259, 2018
2018
-
[31]
Demonstration of dual av nodal pathways in patients with paroxysmal supraventricular tachycardia,
P. Denes, D. Wu, R. C. Dhingra, R. Chuquimia, and K. M. Rosen, “Demonstration of dual av nodal pathways in patients with paroxysmal supraventricular tachycardia,” Circulation, vol. 48, no. 3, pp. 549–555, 1973
1973
-
[32]
Characterization of atrioventricular nodal behavior and ventricular response during atrial fibrillation before and after a selective slow- pathway ablation,
Z. Blanck, A. A. Dhala, J. Sra, S. S. Deshpande, A. J. An- derson, M. Akhtar, and M. R. Jazayeri, “Characterization of atrioventricular nodal behavior and ventricular response during atrial fibrillation before and after a selective slow- pathway ablation,” Circulation, vol. 91...
1995
-
[33]
Tilt test: a review,
L. Aponte-Becerra and P. Novak, “Tilt test: a review,” Journal of Clinical Neurophysiology, vol. 38, no. 4, pp. 279–286, 2021
2021
-
[34]
An atrioventricular node model incorporating autonomic tone,
F. Plappert, M. Wallman, M. Abdollahpur, P. G. Platonov, S. ¨Ostenson, and F. Sandberg, “An atrioventricular node model incorporating autonomic tone,” Frontiers in Physiology, p. 1814, 2022
2022
-
[35]
Role of the atrial rate as a factor modulating ventricular response during atrial fib- rillation,
A. M. Climent, M. S. Guillem, D. Husser, F. Castells, J. Millet, and A. Bollmann, “Role of the atrial rate as a factor modulating ventricular response during atrial fib- rillation,” Pacing and clinical electrophysiology, vol. 33, no. 12, pp. 1510–1517, 2010
2010
Reviewed August 6, 2026 · model on record in the stance chip above.
Discussion (0). Continue with ORCID to comment.