Peak-to-Peak Voltage Mapping Reveals Dynamic Arrhythmogenic Substrate Behavior in Isolated Rabbit Hearts

Q: What are the key findings of this study?

Induced ventricular tachycardia significantly reduced median peak-to-peak epicardial voltage amplitudes by 21.68 mV compared to sinus rhythm in isolated rabbit hearts.

Q: What is the clinical evidence from this study?

Population: Cardiac arrhythmias (n=9). Intervention: Induced arrhythmias (AT, VT, VF) vs. Sinus rhythm. Primary outcome: Peak-to-peak amplitude during ventricular tachycardia (VT) vs sinus rhythm (SR) (Median paired difference 21.68 mV, 95% CI 20.60-23.38, p=<0.0001).

Q: What does this research mean for the field?

Cardiac arrhythmias significantly reduce epicardial peak-to-peak electrogram amplitudes compared to sinus rhythm, generating both dynamic rhythm-dependent and spatially persistent low-voltage substrate areas in isolated rabbit hearts. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To establish chamber-specific epicardial voltage thresholds for healthy tissue and characterize dynamic arrhythmogenic substrate behavior during tachyarrhythmias in isolated rabbit hearts.

José Gomes; Vinicius Silva; Tainan Neves; Jimena Siles; João Loures Salinet

doi:10.1007/s10439-026-04382-5

September 26, 2026Annals of Biomedical EngineeringOpen Access

Peak-to-Peak Voltage Mapping Reveals Dynamic Arrhythmogenic Substrate Behavior in Isolated Rabbit Hearts

View Full Paper

Ask AI

Bookmark

Share

Key result

Induced VT reduces epicardial voltage amplitudes by ~73% versus SR in isolated rabbit hearts.

Median paired difference −21.68 mV
95% CI 20.60-23.38
P<0.0001
n=9

Key Points

To establish chamber-specific epicardial voltage thresholds for healthy tissue and characterize dynamic arrhythmogenic substrate behavior during tachyarrhythmias in isolated rabbit hearts.
Perfused isolated New Zealand White rabbit hearts (n = 9) in a Langendorff system.
Acquired epicardial unipolar and derived bipolar electrograms from the right atrium (RA), left atrium (LA), and ventricular epicardium (V) using custom multi-electrode arrays.
Established healthy tissue thresholds using the 95th percentile during sinus rhythm (SR) and assessed voltage alterations during induced atrial tachycardia (AT), ventricular tachycardia (VT), and ventricular fibrillation (VF).
Healthy 95th percentile unipolar voltage cut-offs were 7.4 mV (RA), 8.9 mV (LA), and 17.4 mV (V), while bipolar cut-offs were 4.1 mV (RA), 5.7 mV (LA), and 9.5 mV (V).
Ventricular peak-to-peak amplitude dropped from 31.0 mV in SR to 8.3 mV in VT (p < 0.0001; median paired difference 21.68 mV, 95% CI 20.60 to 23.38 mV) and from 23.6 mV in SR to 4.8 mV in VF (p < 0.0001; median paired difference 15.95 mV, 95% CI 15.01 to 17.30 mV).
Atrial peak-to-peak amplitude declined during AT from 18.2 mV to 16.1 mV in RA (p < 0.001; median paired difference 2.95 mV, 95% CI 1.37 to 3.91 mV) and from 28.2 mV to 9.9 mV in LA (p < 0.0001; median paired difference 15.94 mV, 95% CI 14.97 to 17.82 mV).

Structured PICO

P

Population

9 isolated New Zealand White rabbit hearts (aged 2-3 years) were perfused ex vivo to establish epicardial voltage thresholds and investigate arrhythmogenic substrate dynamics.

I

Intervention

Induced atrial tachycardia (AT), ventricular tachycardia (VT), and ventricular fibrillation (VF) via programmed electrical stimulation.

C

Comparator

Baseline sinus rhythm (SR) in the same hearts.

O

Outcome

Chamber-specific epicardial voltage thresholds and peak-to-peak amplitude variability across different rhythms.surrogate

Main Result

Mean Difference: 21.68 (95% CI 20.6–23.38)

Absolute Event Rate: 8.3% vs 31%

p-value: p=<0.0001

Limitations

Arrhythmias investigated involved distinct electrophysiological mechanisms and were analyzed in different cardiac chambers, limiting direct comparisons.
Analyses during induced arrhythmias were obtained in the continuous presence of blebbistatin, carbachol, and pinacidil, which may influence conduction and EGM amplitudes.
Proposed voltage thresholds are specific to the custom MEA geometry, interelectrode spacing, and ex vivo Langendorff preparation employed, requiring validation before extrapolation.

Ask about this paper

Answers are grounded in this paper and cite their sources.

Implication

The study establishes reference epicardial voltage thresholds for the isolated rabbit heart model and demonstrates that arrhythmias dynamically reduce peak-to-peak amplitudes, revealing functional arrhythmogenic substrate behaviors.

Abstract

Cardiac arrhythmias are associated with structural and electrical remodeling processes that generate heterogeneous arrhythmogenic substrates characterized by low-voltage areas and abnormal conduction. Although electroanatomical voltage mapping is widely used for substrate characterization, epicardial voltage thresholds remain highly dependent on species, chamber, and recording configuration, and have not been systematically established for isolated rabbit hearts. We hypothesized that healthy rabbit epicardial tissue exhibits reproducible chamber-specific voltage distributions and that arrhythmias produce dynamic rhythm-dependent low-voltage areas substrate behavior. Isolated New Zealand White rabbit hearts ( n = 9) were perfused using a Langendorff system and mapped using custom epicardial multi-electrode arrays. Unipolar EGMs were acquired from the right atrium (RA), left atrium (LA), and ventricular epicardium (V), while bipolar EGMs were derived from adjacent electrodes. Chamber-specific voltage thresholds were determined from sinus rhythm (SR) recordings using 95 th percentile criterion. Voltage dynamics were further investigated during induced atrial tachycardia (AT), ventricular tachycardia (VT), and ventricular fibrillation (VF). Unipolar voltage thresholds were 7.4 mV (RA), 8.9 mV (LA), and 17.4 mV (V), whereas bipolar thresholds were 4.1 mV, 5.7 mV, and 9.5 mV, respectively. Arrhythmias significantly reduced peak-to-peak amplitudes compared with SR ( p < 0.05), particularly during VT and VF. Longitudinal voltage mapping revealed both transient rhythm-dependent low-voltage areas and spatially persistent low-voltage areas, suggesting distinct functional substrate behaviors during arrhythmogenesis. These findings establish reference epicardial voltage thresholds for the rabbit heart model and demonstrate the utility of voltage mapping for investigating dynamic arrhythmogenic substrate organization under controlled ex vivo conditions.

Discussion

No takes yet. Share an insight, caveat, or question.

Cite This Study

Gomes et al. (2026) studied Cardiac arrhythmias (n=9). Induced arrhythmias (AT, VT, VF) vs. Sinus rhythm was evaluated on Peak-to-peak amplitude during ventricular tachycardia (VT) vs sinus rhythm (SR) (Median paired difference 21.68 mV, 95% CI 20.60-23.38, p=<0.0001). Induced ventricular tachycardia significantly reduced median peak-to-peak epicardial voltage amplitudes by 21.68 mV compared to sinus rhythm in isolated rabbit hearts.

synapsesocial.com/papers/6ab9b5e97822ec8fc3d91318 https://doi.org/10.1007/s10439-026-04382-5

View Full Paper

Ask AI

Bookmark

Share

Peak-to-Peak Voltage Mapping Reveals Dynamic Arrhythmogenic Substrate Behavior in Isolated Rabbit Hearts

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Peak-to-Peak Voltage Mapping Reveals Dynamic Arrhythmogenic Substrate Behavior in Isolated Rabbit Hearts

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Keep reading

Keep reading