Related Experiment Video
Updated: Jan 6, 2026
Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Activation During Sinus Rhythm in Ventricles With Healed Infarction: Differentiation Between Arrhythmogenic and
Markus Rottmann1, Andre G Kleber1, Michael Barkagan1
1Harvard-Thorndike Electrophysiology Institute, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Insights
Activation slowing during sinus rhythm (SR) identifies infarct regions vulnerable to ventricular tachycardia (VT). These slow activation sites correlate with the VT circuit
Area of Science:
- Cardiology
- Electrophysiology
- Medical Imaging
Background:
- Infarct-related ventricular tachycardia (VT) circuits often involve areas of slow electrical activation during sinus rhythm (SR).
- The precise relationship between SR activation slowing, reentry vulnerability, and VT circuit components remains unclear.
Purpose of the Study:
- To investigate the link between SR activation slowing and reentry vulnerability.
- To correlate areas of SR activation slowing with specific VT circuit components.
Main Methods:
- A porcine model of healed myocardial infarction was used.
- Endocardial activation velocity was compared during SR and VT using activation and entrainment mapping to define isthmus and bystander sites.
Main Results:
- Infarctions with inducible VT exhibited significantly greater SR activation slowing compared to non-inducible ones (cutoff ≤0.1 m/s, P=0.015).
- Maximal SR endocardial slowing regions corresponded to VT isthmus sites, while bystander sites showed near-normal SR activation.
- VT circuits frequently displayed complex conduction patterns, including intramural bridges.
Conclusions:
- Endocardial activation slowing during SR can predict infarction vulnerability to VT.
- SR slow activation sites are directly associated with VT isthmus formation, not bystander regions.
Background:
In infarct-related ventricular tachycardia (VT), the circuit often corresponds to a location characterized by activation slowing during sinus rhythm (SR). However, the relationship between activation slowing during SR and vulnerability for reentry and correlation to components of the VT circuit are unknown. This study examined the relationship between activation slowing during SR and vulnerability for reentry and correlated these areas with components of the circuit.
Methods:
In a porcine model of healed infarction, the spatial distribution of endocardial activation velocity was compared between SR and VT. Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit.
Results:
Of 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1 m/s differentiated inducible from noninducible infarctions (P=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (area under curve=0.84 95% CI, 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. Regions forming the VT isthmus borders had faster activation during SR while regions forming the inner isthmus were activated faster during VT.
Conclusions:
Endocardial activation slowing during SR may differentiate infarctions vulnerable for VT from those less vulnerable for VT. Sites of slow activation during SR correspond to sites forming the VT isthmus but not to bystander sites.
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