Conduction Velocity Dispersion Predicts Postinfarct Ventricular Tachycardia Circuit Sites and Associates With
Lingyu Xu1, Sohail Zahid2, Mirmilad Khoshknab1
1Cardiovascular Medicine Division, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Insights
Regional conduction velocity (CV) dispersion is a better predictor of ventricular tachycardia (VT) circuits than repolarization dispersion in post-heart attack patients. Myocardial lipomatous metaplasia (LM) is identified as a key substrate for this CV dispersion.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Imaging
Background:
- Regional myocardial conduction velocity (CV) dispersion has not been previously studied in patients with ventricular tachycardia (VT) after myocardial infarction.
- Understanding the factors influencing VT in post-infarct patients is crucial for improving patient outcomes.
Purpose of the Study:
- To compare the association of CV dispersion versus repolarization dispersion with ventricular tachycardia (VT) circuit sites.
- To investigate myocardial lipomatous metaplasia (LM) and fibrosis as potential substrates for CV dispersion.
Main Methods:
- Utilized cardiac magnetic resonance and computed tomography to characterize infarct tissue, LM, and fibrosis in 33 post-infarct VT patients.
- Registered imaging data with electroanatomic maps to assess regional CV and Activation Recovery Interval (ARI) dispersion.
- Calculated CV and ARI dispersion using the coefficient of variation (CoV) per American Heart Association (AHA) segment.
Main Results:
- Regional CV dispersion showed a significantly larger range (median 0.65) compared to ARI dispersion (median 0.24).
- CV dispersion was a more robust predictor of critical VT sites than ARI dispersion.
- Regional lipomatous metaplasia (LM) area demonstrated a stronger association with CV dispersion than fibrosis area.
Conclusions:
- Regional CV dispersion is a stronger predictor of VT circuit sites compared to repolarization dispersion.
- Myocardial lipomatous metaplasia (LM) serves as a critical substrate contributing to regional CV dispersion in post-infarct hearts.
Background:
Regional myocardial conduction velocity (CV) dispersion has not been studied in postinfarct patients with ventricular tachycardia (VT).
Objectives:
This study sought to compare the following: 1) the association of CV dispersion vs repolarization dispersion with VT circuit sites; and 2) myocardial lipomatous metaplasia (LM) vs fibrosis as the anatomic substrate for CV dispersion.
Methods:
Among 33 postinfarct patients with VT, we characterized dense and border zone infarct tissue by late gadolinium enhancement cardiac magnetic resonance, and LM by computed tomography, with both images registered with electroanatomic maps. Activation recovery interval (ARI) was the time interval from the minimum derivative within the QRS complex to the maximum derivative within the T-wave on unipolar electrograms. CV at each EAM point was the mean CV between that point and 5 adjacent points along the activation wave front. CV and ARI dispersion were the coefficient of variation (CoV) of CV and ARI per American Heart Association (AHA) segment, respectively.
Results:
Regional CV dispersion exhibited a much larger range than ARI dispersion, with median 0.65 vs 0.24; P < 0.001. CV dispersion was a more robust predictor of the number of critical VT sites per AHA segment than ARI dispersion. Regional LM area was more strongly associated with CV dispersion than fibrosis area. LM area was larger (median 0.44 vs 0.20 cm2; P < 0.001) in AHA segments with mean CV <36 cm/s and CoV_CV >0.65 than those with mean CV <36 cm/s and CoV_CV <0.65.
Conclusions:
Regional CV dispersion more strongly predicts VT circuit sites than repolarization dispersion, and LM is a critical substrate for CV dispersion.
More Related Videos
Related Concept Videos
Conduction System of the Heart
The pacemaker cells are located in two primary nodes: the sinoatrial (SA) node and the atrioventricular (AV) node. The SA node pacemaker cells can autonomously depolarize, triggering an action potential that leads to the...
Dysrhythmias III: Characteristics of Dysrhythmias
Myocarditis I: Introduction
Electrophysiology of Normal Cardiac Rhythm
Coronary Artery Disease II: Pathophysiology
Cardiac Action Potential
The cardiac action potential process involves a series of phases characterized by the movement of ions across the cardiac cell membranes, leading to the depolarization and repolarization of the cardiac myocytes.
Ionic Basis of Cardiac Action Potentials


