Distinct Electrogram Features and Ventricular Arrhythmia Induction Modes Between Repolarization and Conduction
Estelle Renard1, Elodie Surget1, Richard D Walton1
1IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France.
Background:
Recent clinical studies have indicated the presence of localized electrical abnormalities in idiopathic ventricular fibrillation and J-wave syndrome patients.
Objectives:
This study aims to characterize the specific electrical signatures of localized repolarization and conduction heterogeneities and their respective role in vulnerability to arrhythmias.
Methods:
Optical mapping was performed in porcine right ventricles with local: 1) repolarization shortening; 2) conduction slowing; or 3) structural heterogeneity induced by locally perfusing: 1) pinacidil (20 μmol/L, n = 13); or 2) flecainide (2 μmol/L, n = 13) via an epicardial catheter; or 3) by local epicardial tissue destruction (9 radiofrequency lesions n = 12). Electrograms were recorded (n = 5 in each group) and spontaneous and induced arrhythmias were quantified and optically mapped.
Results:
Electrograms were normal in (1) but showed local fragmentation in 40% of preparations in (2) with greater effects observed at high pacing frequencies dependent on the wavefront direction. In (3), the structural substrate alone increased the width and number of peaks in the electrograms, and addition of flecainide induced pronounced fragmentation (≥3 peaks and ≥70 ms) in all cases. Occurrence of spontaneous arrhythmias was significantly increased in (1) and (2) (P < 0.0001 and 0.05, respectively, vs baseline) and were triggered by ectopies. Vulnerability to arrhythmias at high pacing frequencies (≥2 Hz) was the lowest in (1) and greatest in (2).
Conclusions:
Microstructural substrates have the most pronounced impact on electrograms, especially when combined with sodium channel blockers, whereas local action potential duration shortening does not lead to electrogram fragmentation even though it is associated with the highest prevalence of spontaneous arrhythmias.
Related Concept Videos
01:30Cardiac 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
01:19Electrophysiology of Normal Cardiac Rhythm
01:28Electrocardiogram Fundamentals
An electrocardiogram (ECG) is a diagnostic tool for identifying cardiac conditions such as arrhythmias, conduction abnormalities, and myocardial ischemia.
Definition
An electrocardiogram (ECG) visualizes the heart's electrical activity by tracing the electrical movement associated with each heartbeat on a graph or monitor. As the heart beats, an electrical wave passes through it, correlating with the cardiac cycle events.
Parts of an ECG
An ECG utilizes electrodes on the skin...
01:29Electrocardiogram
Three major waveforms are present in a typical ECG recording: the P wave, the QRS complex, and...
01:28Mechanism of Cardiac Arrhythmias
01:25Correlation between ECG and Cardiac Cycle
A cardiac action potential originates in the SA node and spreads throughout the atria and the AV node in approximately 0.03 seconds. This results in the P wave in an ECG and triggers atrial contraction. The action potential is then briefly slowed at the AV node, allowing the atria to contract and fill the ventricles with blood before...