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Published on: April 21, 2014
Mechanisms underlying spontaneous and induced ventricular arrhythmias in patients with idiopathic dilated
S M Pogwizd1, J P McKenzie, M E Cain
1Cardiovascular Division, Washington University School of Medicine St. Louis, MO, USA.
Insights
Ventricular arrhythmias in nonischemic cardiomyopathy originate from focal mechanisms in the subendocardium or subepicardium. This study used 3D mapping to reveal these electrophysiological mechanisms in patients with idiopathic dilated cardiomyopathy.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Arrhythmias
Background:
- Nonischemic cardiomyopathy presents a significant challenge in understanding ventricular arrhythmias.
- Idiopathic dilated cardiomyopathy often leads to life-threatening arrhythmias.
- Electrophysiological mechanisms of these arrhythmias require precise definition.
Purpose of the Study:
- To elucidate the electrophysiological mechanisms underlying inducible and spontaneous ventricular arrhythmias.
- To investigate the role of conduction delay and block in arrhythmia initiation.
- To correlate arrhythmogenic sites with myocardial fibrosis.
Main Methods:
- Three-dimensional intraoperative mapping was conducted in 6 patients with idiopathic dilated cardiomyopathy.
- Mapping involved 156 intramural sites to analyze ventricular tachycardia (VT) and spontaneous arrhythmias.
- Programmed electrical stimulation was used to induce arrhythmias.
Main Results:
- High electrode density allowed mechanism determination for most induced and spontaneous ventricular arrhythmias.
- Extrastimuli revealed progressive conduction delay and intramural block due to slow conduction.
- Ventricular tachycardia initiation occurred via a focal mechanism at subendocardial or subepicardial sites, distinct from areas of significant fibrosis and conduction delay.
Conclusions:
- Both spontaneous and induced ventricular arrhythmias in end-stage idiopathic cardiomyopathy originate from focal mechanisms.
- Arrhythmias can initiate in either the subendocardium or subepicardium.
- Fibrosis plays a role in conduction abnormalities but is spatially separated from arrhythmia initiation sites.
Background:
To define the electrophysiological mechanism(s) of inducible and spontaneously occurring ventricular arrhythmias associated with nonischemic cardiomyopathy, 3-dimensional intraoperative mapping from 156 intramural sites was performed in 6 patients with idiopathic dilated cardiomyopathy undergoing cardiac transplantation.
Methods And Results:
Electrode density was sufficient to determine the mechanism for 52 of 74 beats of nonsustained ventricular tachycardia (VT) induced by programmed stimulation and 9 of 11 beats of spontaneous ventricular arrhythmias. The first, second, and third extrastimuli (S2 through S4) conducted with progressively greater degrees of conduction delay (total activation times [TAs] of 144+/-5, 166+/-5, and 194+/-5 ms, respectively) owing to slow conduction and on occasion intramural block. The first beats of induced VT arose from subendocardial or subepicardial sites distant from areas of marked conduction delay by a focal mechanism on the basis of the absence of intervening electrical activity between the termination of the last extrastimulus and the initiation of VT (123+/-31 ms). Subsequent beats arose by a focal mechanism and conducted with a TA of 127+/-6 ms (P=NS versus initiating beats of VT [118+/-9 ms]). Spontaneous ventricular arrhythmias initiated in the subendocardium by a focal mechanism and conducted with a TA of 138+/-5 ms. Tissue analysis demonstrated a variable degree of interstitial fibrosis at sites of focal activation. Sites of conduction delay or block typically exhibited marked interstitial and/or replacement fibrosis but were spatially distant from sites initiating VT.
Conclusions:
Spontaneous and induced ventricular arrhythmias in patients with end-stage idiopathic cardiomyopathy can arise in the subendocardium or subepicardium by a focal mechanism.
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