Myocardial Structural Associations with Local Electrograms: A Study of Post-Infarct Ventricular Tachycardia Pathophysiology and Magnetic Resonance Based Non-Invasive Mapping
Background—The association of scar on late-gadolinium enhancement cardiac magnetic resonance (LGE-CMR) with local electrograms on electroanatomic mapping (EAM) has been investigated. We aimed to quantify these associations to gain insights regarding LGE-CMR image characteristics of tissues and critical sites that support post-infarct ventricular tachycardia (VT).
Methods and Results—LGE-CMR was performed in 23 patients with ischemic cardiomyopathy before VT ablation. Left ventricular wall thickness and post-infarct scar thickness were measured in each of 20 sectors per LGE-CMR short-axis plane. EAM points were retrospectively registered to the corresponding LGE-CMR images. Multivariable regression analysis, clustered by patient, revealed significant associations between left ventricular wall thickness, post infarct scar thickness, and intramural scar location on LGE-CMR, and local endocardial electrogram bipolar/unipolar voltage, duration, and deflections on EAM. Antero-posterior and septal/lateral scar localization was also associated with bipolar and unipolar voltage. Anti-arrhythmic drug use was associated with electrogram duration. Critical sites of post-infarct VT were associated with >25% scar transmurality and slow conduction sites with >40 msec stimulus-QRS time were associated with >75% scar transmurality.
Conclusions—Critical sites for maintenance of post-infarct VT are confined to areas with >25% scar transmurality. Our data provides insights into the structural substrates for delayed conduction and VT, and may reduce procedural time devoted to substrate mapping, overcome limitations of invasive mapping due to sampling density, and enhance magnetic resonance based ablation by feature extraction from complex images.
- ischemic heart disease
- magnetic resonance imaging
- ventricular tachycardia
- late gadolinium enhancement
- Received February 9, 2012.
- Accepted November 2, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited