Substrate mapping for unstable ventricular tachycardia

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Date of download: 6/27/2016 Copyright © The American College of Cardiology. All rights reserved. From: Repetitive monomorphic ventricular tachycardia originating.

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Presentation transcript:

Substrate mapping for unstable ventricular tachycardia Pasquale Santangeli, MD, Francis E. Marchlinski, MD, FHRS Heart Rhythm Volume 13, Issue 2, Pages 569-583 (February 2016) DOI: 10.1016/j.hrthm.2015.09.023 Copyright © 2016 Heart Rhythm Society Terms and Conditions

Figure 1 Impact of different wavefronts of activation on late potential mapping. Left: Substrate map of a patient with prior anterior myocardial infarction presenting with recurrent ventricular tachycardia. Right: Example of bipolar recordings from a multipolar catheter (PR) positioned within the abnormal substrate during biventricular (BIV) vs right ventricular (RV) pacing. At the same recording site, late potentials are recorded only with RV pacing. Heart Rhythm 2016 13, 569-583DOI: (10.1016/j.hrthm.2015.09.023) Copyright © 2016 Heart Rhythm Society Terms and Conditions

Figure 2 Effect of different pacing outputs on the ventricular activation sequence and surface ECG morphology when pacing from the abnormal substrate in the periaortic region (LV endo). For outputs ≤20 mA, a sudden change in ventricular activation (as highlighted by the change in the ventricular activation sequence recorded at the decapolar catheter positioned in the great cardiac vein/anterior interventricular vein) and paced QRS morphology with different stimulus to QRS are noted. Heart Rhythm 2016 13, 569-583DOI: (10.1016/j.hrthm.2015.09.023) Copyright © 2016 Heart Rhythm Society Terms and Conditions

Figure 3 Impact of left ventricular hypertrophy on unipolar voltages. In this patient with nonischemic cardiomyopathy and left ventricular hypertrophy, a confluent area of unipolar voltage abnormalities concordant with the area of late gadolinium enhancement on cardiac magnetic resonance (right, arrows) is revealed after manual adjustment of the upper cutoff value of normal unipolar voltages on three-dimensional electroanatomic map. LV = left ventricle. Heart Rhythm 2016 13, 569-583DOI: (10.1016/j.hrthm.2015.09.023) Copyright © 2016 Heart Rhythm Society Terms and Conditions

Figure 4 Effect of electrically silent structures (eg, aortic root) on adjacent unipolar voltages. Shown are septal (left) and posteroanterior (right) views of a detailed right ventricular unipolar voltage map in a patient with no evidence of structural heart disease and completely normal cardiac magnetic resonance. The posterior septum consistently appears to have low voltages due to interposition of the aortic root. RVOT = right ventricular outflow tract. Heart Rhythm 2016 13, 569-583DOI: (10.1016/j.hrthm.2015.09.023) Copyright © 2016 Heart Rhythm Society Terms and Conditions

Figure 5 Evidence of a large field of view of bipolar recordings from a standard open-irrigated mapping and ablation catheter. The ablation catheter is positioned in the endocardial inferolateral left ventricle, and a decapolar catheter is positioned in the epicardium opposite to the site recorded by the ablation catheter (top left). The endocardial recording from the ablation catheter shows an abnormal electrogram with a sharp early component (potential “A”) and a blunt late component (potential “B”). The late endocardial component is on time with the epicardial late potentials (top right). Pacing from the epicardium pulls in the late endocardial component, demonstrating endocardial far-field recording from the adjacent epicardium. Heart Rhythm 2016 13, 569-583DOI: (10.1016/j.hrthm.2015.09.023) Copyright © 2016 Heart Rhythm Society Terms and Conditions

Figure 6 Inability to eliminate late potentials despite aggressive ablation. In this patient with prior inferior myocardial infarction, a substrate-based ablation approach targeting late potentials was adopted. At the end of the ablation set, persistence of late potentials was recorded at the apical border of the abnormal substrate. Late potentials activation demonstrated a focal site of breakthrough from the apical aspect of the scar, below the posteromedial papillary muscle. At that site, an area of abnormal echogenicity was noted at intracardiac echocardiography, which extended below the insertion of the posteromedial papillary muscle. Aggressive ablation at that site failed to eliminate late potentials. This suggested that a portion of the abnormal substrate extended below the posteromedial papillary muscle and could not be effectively targeted with ablation because protected by the intracavitary structure. LP = late potential. Heart Rhythm 2016 13, 569-583DOI: (10.1016/j.hrthm.2015.09.023) Copyright © 2016 Heart Rhythm Society Terms and Conditions