Fundamental Differences in Electrophysiologic and Electroanatomic Substrate Between Ischemic Cardiomyopathy Patients With and Without Clinical Ventricular Tachycardia
Received 15 January 2009; received in revised form 30 March 2009; accepted 20 April 2009.
Refers to article:
Why Are (Only) Some Infarcted Hearts Arrhythmogenic?⁎Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
James P. Daubert
Journal of the American College of Cardiology
7 July 2009 (Vol. 54, Issue 2, Pages 174-175) Full Text |
Full-Text PDF (115 KB)
Objectives
The aim of this study was to compare the electrophysiologic substrate in ischemic cardiomyopathy (ICM) patients with and without sustained monomorphic ventricular tachycardia (SMVT).
Background
Despite the universal presence of potentially arrhythmogenic left ventricular (LV) scarring, it is not clear why the majority of ICM patients never develop SMVT.
Methods
Detailed electroanatomic mapping of the LV endocardium was performed in 17 stable control ICM patients (16 males) without clinical SMVT. They were compared with 17 ICM patients (15 males) with spontaneous SMVT. Standard definitions of low-voltage zones and fractionated, isolated, and very late potentials were used.
Results
There were no significant baseline differences between the groups in terms of LV diameter, ejection fraction (27% vs. 28%), infarct territory, or time from infarction. However, control patients had smaller total low-voltage area ≤1.5 mv (30% of surface area vs. 55%, p < 0.001); smaller very low-voltage area <0.5 mv (7.3% vs. 29%, p < 0.001); higher mean voltage of low-voltage zones; fewer fractionated, isolated, and very late potentials with lower density of these scar-related electrograms per unit low-voltage area; and less SMVT inducibility. Potential conducting channels within dense scar and adjacent to the mitral annulus were more frequent in SMVT patients.
Conclusions
Compared with ICM patients with SMVT, an otherwise similar control group demonstrated markedly smaller endocardial low-voltage zones, lower scar-related electrogram density, and fewer conducting channels with faster conduction velocity. These findings may explain why some ICM patients develop SMVT and others do not.
Department of Cardiology, Royal Melbourne Hospital and the Department of Medicine, University of Melbourne, Melbourne, Australia
Reprint requests and correspondence: Prof. Jonathan M. Kalman, Department of Cardiology, Royal Melbourne Hospital, Grattan Street, Parkville, Victoria, Australia 3050
Drs. Haqqani and Roberts-Thomson are the recipients of Postgraduate Medical Scholarships from the National Health and Medical Research Council of Australia as well as Cardiovascular Lipid Grants.
ABSTRACT