Lingyu Xu MD, PhD , Mirmilad Khoshknab MD , Juwann Moss BS , Lauren C. Yang BA , Ronald D. Berger MD, PhD , Jonathan Chrispin MD , David Callans MD , Francis E. Marchlinski MD , Stefan L. Zimmerman MD , Yuchi Han MD , Natalia Trayanova PhD , Walter R. Witschey PhD , Benoit Desjardins MD, PhD , Saman Nazarian MD, PhD
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引用次数: 0
Abstract
Background
Ventricular tachycardia (VT) substrate in patients with nonischemic cardiomyopathy (NICM) is complex in distribution and intramural location.
Objectives
This study sought to test the hypothesis that myocardial lipomatous metaplasia (LM) is a vital anatomic substrate for VT corridors in patients with NICM and VT, and that LM stabilizes current propagation in VT corridors.
Methods
Among 49 patients with NICM in the 2-center INFINITY (Prospective Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy) Study, potential VT viable corridors within the myocardial scar and/or LM were computed from late gadolinium enhancement cardiac magnetic resonance images and were registered with electroanatomical maps. Corridors passing through VT entrance, isthmus, and/or exit sites, estimated by entrainment or pace mapping, were defined as VT corridors. LM was separately distinguished from scar using computed tomography. The SD of current amplitude along each corridor was measured.
Results
Compared with 151 non-VT corridors, 35 VT corridors traversed a substantially higher volume of LM, with a median 236.6 mg (IQR: 13.5-903.4 mg) vs 5.8 mg (IQR: 0.0-57.9 mg) (P < 0.001). Among corridors with computable current amplitude, 28 VT corridors exhibited substantially lower current variation along the corridors, with SD 8.0 μA (25th-75th percentile: 6.1-10.3 μA) vs 14.9 μA (25th-75th percentile: 8.5-23.7 μA) among 71 non-VT corridors (P < 0.001). Individual VT circuit sites (95 out 118) were highly colocalized with LM.
Conclusions
VT circuitry corridors in NICM are more likely to traverse LM and exhibit reduced current amplitude variation compared with bystander corridors.
期刊介绍:
JACC: Clinical Electrophysiology is one of a family of specialist journals launched by the renowned Journal of the American College of Cardiology (JACC). It encompasses all aspects of the epidemiology, pathogenesis, diagnosis and treatment of cardiac arrhythmias. Submissions of original research and state-of-the-art reviews from cardiology, cardiovascular surgery, neurology, outcomes research, and related fields are encouraged. Experimental and preclinical work that directly relates to diagnostic or therapeutic interventions are also encouraged. In general, case reports will not be considered for publication.