Joy, G;
Lopes, LR;
Webber, M;
Ardissino, AM;
Wilson, J;
Chan, F;
Pierce, I;
Hughes, RK;
Moschonas, K;
Shiwani, H;
et al.
Joy, G; Lopes, LR; Webber, M; Ardissino, AM; Wilson, J; Chan, F; Pierce, I; Hughes, RK; Moschonas, K; Shiwani, H; Jamieson, R; Velazquez, PP; Vijayakumar, R; Dall Armellina, E; Macfarlane, PW; Manisty, C; Kellman, P; Davies, RH; Tome, M; Koncar, V; Tao, X; Guger, C; Rudy, Y; Hughes, AD; Lambiase, PD; Moon, JC; Orini, M; Captur, G
(2024)
Electrophysiological Characterization of Subclinical and Overt Hypertrophic Cardiomyopathy by Magnetic Resonance Imaging-Guided Electrocardiography.
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 83 (11).
pp. 1042-1055.
ISSN 0735-1097
https://doi.org/10.1016/j.jacc.2024.01.006
SGUL Authors: Tome, Maria Teresa
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Abstract
Background Ventricular arrhythmia in hypertrophic cardiomyopathy (HCM) relates to adverse structural change and genetic status. Cardiovascular magnetic resonance (CMR)–guided electrocardiographic imaging (ECGI) noninvasively maps cardiac structural and electrophysiological (EP) properties. Objectives The purpose of this study was to establish whether in subclinical HCM (genotype [G]+ left ventricular hypertrophy [LVH]−), ECGI detects early EP abnormality, and in overt HCM, whether the EP substrate relates to genetic status (G+/G−LVH+) and structural phenotype. Methods This was a prospective 211-participant CMR-ECGI multicenter study of 70 G+LVH−, 104 LVH+ (51 G+/53 G−), and 37 healthy volunteers (HVs). Local activation time (AT), corrected repolarization time, corrected activation-recovery interval, spatial gradients (GAT/GRTc), and signal fractionation were derived from 1,000 epicardial sites per participant. Maximal wall thickness and scar burden were derived from CMR. A support vector machine was built to discriminate G+LVH− from HV and low-risk HCM from those with intermediate/high-risk score or nonsustained ventricular tachycardia. Results Compared with HV, subclinical HCM showed mean AT prolongation (P = 0.008) even with normal 12-lead electrocardiograms (ECGs) (P = 0.009), and repolarization was more spatially heterogenous (GRTc: P = 0.005) (23% had normal ECGs). Corrected activation-recovery interval was prolonged in overt vs subclinical HCM (P < 0.001). Mean AT was associated with maximal wall thickness; spatial conduction heterogeneity (GAT) and fractionation were associated with scar (all P < 0.05), and G+LVH+ had more fractionation than G−LVH+ (P = 0.002). The support vector machine discriminated subclinical HCM from HV (10-fold cross-validation accuracy 80% [95% CI: 73%-85%]) and identified patients at higher risk of sudden cardiac death (accuracy 82% [95% CI: 78%-86%]). Conclusions In the absence of LVH or 12-lead ECG abnormalities, HCM sarcomere gene mutation carriers express an aberrant EP phenotype detected by ECGI. In overt HCM, abnormalities occur more severely with adverse structural change and positive genetic status.
Item Type: | Article | |||||||||||||||
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Additional Information: | © 2024 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). | |||||||||||||||
Keywords: | cardiac magnetic resonance imaging, ECG imaging, electrophysiology, hypertrophic cardiomyopathy, 1102 Cardiorespiratory Medicine and Haematology, 1117 Public Health and Health Services, Cardiovascular System & Hematology | |||||||||||||||
SGUL Research Institute / Research Centre: | ?? 63 ?? | |||||||||||||||
Journal or Publication Title: | JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY | |||||||||||||||
ISSN: | 0735-1097 | |||||||||||||||
Publisher License: | Creative Commons: Attribution-Noncommercial-No Derivative Works 4.0 | |||||||||||||||
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Web of Science ID: | WOS:001225745100001 | |||||||||||||||
URI: | https://openaccess.sgul.ac.uk/id/eprint/116535 | |||||||||||||||
Publisher's version: | https://doi.org/10.1016/j.jacc.2024.01.006 |
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