TY - JOUR
T1 - Mechanisms of Arrhythmogenicity in Hypertrophic Cardiomyopathy
T2 - Insight From Non-invasive Electrocardiographic Imaging
AU - Perez-Alday, Erick A.
AU - Haq, Kazi T.
AU - German, David M.
AU - Hamilton, Christopher
AU - Johnson, Kyle
AU - Phan, Francis
AU - Rogovoy, Nichole M.
AU - Yang, Katherine
AU - Wirth, Ashley
AU - Thomas, Jason A.
AU - Dalouk, Khidir
AU - Fuss, Cristina
AU - Ferencik, Maros
AU - Heitner, Stephen
AU - Tereshchenko, Larisa G.
N1 - Publisher Copyright:
© Copyright © 2020 Perez-Alday, Haq, German, Hamilton, Johnson, Phan, Rogovoy, Yang, Wirth, Thomas, Dalouk, Fuss, Ferencik, Heitner and Tereshchenko.
PY - 2020/4/24
Y1 - 2020/4/24
N2 - Background: Mechanisms of arrhythmogenicity in hypertrophic cardiomyopathy (HCM) are not well understood. Objective: To characterize an electrophysiological substrate of HCM in comparison to ischemic cardiomyopathy (ICM), or healthy individuals. Methods: We conducted a prospective case-control study. The study enrolled HCM patients at high risk for ventricular tachyarrhythmia (VT) [n = 10; age 61 ± 9 years; left ventricular ejection fraction (LVEF) 60 ± 9%], and three comparison groups: healthy individuals (n = 10; age 28 ± 6 years; LVEF > 70%), ICM patients with LV hypertrophy (LVH) and known VT (n = 10; age 64 ± 9 years; LVEF 31 ± 15%), and ICM patients with LVH and no known VT (n = 10; age 70 ± 7 years; LVEF 46 ± 16%). All participants underwent 12-lead ECG, cardiac CT or MRI, and 128-electrode body surface mapping (BioSemi ActiveTwo, Netherlands). Non-invasive voltage and activation maps were reconstructed using the open-source SCIRun (University of Utah) inverse problem-solving environment. Results: In the epicardial basal anterior segment, HCM patients had the greatest ventricular activation dispersion [16.4 ± 5.5 vs. 13.1 ± 2.7 (ICM with VT) vs. 13.8 ± 4.3 (ICM no VT) vs. 8.1 ± 2.4 ms (Healthy); P = 0.0007], the largest unipolar voltage [1094 ± 211 vs. 934 ± 189 (ICM with VT) vs. 898 ± 358 (ICM no VT) vs. 842 ± 90 μV (Healthy); P = 0.023], and the greatest voltage dispersion [median (interquartile range) 215 (161–281) vs. 189 (143–208) (ICM with VT) vs. 158 (109–236) (ICM no VT) vs. 110 (106–168) μV (Healthy); P = 0.041]. Differences were also observed in other endo-and epicardial basal and apical segments. Conclusion: HCM is characterized by a greater activation dispersion in basal segments, a larger voltage, and a larger voltage dispersion through LV. Clinical Trial Registration: www.clinicaltrials.gov Unique identifier: NCT02806479.
AB - Background: Mechanisms of arrhythmogenicity in hypertrophic cardiomyopathy (HCM) are not well understood. Objective: To characterize an electrophysiological substrate of HCM in comparison to ischemic cardiomyopathy (ICM), or healthy individuals. Methods: We conducted a prospective case-control study. The study enrolled HCM patients at high risk for ventricular tachyarrhythmia (VT) [n = 10; age 61 ± 9 years; left ventricular ejection fraction (LVEF) 60 ± 9%], and three comparison groups: healthy individuals (n = 10; age 28 ± 6 years; LVEF > 70%), ICM patients with LV hypertrophy (LVH) and known VT (n = 10; age 64 ± 9 years; LVEF 31 ± 15%), and ICM patients with LVH and no known VT (n = 10; age 70 ± 7 years; LVEF 46 ± 16%). All participants underwent 12-lead ECG, cardiac CT or MRI, and 128-electrode body surface mapping (BioSemi ActiveTwo, Netherlands). Non-invasive voltage and activation maps were reconstructed using the open-source SCIRun (University of Utah) inverse problem-solving environment. Results: In the epicardial basal anterior segment, HCM patients had the greatest ventricular activation dispersion [16.4 ± 5.5 vs. 13.1 ± 2.7 (ICM with VT) vs. 13.8 ± 4.3 (ICM no VT) vs. 8.1 ± 2.4 ms (Healthy); P = 0.0007], the largest unipolar voltage [1094 ± 211 vs. 934 ± 189 (ICM with VT) vs. 898 ± 358 (ICM no VT) vs. 842 ± 90 μV (Healthy); P = 0.023], and the greatest voltage dispersion [median (interquartile range) 215 (161–281) vs. 189 (143–208) (ICM with VT) vs. 158 (109–236) (ICM no VT) vs. 110 (106–168) μV (Healthy); P = 0.041]. Differences were also observed in other endo-and epicardial basal and apical segments. Conclusion: HCM is characterized by a greater activation dispersion in basal segments, a larger voltage, and a larger voltage dispersion through LV. Clinical Trial Registration: www.clinicaltrials.gov Unique identifier: NCT02806479.
KW - body surface mapping
KW - conduction velocity
KW - electrocardiographic imaging
KW - hypertrophic cardiomyopathy
KW - noninvasive
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U2 - 10.3389/fphys.2020.00344
DO - 10.3389/fphys.2020.00344
M3 - Article
AN - SCOPUS:85084346892
SN - 1664-042X
VL - 11
JO - Frontiers in Physiology
JF - Frontiers in Physiology
M1 - 344
ER -