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 - Funding Information:
The authors declare that this study received funding from Gilead Sciences, Inc. as a physician-initiated study (LT). The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this article or the decision to submit it for publication. This work was partially supported by 1R01HL118277 and 2R56HL118277 (LT).
Funding Information:
We thank the study participants and staff. We thank William Woodward, ARMRIT, for the help with the CMR data acquisition. Funding. The authors declare that this study received funding from Gilead Sciences, Inc. as a physician-initiated study (LT). The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this article or the decision to submit it for publication. This work was partially supported by 1R01HL118277 and 2R56HL118277 (LT).
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
UR - http://www.scopus.com/inward/record.url?scp=85084346892&partnerID=8YFLogxK
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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 -