AUTHOR=Perez-Alday Erick A. , Haq Kazi T. , German David M. , Hamilton Christopher , Johnson Kyle , Phan Francis , Rogovoy Nichole M. , Yang Katherine , Wirth Ashley , Thomas Jason A. , Dalouk Khidir , Fuss Cristina , Ferencik Maros , Heitner Stephen , Tereshchenko Larisa G. 

TITLE=Mechanisms of Arrhythmogenicity in Hypertrophic Cardiomyopathy: Insight From Non-invasive Electrocardiographic Imaging

JOURNAL=Frontiers in Physiology

VOLUME=11

YEAR=2020

URL=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2020.00344

DOI=10.3389/fphys.2020.00344

ISSN=1664-042X

ABSTRACT=<sec><title>Background</title><p>Mechanisms of arrhythmogenicity in hypertrophic cardiomyopathy (HCM) are not well understood.</p></sec><sec><title>Objective</title><p>To characterize an electrophysiological substrate of HCM in comparison to ischemic cardiomyopathy (ICM), or healthy individuals.</p></sec><sec><title>Methods</title><p>We conducted a prospective case-control study. The study enrolled HCM patients at high risk for ventricular tachyarrhythmia (VT) [<italic>n</italic> = 10; age 61 ± 9 years; left ventricular ejection fraction (LVEF) 60 ± 9%], and three comparison groups: healthy individuals (<italic>n</italic> = 10; age 28 ± 6 years; LVEF &gt; 70%), ICM patients with LV hypertrophy (LVH) and known VT (<italic>n</italic> = 10; age 64 ± 9 years; LVEF 31 ± 15%), and ICM patients with LVH and no known VT (<italic>n</italic> = 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.</p></sec><sec><title>Results</title><p>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); <italic>P</italic> = 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); <italic>P</italic> = 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); <italic>P</italic> = 0.041]. Differences were also observed in other endo-and epicardial basal and apical segments.</p></sec><sec><title>Conclusion</title><p>HCM is characterized by a greater activation dispersion in basal segments, a larger voltage, and a larger voltage dispersion through LV.</p></sec><sec><title>Clinical Trial Registration</title><p><ext-link ext-link-type="uri" xlink:href="http://www.clinicaltrials.gov" xmlns:xlink="http://www.w3.org/1999/xlink">www.clinicaltrials.gov</ext-link> Unique identifier: NCT02806479.</p></sec>