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

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

doi:10.3389/fphys.2020.00344

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

Front Physiol. 2020 Apr 24:11:344. doi: 10.3389/fphys.2020.00344. eCollection 2020.

Authors

Erick A Perez-Alday¹, Kazi T Haq¹, David M German¹, Christopher Hamilton¹, Kyle Johnson¹, Francis Phan¹, Nichole M Rogovoy¹, Katherine Yang^{1

2}, Ashley Wirth¹, Jason A Thomas¹, Khidir Dalouk^{1

3}, Cristina Fuss⁴, Maros Ferencik¹, Stephen Heitner¹, Larisa G Tereshchenko¹

Affiliations

¹ Department of Medicine, Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, United States.
² Sidney Kimmel Medical College, Philadelphia, PA, United States.
³ Portland VA Medical Center, Portland, OR, United States.
⁴ Department of Diagnostic Radiology, Oregon Health & Science University, Portland, OR, United States.

Abstract

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.

Keywords: body surface mapping; conduction velocity; electrocardiographic imaging; hypertrophic cardiomyopathy; noninvasive.

Associated data

ClinicalTrials.gov/NCT02806479

Abstract

Associated data

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