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
Department of Medicine, Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, United States.
Sidney Kimmel Medical College, Philadelphia, PA, United States.
Front Physiol. 2020 Apr 24;11:344. doi: 10.3389/fphys.2020.00344. eCollection 2020.
Mechanisms of arrhythmogenicity in hypertrophic cardiomyopathy (HCM) are not well understood.
To characterize an electrophysiological substrate of HCM in comparison to ischemic cardiomyopathy (ICM), or healthy individuals.
We conducted a prospective case-control study. The study enrolled HCM patients at high risk for ventricular tachyarrhythmia (VT) [ = 10; age 61 ± 9 years; left ventricular ejection fraction (LVEF) 60 ± 9%], and three comparison groups: healthy individuals ( = 10; age 28 ± 6 years; LVEF > 70%), ICM patients with LV hypertrophy (LVH) and known VT ( = 10; age 64 ± 9 years; LVEF 31 ± 15%), and ICM patients with LVH and no known VT ( = 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.
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); = 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); = 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); = 0.041]. Differences were also observed in other endo-and epicardial basal and apical segments.
HCM is characterized by a greater activation dispersion in basal segments, a larger voltage, and a larger voltage dispersion through LV.
www.clinicaltrials.gov Unique identifier: NCT02806479.
肥厚型心肌病（HCM）的致心律失常机制尚未完全明确。
与缺血性心肌病（ICM）或健康个体相比，明确HCM的电生理基质。
我们进行了一项前瞻性病例对照研究。该研究纳入了有室性快速心律失常（VT）高风险的HCM患者[ = 10；年龄61±9岁；左心室射血分数（LVEF）60±9%]，以及三个对照组：健康个体（ = 10；年龄28±6岁；LVEF>70%）、有左心室肥厚（LVH）且已知有VT的ICM患者（ = 10；年龄64±9岁；LVEF 31±15%）和有LVH但无已知VT的ICM患者（ = 10；年龄70±7岁；LVEF 46±16%）。所有参与者均接受了12导联心电图、心脏CT或MRI检查，以及128电极体表标测（荷兰BioSemi ActiveTwo）。使用开源的SCIRun（犹他大学）逆问题解决环境重建无创电压和激动标测图。
在心外膜基底前节段，HCM患者的心室激动离散度最大[16.4±5.5 vs. 13.1±2.7（有VT的ICM）vs. 13.8±4.3（无VT的ICM）vs. 8.1±2.4毫秒（健康者）； = 0.0007]，单极电压最高[1094±211 vs. 934±189（有VT的ICM）vs. 898±358（无VT的ICM）vs. 842±90微伏（健康者）； = 0.023]，电压离散度也最大[中位数（四分位间距）215（161 - 281）vs. 189（143 - 208）（有VT的ICM）vs. 158（109 - 236）（无VT的ICM）vs. 110（106 - 168）微伏（健康者）； = 0.041]。在内膜和外膜的其他基底和心尖节段也观察到了差异。
HCM的特征是基底节段激动离散度更大、电压更高以及左心室内电压离散度更大。
www.clinicaltrials.gov 唯一标识符：NCT02806479。
