Dynamic conduction and repolarisation changes in early arrhythmogenic right ventricular cardiomyopathy versus benign outflow tract ectopy demonstrated by high density mapping & paced surface ECG analysis.

Dynamic conduction and repolarisation changes in early arrhythmogenic right ventricular cardiomyopathy versus benign outflow tract ectopy demonstrated by high density mapping & paced surface ECG analysis.
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DOI:
10.1371/journal.pone.0099125
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Lambiase PD
Lambiase PD
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Finlay MC;Ahmed AK;Sugrue A;Bhar-Amato J;Quarta G;Pantazis A;Ciaccio EJ;Syrris P;Sen-Chowdhry S;Ben-Simon R;Chow AW;Lowe MD;Segal OR;McKenna WJ;Lambiase PD

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致心律失常性右室心肌病(ARVC)的隐匿期可能最初表现为电生理。还没有研究通过动态传导/复极动力学来区分良性右室流出道异位(RVOT异位)和ARVC的早期。我们研究了区分早期ARVC疾病表达和RVOT异位的动态心内膜电生理变化。22例无右室结构异常的ARVC患者(12例根据家族史和突变携带者确定,10例可能)接受了右室高密度非接触标测。这些数据与14例RVOT异位和12例室上性心动过速和正常心脏患者的数据进行了比较。在标准的S1-S2重建方案中评估心内膜和体表心电图的传导和复极参数。在窦性心律或稳态起搏时,明确的无RV器质性病变的ARVC与RVOT异位不能明确区分。室性早搏患者(43±20ms)较右室流出道异位患者(36±14ms,p = 0.03)或正常人(25±16ms,p = 0.008)明显延长,复极时间曲线呈渐进性分离。ARVC组RVOT复极时间延长最大(明确ARVC:18±20ms;RVOT异位:5±14,正常:1±18,p<0.05)。这些心内测量的体表心电图相关指标显示,与稳态相比,体表心电图J点ERP前刺激增加了48ms以上,对区分明确的ARVC与其他组的特异度和敏感度分别为88%和68%。这项技术不能区分仅有ARVC遗传易感性的患者(可能是ARVC)和对照组。在发现RV结构异常之前,动态传导和复极的显著变化在早期ARVC中就很明显,在可能的ARVC患者中出现的程度较小。动态电生理参数的研究可能有助于通过心内膜电信号或起搏心电参数识别无疾病家系的患者的隐匿性ARVC。
The concealed phase of arrhythmogenic right ventricular cardiomyopathy (ARVC) may initially manifest electrophysiologically. No studies have examined dynamic conduction/repolarization kinetics to distinguish benign right ventricular outflow tract ectopy (RVOT ectopy) from ARVC's early phase. We investigated dynamic endocardial electrophysiological changes that differentiate early ARVC disease expression from RVOT ectopy. 22 ARVC (12 definite based upon family history and mutation carrier status, 10 probable) patients without right ventricular structural anomalies underwent high-density non-contact mapping of the right ventricle. These were compared to data from 14 RVOT ectopy and 12 patients with supraventricular tachycardias and normal hearts. Endocardial & surface ECG conduction and repolarization parameters were assessed during a standard S1-S2 restitution protocol. Definite ARVC without RV structural disease could not be clearly distinguished from RVOT ectopy during sinus rhythm or during steady state pacing. Delay in Activation Times at coupling intervals just above the ventricular effective refractory period (VERP) increased in definite ARVC (43±20 ms) more than RVOT ectopy patients (36±14 ms, p = 0.03) or Normals (25±16 ms, p = 0.008) and a progressive separation of the repolarisation time curves between groups existed. Repolarization time increases in the RVOT were also greatest in ARVC (definite ARVC: 18±20 ms; RVOT ectopy: 5±14, Normal: 1±18, p<0.05). Surface ECG correlates of these intracardiac measurements demonstrated an increase of greater than 48 ms in stimulus to surface ECG J-point pre-ERP versus steady state, with an 88% specificity and 68% sensitivity in distinguishing definite ARVC from the other groups. This technique could not distinguish patients with genetic predisposition to ARVC only (probable ARVC) from controls. Significant changes in dynamic conduction and repolarization are apparent in early ARVC before detectable RV structural abnormalities, and were present to a lesser degree in probable ARVC patients. Investigation of dynamic electrophysiological parameters may be useful to identify concealed ARVC in patients without disease pedigrees by using endocardial electrogram or paced ECG parameters.
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