Leong Kevin M W, Ng Fu Siong, Yao Cheng, Roney Caroline, Taraborrelli Patricia, Linton Nicholas W F, Whinnett Zachary I, Lefroy David C, Davies D Wyn, Boon Lim Phang, Harding Sian E, Peters Nicholas S, Kanagaratnam Prapa, Varnava Amanda M
From the National Heart and Lung Institute, Imperial College London, United Kingdom (K.M.W.L., F.S.N., C.R., N.W.F.L., Z.I.W., P.B.L., S.E.H., N.S.P., P.K.); Imperial College Healthcare NHS Trust, London, United Kingdom (K.M.W.L., F.S.N., P.T., N.W.F.L., Z.I.W., D.C.L., D.W.D., P.B.L., N.S.P., P.K., A.M.V.); and Medtronic Ltd, Watford, United Kingdom (C.Y.).
Circ Arrhythm Electrophysiol. 2017 Oct;10(10). doi: 10.1161/CIRCEP.117.005107.
The substrate location and underlying electrophysiological mechanisms that contribute to the characteristic ECG pattern of Brugada syndrome (BrS) are still debated. Using noninvasive electrocardiographical imaging, we studied whole heart conduction and repolarization patterns during ajmaline challenge in BrS individuals.
A total of 13 participants (mean age, 44±12 years; 8 men), 11 concealed patients with type I BrS and 2 healthy controls, underwent an ajmaline infusion with electrocardiographical imaging and ECG recordings. Electrocardiographical imaging activation recovery intervals and activation timings across the right ventricle (RV) body, outflow tract (RVOT), and left ventricle were calculated and analyzed at baseline and when type I BrS pattern manifested after ajmaline infusion. Peak J-ST point elevation was calculated from the surface ECG and compared with the electrocardiographical imaging-derived parameters at the same time point. After ajmaline infusion, the RVOT had the greatest increase in conduction delay (5.4±2.8 versus 2.0±2.8 versus 1.1±1.6 ms; =0.007) and activation recovery intervals prolongation (69±32 versus 39±29 versus 21±12 ms; =0.0005) compared with RV or left ventricle. In controls, there was minimal change in J-ST point elevation, conduction delay, or activation recovery intervals at all sites with ajmaline. In patients with BrS, conduction delay in RVOT, but not RV or left ventricle, correlated to the degree of J-ST point elevation (Pearson , 0.81; <0.001). No correlation was found between J-ST point elevation and activation recovery intervals prolongation in the RVOT, RV, or left ventricle.
Magnitude of ST (J point) elevation in the type I BrS pattern is attributed to degree of conduction delay in the RVOT and not prolongation in repolarization time.
导致Brugada综合征（BrS）特征性心电图模式的底物位置及潜在电生理机制仍存在争议。我们使用无创心电图成像技术，研究了BrS患者在阿义马林激发试验期间的全心传导和复极模式。
共有13名参与者（平均年龄44±12岁；8名男性），其中11名隐匿性I型BrS患者和2名健康对照者接受了阿义马林静脉输注，并进行了心电图成像和心电图记录。在基线时以及阿义马林输注后I型BrS模式出现时，计算并分析了右心室（RV）体部、流出道（RVOT）和左心室的心电图成像激活恢复间期和激活时间。从体表心电图计算J点ST段抬高峰值，并与同一时间点心电图成像得出的参数进行比较。阿义马林输注后，与RV或左心室相比，RVOT的传导延迟增加幅度最大（5.4±2.8对2.0±2.8对1.1±1.6毫秒；P=0.007），激活恢复间期延长幅度最大（69±32对39±29对21±12毫秒；P=0.0005）。在对照者中，阿义马林作用下所有部位的J点ST段抬高、传导延迟或激活恢复间期变化极小。在BrS患者中，RVOT的传导延迟（而非RV或左心室）与J点ST段抬高程度相关（Pearson相关系数，0.81；P<0.001）。RVOT、RV或左心室的J点ST段抬高与激活恢复间期延长之间未发现相关性。
I型BrS模式中ST（J点）抬高幅度归因于RVOT的传导延迟程度，而非复极时间延长。
