Heart Center, Department of Clinical and Experimental Cardiology, Amsterdam UMC, University of Amsterdam, Cardiovascular Sciences, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
Department of Medical Informatics, Erasmus MC, University Medical Center Rotterdam, Doctor Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Int J Mol Sci. 2021 Jan 6;22(2):484. doi: 10.3390/ijms22020484.
Patients with Brugada syndrome (BrS) can show a leftward deviation of the frontal QRS-axis upon provocation with sodium channel blockers. The cause of this axis change is unclear. In this study, we aimed to determine (1) the prevalence of this left axis deviation and (2) to evaluate its cause, using the insights that could be derived from vectorcardiograms. Hence, from a large cohort of patients who underwent ajmaline provocation testing ( = 1430), we selected patients in whom a type-1 BrS-ECG was evoked ( = 345). Depolarization and repolarization parameters were analyzed for reconstructed vectorcardiograms and were compared between patients with and without a >30° leftward axis shift. We found (1) that the prevalence of a left axis deviation during provocation testing was 18% and (2) that this left axis deviation was not explained by terminal conduction slowing in the right ventricular outflow tract (4th QRS-loop quartile: +17 ± 14 ms versus +13 ± 15 ms, nonsignificant) but was associated with a more proximal conduction slowing (1st QRS-loop quartile: +12[8;18] ms versus +8[4;12] ms, < 0.001 and 3rd QRS-loop quartile: +12 ± 10 ms versus +5 ± 7 ms, < 0.001). There was no important heterogeneity of the action potential morphology (no difference in the ventricular gradient), but a left axis deviation did result in a discordant repolarization (spatial QRS-T angle: 122[59;147]° versus 44[25;91]°, < 0.001). Thus, although the development of the type-1 BrS-ECG is characterized by a terminal conduction delay in the right ventricle, BrS-patients with a left axis deviation upon sodium channel blocker provocation have an additional proximal conduction slowing, which is associated with a subsequent discordant repolarization. Whether this has implications for risk stratification is still undetermined.
患有 Brugada 综合征(BrS)的患者在使用钠通道阻滞剂激发时可能会出现额面 QRS 轴左偏。这种轴改变的原因尚不清楚。在这项研究中,我们旨在确定(1)这种左轴偏离的发生率,以及(2)使用可以从向量心电图中得出的见解来评估其原因。因此,我们从接受阿马林激发试验的大量患者队列中(=1430 例)选择了出现 1 型 BrS-ECG 的患者(=345 例)。我们分析了重建向量心电图的去极化和复极参数,并比较了有和无 >30°左偏轴转移的患者之间的差异。我们发现(1)在激发试验期间,轴左偏的发生率为 18%,(2)这种左轴偏离不能用右心室流出道的终末传导减慢来解释(第 4 个 QRS 环四分位:+17±14ms 比+13±15ms,无统计学意义),但与更近端的传导减慢有关(第 1 个 QRS 环四分位:+12[8;18]ms 比+8[4;12]ms,<0.001,第 3 个 QRS 环四分位:+12±10ms 比+5±7ms,<0.001)。动作电位形态没有明显的异质性(心室梯度没有差异),但是轴左偏确实导致复极不同步(空间 QRS-T 角:122[59;147]°比 44[25;91]°,<0.001)。因此,尽管 1 型 BrS-ECG 的发生特征是右心室终末传导延迟,但在钠通道阻滞剂激发时出现左轴偏离的 BrS 患者有额外的近端传导减慢,这与随后的复极不同步有关。这是否对危险分层有影响仍不确定。