Corino Valentina D A, Sandberg Frida, Mainardi Luca T, Platonov Pyotr G, Sörnmo Leif
Department of Electronics, Information and Bioengineering, Politecnico of Milano, Italy.
Department of Biomedical Engineering and Center for Integrative Electrocardiology at Lund University (CIEL), Lund University, Lund, Sweden.
Ann Noninvasive Electrocardiol. 2015 Nov;20(6):534-41. doi: 10.1111/anec.12253. Epub 2014 Dec 26.
During atrial fibrillation (AF), conventional electrophysiological techniques for assessment of refractory period or conduction velocity of the atrioventricular (AV) node cannot be used. We aimed at evaluating changes in AV nodal properties during administration of tecadenoson and esmolol using a novel ECG-based method.
Fourteen patients (age 58 ± 8 years, 10 men) with AF were randomly assigned to either 75 or 300 μg intravenous tecadenoson. After tecadenoson wash-out, patients received esmolol continuously (100 μg/kg per min for 10 mins, then 50 μg/kg per min for 50 mins). Atrial fibrillatory rate (AFR) and heart rate (HR) were assessed in 15-min segments. Using the novel method, we assessed the absolute refractory periods of the slow and fast pathways (aRPs and aRPf) of the AV node to produce an estimate of the functional refractory period.
During esmolol infusion, AFR and HR were significantly decreased and the absolute refractory period was significantly prolonged in both pathways (aRPs: 387 ± 73 vs 409 ± 62 ms, P < 0.05; aRPf: 490 ± 80 vs 529 ± 58 ms, P < 0.05). During both tecadenoson doses, HR decreased significantly and AFR was unchanged. Both aRPs and aRPf were prolonged for a 75 μg dose (aRPs: 322 ± 97 vs 476 ± 75 ms, P < 0.05; aRPf: 456 ± 102 vs 512 ± 55 ms, P < 0.05) whereas a trend toward prolongation was observed for a 300 μg dose.
The estimated parameters reflect expected changes in AV nodal properties, i.e., slower conduction through the AV node for tecadenoson and prolongation of the AV node refractory period for esmolol. Thus, the proposed approach may be used to assess drug effects on the AV node in AF patients.
在心房颤动(AF)期间,无法使用传统的电生理技术来评估房室(AV)结的不应期或传导速度。我们旨在使用一种基于心电图的新方法评估替卡地松和艾司洛尔给药期间AV结特性的变化。
14例AF患者(年龄58±8岁,男性10例)被随机分配接受75或300μg静脉注射替卡地松。替卡地松洗脱后,患者持续接受艾司洛尔(100μg/kg每分钟,持续10分钟,然后50μg/kg每分钟,持续50分钟)。以15分钟为时间段评估心房颤动率(AFR)和心率(HR)。使用新方法,我们评估了AV结慢径路和快径路的绝对不应期(aRPs和aRPf),以估算功能不应期。
在输注艾司洛尔期间,AFR和HR显著降低,两条径路的绝对不应期均显著延长(aRPs:387±73对409±62毫秒,P<0.05;aRPf:490±80对529±58毫秒,P<0.05)。在两种替卡地松剂量下,HR均显著降低,AFR未改变。75μg剂量时aRPs和aRPf均延长(aRPs:322±97对476±75毫秒,P<0.05;aRPf:456±102对512±55毫秒,P<0.05),而300μg剂量时观察到延长趋势。
估算参数反映了AV结特性的预期变化,即替卡地松使AV结传导减慢,艾司洛尔使AV结不应期延长。因此,所提出的方法可用于评估AF患者中药物对AV结的作用。