Williams Steven E, Linton Nick, O'Neill Louisa, Harrison James, Whitaker John, Mukherjee Rahul, Rinaldi Christopher A, Gill Jaswinder, Niederer Steven, Wright Matthew, O'Neill Mark
Division of Imaging Sciences and Biomedical Imaging, King's College London.
Cardiovascular Division, Guy's and St. Thomas' NHS Foundation Trust.
J Cardiovasc Electrophysiol. 2017 Sep;28(9):1028-1036. doi: 10.1111/jce.13282.
Bipolar voltage is used during electroanatomic mapping to define abnormal myocardium, but the effect of activation rate on bipolar voltage is not known. We hypothesized that bipolar voltage may change in response to activation rate. By examining corresponding unipolar signals we sought to determine the mechanisms of such changes.
LA extrastimulus mapping was performed during CS pacing in 10 patients undergoing first time paroxysmal atrial fibrillation ablation. Bipolar and unipolar electrograms were recorded using a PentaRay catheter (4-4-4 spacing) and indifferent IVC electrode, respectively. An S1S2 pacing protocol was delivered with extrastimulus coupling interval reducing from 350 to 200 milliseconds. At each recording site (119 ± 37 per LA), bipolar peak-to-peak voltage, unipolar peak to peak voltage and activation delay between unipole pairs was measured. Four patterns of bipolar voltage/extrastimulus coupling interval curves were seen: voltage attenuation with plateau voltage >1 mV (48 ± 15%) or <1 mV (22 ± 15%), and voltage unaffected by coupling interval with plateau voltage >1 mV (17 ± 10%) or <1 mV (13 ± 8%). Electrograms showing bipolar voltage attenuation were associated with significantly greater unipolar voltage attenuation at low (25 ± 28 mV/s vs. 9 ± 11 mV/s) and high (23 ± 29 mV/s vs. 6 ± 12 mV/s) plateau voltage sites (P < 0.001). There was a small but significant increase in conduction delay between unipole pairs at sites showing bipolar voltage attenuation (P = 0.026).
Bipolar electrogram voltage is dependent on activation rate at a significant proportion of sites. Changes in unipolar voltage and timing underlie these effects. These observations have important implications for use of voltage mapping to delineate abnormal atrial substrate.
在电解剖标测过程中,双极电压用于定义异常心肌,但激活速率对双极电压的影响尚不清楚。我们推测双极电压可能会随着激活速率的变化而改变。通过检查相应的单极信号,我们试图确定这种变化的机制。
对10例首次接受阵发性心房颤动消融的患者在冠状窦起搏期间进行左心房额外刺激标测。分别使用PentaRay导管(4-4-4间距)和无关的下腔静脉电极记录双极和单极电图。采用S1S2起搏方案,额外刺激耦合间期从350毫秒缩短至200毫秒。在每个记录部位(每个左心房119±37个),测量双极峰-峰值电压、单极峰-峰值电压以及单极电极对之间的激活延迟。观察到双极电压/额外刺激耦合间期曲线有四种模式:平台期电压>1mV时电压衰减(48±15%)或<1mV时电压衰减(22±15%),以及平台期电压>1mV(17±10%)或<1mV(13±8%)时电压不受耦合间期影响。显示双极电压衰减的电图在低平台期电压部位(25±28mV/s对9±11mV/s)和高平台期电压部位(23±29mV/s对6±12mV/s)与显著更大的单极电压衰减相关(P<0.001)。在显示双极电压衰减的部位,单极电极对之间的传导延迟有小但显著的增加(P=0.026)。
在相当一部分部位,双极电图电压取决于激活速率。单极电压和时间的变化是这些影响的基础。这些观察结果对使用电压标测来描绘异常心房基质具有重要意义。