Ciaccio Edward J, Coromilas James, Wan Elaine Y, Yarmohammadi Hirad, Saluja Deepak S, Peters Nicholas S, Garan Hasan, Biviano Angelo B
Department of Medicine - Division of Cardiology, Columbia University College of Physicians and Surgeons, New York, NY, USA; ElectroCardioMaths Programme, Imperial Centre for Cardiac Engineering, Imperial College London, London, UK.
Department of Medicine - Division of Cardiovascular Disease and Hypertension, Rutgers University, New Brunswick, NJ, USA.
Comput Methods Programs Biomed. 2023 Nov;241:107764. doi: 10.1016/j.cmpb.2023.107764. Epub 2023 Aug 13.
A quantitative analysis of the components of reentrant ventricular tachycardia (VT) circuitry could improve understanding of its onset and perpetuation.
In 19 canine experiments, the left anterior descending coronary artery was ligated to generate a subepicardial infarct. The border zone resided at the epicardial surface of the anterior left ventricle and was mapped 3-5 days postinfarction with a 196-312 bipolar multielectrode array. Monomorphic VT was inducible by extrastimulation. Activation maps revealed an epicardial double-loop reentrant circuit and isthmus, causing VT. Several circuit parameters were analyzed: the coupling interval for VT induction, VT cycle length, the lateral isthmus boundary (LIB) lengths, and isthmus width and angle.
The extrastimulus interval for VT induction and the VT cycle length were strongly correlated (p < 0.001). Both the extrastimulus interval and VT cycle length were correlated to the shortest LIB (p < 0.005). A derivation was developed to suggest that when conduction block at the shorter LIB is functional, the VT cycle length may depend on the local refractory period and the delay from wavefront pivot around the LIB. Isthmus width and angle were uncorrelated to other parameters.
The shorter LIB is correlated to VT cycle length, hence its circuit loop may drive reentrant VT. The extrastimulation interval, VT cycle length, and shorter LIB are intertwined, and may depend upon the local refractory period. Isthmus width and angle are less correlated, perhaps being more related to electrical discontinuity caused by alterations in infarct shape at depth.
对折返性室性心动过速(VT)环路的组成部分进行定量分析,有助于加深对其发作和持续机制的理解。
在19只犬类实验中,结扎左前降支冠状动脉以形成心外膜下梗死。梗死边缘区位于左心室前壁的心外膜表面,在梗死后3 - 5天使用196 - 312极双极多电极阵列进行标测。通过额外刺激可诱发单形性室性心动过速。激动标测显示存在一个心外膜双环折返环路和峡部,导致室性心动过速。分析了几个环路参数:诱发室性心动过速的耦合间期、室性心动过速周期长度、外侧峡部边界(LIB)长度以及峡部宽度和角度。
诱发室性心动过速的额外刺激间期与室性心动过速周期长度密切相关(p < 0.001)。额外刺激间期和室性心动过速周期长度均与最短的LIB相关(p < 0.005)。推导出一个公式,表明当较短LIB处的传导阻滞起作用时,室性心动过速周期长度可能取决于局部不应期以及波阵面围绕LIB的折返延迟。峡部宽度和角度与其他参数无关。
较短的LIB与室性心动过速周期长度相关,因此其环路可能驱动折返性室性心动过速。额外刺激间期、室性心动过速周期长度和较短的LIB相互关联,可能取决于局部不应期。峡部宽度和角度的相关性较小,可能与深部梗死形状改变引起的电不连续性更相关。