Sivagangabalan Gopal, Pouliopoulos Jim, Huang Kaimin, Barry Michael A, Lu Juntang, Thomas Stuart P, Ross David L, Thiagalingam Aravinda, Kovoor Pramesh
Cardiology Department, Westmead Hospital, Sydney, Australia.
Circ Arrhythm Electrophysiol. 2009 Aug;2(4):441-9. doi: 10.1161/CIRCEP.108.842872. Epub 2009 May 22.
We assessed a novel simultaneous biventricular mapping and ablation approach for septal ventricular tachycardia (VT) in a chronic ovine infarct model.
In 8 sheep with inducible VT, mapping and ablation were performed 9+/-3 months after percutaneously induced myocardial infarction, with left ventricular ejection fraction 23+/-8%. Scar was identified by EnSite Dynamic Substrate Mapping plus CARTO voltage mapping. Thirty VT episodes (cycle length, 235+/-42 ms) were mapped with simultaneous analyses using EnSite arrays deployed in both the left ventricle and the right ventricle. Short ablation lines were created perpendicular to the breakout pathway along the scar border in the ventricle with earliest activity. If septal VT was still inducible, this line was extended before ablation in the second chamber. The end point of noninducibility of VT was achieved in all animals. The mean difference in delay in noncontact breakout timing between the ventricles was shorter for VT with (n=18) than without (n=12) septal breakout (32+/-7.8 ms, P<0.001). In 5 of 6 animals, after ablation in one ventricle, septal VT was still inducible with a common breakout site in the second ventricle. After septal ablation in the second ventricle, VT was no longer inducible. In the 6 animals in which septal VT had been ablated, transmural septal ablation was identified at the scar border, with overlapping left ventricular and right ventricular ablation lesions present in 5 of 6 (septal thickness 8 to 17 mm) and left ventricular endocardial ablation being transmural in 1 of 6 (6 mm).
Biventricular scar and VT activation mapping correctly localizes septal VT pathways, directing ablation from one or both septal endocardial aspects. Creation of a transmural septal lesion at the scar border interrupting VT exit points is highly effective at ablating septal VT.
我们在慢性绵羊梗死模型中评估了一种用于间隔性室性心动过速（VT）的新型同步双心室标测与消融方法。
对8只可诱发VT的绵羊，在经皮诱导心肌梗死后9±3个月进行标测与消融，左心室射血分数为23±8%。通过EnSite动态基质标测加CARTO电压标测识别瘢痕。使用分别置于左心室和右心室的EnSite阵列同步分析，对30次VT发作（周期长度为235±42毫秒）进行标测。在最早出现激动的心室中，沿瘢痕边界垂直于突破路径创建短消融线。如果间隔性VT仍可诱发，则在第二个腔室消融前延长该线。所有动物均达到VT不能诱发的终点。对于有间隔突破（n = 18）的VT，心室间非接触突破时间延迟的平均差异比无间隔突破（n = 12）的VT短（32±7.8毫秒，P<0.001）。6只动物中有5只，在一个心室消融后，间隔性VT仍可诱发，且在第二个心室有共同的突破位点。在第二个心室进行间隔消融后，VT不再能诱发。在6只已消融间隔性VT的动物中，在瘢痕边界处识别出透壁性间隔消融，6只中有5只（间隔厚度8至17毫米）存在左心室和右心室消融灶重叠，6只中有1只（6毫米）左心室内膜消融是透壁的。
双心室瘢痕和VT激动标测可正确定位间隔性VT路径，指导从间隔的心内膜一侧或两侧进行消融。在瘢痕边界处创建中断VT出口点的透壁性间隔病变对消融间隔性VT非常有效。
