Relationship of frequent postinfarction premature ventricular complexes to the reentry circuit of scar-related ventricular tachycardia
Relationship of frequent postinfarction premature ventricular complexes to the reentry circuit of scar-related ventricular tachycardia
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DOI：
10.1016/j.hrthm.2007.11.026
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发表时间：
2008-03-01
期刊：
影响因子：
5.5
通讯作者：
Morady, Fred
中科院分区：
文献类型：
--
作者：
Bogun, Frank;Crawford, Thomas;Morady, Fred
背景梗死后折返性室性心动过速（VT）通常是疤痕相关的。然而，在心肌梗死愈合的情况下，室性早搏 (PVC) 的起源部位尚未得到很好的表征。 目的 本研究的目的是确定梗死后 VT 患者中频繁 PVC 的起源部位，并确定与 VT 退出部位的关系。 方法 对 13 名连续患者（12 名男性，平均年龄 62±8 岁，平均射血分数 0.32 +/-）进行标测和导管消融。 0.12) 既往有心肌梗塞、持续单形性 VT 和 > 10 PVCs/h。 24 小时动态心电图显示，平均 PVC 负荷为 12% +/- 11%。在窦性心律期间构建电解剖左心室电压图以识别疤痕。 PVC 的心内膜激活图与电压图相关，并且最常见的 PVC 被消融。确定 PVC 消融对 VT 诱导性的影响。结果 17 个持续单形 VT 是可重复诱导的。 PVC 共有 34 种不同的形态。 13 名患者中的 12 名患者的 34 种 PVC 形态中的 18 种的起源位点已被确定。可确定起源部位的 18 种 PVC 占这些患者 PVC 负担的 89%。 11 例患者的 PVC 起源部位位于梗死疤痕处，1 例患者的 PVC 起源部位位于边缘区，1 例患者的 PVC 起源部位无法识别。 PVC 起源位点对应于 17 个可重复诱导 VT 中 14 个的 VT 出口位点。成功定位的 PVC 被消融，这使得 VT 不再可诱导。 结论 梗塞后 PVC 通常由梗塞疤痕产生，其起源部位通常对应于折返性 VT 的出口部位。因此，室性早搏的导管消融通常与诱导性室速的丧失有关。
BACKGROUND Postinfarction reentrant ventricular tachycardia (VT) is usually scar-retated. However, the sites of origin of premature ventricular complexes (PVCs) in the setting of healed myocardial infarction have not been well characterized.OBJECTIVE The purpose of this study was to determine the site of origin of frequent PVCs in postinfarction patients with VT and to determine the relationship to VT exit sites.METHODS Mapping and catheter ablation were performed in 13 consecutive patients (12 men, mean age 62 8 years, mean ejection fraction 0.32 +/- 0.12) with prior myocardial infarction, sustained monomorphic VT, and > 10 PVCs/h. The mean PVC burden was 12% +/- 11% on a 24-hour Holter monitor. Electroanatomical left ventricular voltage maps were constructed during sinus rhythm to identify scars. Endocardial activation maps of the PVCs were correlated with the voltage maps, and the most prevalent PVCs were ablated. The effect of PVC ablation on the inducibility of VT was determined.RESULTS Seventeen sustained monomorphic VTs were reproducibly inducible. There were a total of 34 different PVC morphologies. The site of origin was identified for 18 of the 34 PVC morphologies in 12 of 13 patients. The 18 PVCs for which the site of origin could be identified accounted for 89% of the PVC burden in these patients. The site of PVC origin was in the infarct scar in 11 patients, the border zone in 1 patient, and unidentifiable in 1 patient. The site of PVC origin corresponded to the VT exit site for 14 of 17 reproducibly inducible VTs. The PVCs that were successfully mapped were ablated, and this rendered VT no longer inducible.CONCLUSION Postinfarction PVCs usually arise from the infarct scar, and their site of origin often corresponds to the exit site of a reentrant VT. Therefore, catheter ablation of the PVCs often is associated with the loss of inducible VT.