Determinants of postinfarction ventricular tachycardia.

Determinants of postinfarction ventricular tachycardia.
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炎后心室心动过速的决定因素。

DOI:
10.1161/circep.110.945295
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发表时间:
2010-12
期刊:
Circulation. Arrhythmia and electrophysiology
影响因子:
--
通讯作者:
Bogun F
Bogun F
中科院分区:
其他
文献类型:
--
作者:
Crawford T;Cowger J;Desjardins B;Kim HM;Good E;Jongnarangsin K;Oral H;Chugh A;Pelosi F;Morady F;Bogun F

文献摘要

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导致梗死后室性心动过速(VT)发展的结构因素尚不清楚。本研究的目的是分析有和无诱发性室性心动过速患者的梗死结构和电图特征,并确定梗死后室性心动过速的相关因素。24例梗死后患者(中位年龄64 [53,70]岁)接受VT(n=12)或频繁症状性室性早搏(PVC,n=12)的射频导管消融术。消融前进行延迟增强磁共振成像(DE-MRI)。进行电解剖标测,比较有和无诱导性室性心动过速患者的瘢痕面积和瘢痕组织的电图特征。有和无诱导性室性心动过速受试者的中位射血分数分别为27% [22,43]和43% [40,47](p=0.085)。DE-MRI确定的室性心动过速患者的室壁下梗死面积(43 [38,62] cm 2)大于非室性心动过速患者(8 [4,11] cm 2,p=0.002),电解剖图上的单极和双极电压在可诱导患者中显著较低(均p<0.05)。梗塞体积>14%鉴定出12名患者中的11名具有诱导性VT(AUC 0.94,p=0.007)。在电解剖标测中,诱导型患者孤立电位(IP)的不同部位比非诱导型患者更常见(瘢痕内点的13.2% vs. 1.1%; p<0.001)。诱导性室性心动过速的数量与IP不同位点的数量相关(R=0.87,p<0.0001)。梗死后诱导性室性心动过速患者的瘢痕组织与无诱导性室性心动过速患者的瘢痕组织在数量和质量上存在差异。瘢痕大小和IP与VT诱导相关。
Structural factors contributing to the development of post-infarction ventricular tachycardia (VT) are unclear. The purpose of this study was to analyze infarct architecture and electrogram characteristics in patients with and without inducible VT and to identify correlates of post-infarction VT. Twenty-four post-infarction patients (median age 64 [53,70] years) were referred for radiofrequency catheter ablation of VT (n=12) or frequent symptomatic premature ventricular contractions (PVCs, n=12). Delayed-enhanced magnetic resonance imaging (DE-MRI) was obtained prior to ablation. Electroanatomical mapping was performed and scar area and electrogram characteristics of the scar tissue were compared in patients with and without inducible VT. The median ejection fraction in subjects with and without inducible VT was 27% [22,43] and 43% [40,47], respectively (p=0.085). Subendocardial infarct area determined by DE-MRI was larger in patients with inducible VT (43 [38,62] cm2) than those who were non-inducible (8 [4,11] cm2, p=0.002), and unipolar and bipolar voltages on electroanatomical maps were significantly lower in inducible patients (both p<0.05). An infarct volume of >14% identified 11 of 12 patients with inducible VT (AUC 0.94, p=0.007). On electroanatomical mapping, distinct sites with isolated potentials (IPs) were more prevalent in inducible than noninducible patients (13.2% vs. 1.1% of points within scar; p<0.001). The number of inducible VTs correlated with the number of distinct sites with IPs (R=0.87, p<0.0001). Scar tissue in post-infarction patients with inducible VT shows quantitative and qualitative differences from scars in patients without inducible VT. Scar size and IPs are correlated with VT inducibility.