Whole human heart histology to validate electroanatomical voltage mapping in patients with non-ischaemic cardiomyopathy and ventricular tachycardia
Whole human heart histology to validate electroanatomical voltage mapping in patients with non-ischaemic cardiomyopathy and ventricular tachycardia
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DOI：
10.1093/eurheartj/ehy168
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发表时间：
2018-08-14
影响因子：
39.3
通讯作者：
Zeppenfeld, Katja
中科院分区：
文献类型：
--
作者：
Glashan, Claire A.;Androulakis, Alexander F. A.;Zeppenfeld, Katja
目的 电解剖电压图 (EAVM) 是非缺血性心肌病 (NICM) 纤维化识别和风险分层的重要诊断工具；目前，采用了不同的界限。我们的目的是评估 EAVM 通过与整个心脏组织学相结合来检测纤维化的性能，并确定 NICM 室性心动过速 (VT) 患者的纤维化模式。方法和结果 8 名 NICM 和 VT 患者在死亡或心脏移植前接受了 EAVM。 EAVM 数据被投影到整个心脏的切片上。在与 EAVM 部位相对应的透壁活检中评估纤维化的模式、结构和数量。 NICM 活检中的纤维化模式 (n = 507) 变化很大，并且不限于中壁/心外膜下。纤维化结构很少是致密的，但通常是斑片状和/或弥漫性的。在 NICM 中，没有异常纤维化的活检单极电压 (UV) 和双极电压 (BV) 显示与壁厚度 (WT) 呈线性相关。存活心肌的数量与 UV 和 BV 呈线性相关。因此，任何描绘纤维化的截止值都表现不佳。生成一个方程，计算任何位置的纤维化量，给定 WT 和 UV 或 BV 结论 考虑到 WT、纤维化量以及 UV 和 BV 之间的线性关系，寻找任何不同的电压截止值来识别 NICM 中的纤维化是徒劳的。如果 WT 和电压已知，则可以计算纤维化的量。纤维化模式和结构与缺血性心肌病不同，缺血基质的发现可能不适用于 NICM。
Aims Electroanatomical voltage mapping (EAVM) is an important diagnostic tool for fibrosis identification and risk stratification in non-ischaemic cardiomyopathy (NICM); currently, distinct cut-offs are applied. We aimed to evaluate the performance of EAVM to detect fibrosis by integration with whole heart histology and to identify the fibrosis pattern in NICM patients with ventricular tachycardias (VTs)Methods and results Eight patients with NICM and VT underwent EAVM prior to death or heart transplantation. EAVM data was projected onto slices of the entire heart. Pattern, architecture, and amount of fibrosis were assessed in transmural biopsies corresponding to EAVM sites. Fibrosis pattern in NICM biopsies (n = 507) was highly variable and not limited to mid-wall/sub-epicardium. Fibrosis architecture was rarely compact, but typically patchy and/or diffuse. In NICM, biopsies without abnormal fibrosis unipolar voltage (UV) and bipolar voltage (BV) showed a linear association with wall thickness (WT). The amount of viable myocardium showed a linear association with both UV and BV. Accordingly, any cut-off to delineate fibrosis performed poorly. An equation was generated calculating the amount of fibrosis at any location, given WT and UV or BVConclusion Considering the linear relationships between WT, amount of fibrosis and both UV and BV, the search for any distinct voltage cut-off to identify fibrosis in NICM is futile. The amount of fibrosis can be calculated, if WT and voltages are known. Fibrosis pattern and architecture are different from ischaemic cardiomyopathy and findings on ischaemic substrates may not be applicable to NICM.