The functional and molecular imaging characteristics of ischemic ventricular tachycardia (VT) substrate are incompletely understood. Our objective was to compare regional ¹⁸F-FDG PET tracer uptake with detailed electroanatomic maps (EAMs) in a more extensive series of postinfarction VT patients to define the metabolic properties of VT substrate and successful ablation sites. Methods: Three-dimensional (3D) metabolic left ventricular reconstructions were created from perfusion-normalized ¹⁸F-FDG PET images in consecutive patients undergoing VT ablation. PET defects were classified as severe (defined as <50% uptake) or moderate (defined as 50%–70% uptake), as referenced to the maximal 17-segment uptake. Color-coded PET scar reconstructions were coregistered with corresponding high-resolution 3D EAMs, which were classified as indicating dense scarring (defined as voltage < 0.5 mV), normal myocardium (defined as voltage > 1.5 mV), or border zones (defined as voltage of 0.5–1.5 mV). Results: All 56 patients had ischemic cardiomyopathy (ejection fraction, 29% ± 12%). Severe PET defects were larger than dense scarring, at 63.0 ± 48.4 cm² versus 13.8 ± 33.1 cm² (P < 0.001). Similarly, moderate/severe PET defects (≤70%) were larger than areas with abnormal voltage (≤1.5 mV) measuring 105.1 ± 67.2 cm² versus 56.2 ± 62.6 cm² (P < 0.001). Analysis of bipolar voltage (23,389 mapping points) showed decreased voltage among severe PET defects (n = 10,364; 0.5 ± 0.3 mV) and moderate PET defects (n = 5,243; 1.5 ± 0.9 mV, P < 0.01), with normal voltage among normal PET areas (>70% uptake) (n = 7,782, 3.2 ± 1.3 mV, P < 0.001). Eighty-eight percent of VT channel or exit sites (n = 44) were metabolically abnormal (severe PET defect, 78%; moderate PET defect, 10%), whereas 12% (n = 6) were in PET-normal areas. Metabolic channels (n = 26) existed in 45% (n = 25) of patients, with an average length and width of 17.6 ± 12.5 mm and 10.3 ± 4.2 mm, respectively. Metabolic channels were oriented predominantly in the apex or base (86%), harboring VT channel or exit sites in 31%. Metabolic rapid-transition areas (>50% change in ¹⁸F-FDG tracer uptake/15 mm) were detected in 59% of cases (n = 33), colocalizing to VT channels or exit sites (15%) or near these sites (85%, 12.8 ± 8.5 mm). Metabolism–voltage mismatches in which there was a severe PET defect but voltage indicating normal myocardium were seen in 21% of patients (n = 12), 41% of whom were harboring VT channel or exit sites. Conclusion: Abnormal ¹⁸F-FDG uptake categories could be detected using incremental 3D step-up reconstructions. They predicted decreasing bipolar voltages and VT channel or exit sites in about 90% of cases. Additionally, functional imaging allowed detection of novel molecular tissue characteristics within the ischemic VT substrate such as metabolic channels, rapid-transition areas, and metabolism–voltage mismatches demonstrating intrasubstrate heterogeneity and providing possible targets for imaging-guided ablation.

缺血性室性心动过速 (VT) 基质的功能和分子成像特征尚不完全清楚。我们的目标是在更广泛的梗死后 VT 患者系列中比较区域^{18 F-FDG PET 示踪剂摄取与详细的电解剖图 (EAM)，以确定 VT 底物的代谢特性和成功消融部位。}方法：三维 (3D) 代谢左心室重建从灌注标准化¹⁸连续接受 VT 消融的患者的 F-FDG PET 图像。PET 缺陷分为严重（定义为 <50% 摄取）或中度（定义为 50%–70% 摄取），参考最大 17 段摄取。颜色编码的 PET 疤痕重建与相应的高分辨率 3D EAM 共同注册，其被分类为指示密集疤痕（定义为电压 < 0.5 mV）、正常心肌（定义为电压 > 1.5 mV）或边界区域（定义为电压0.5–1.5 mV)。结果：所有 56 名患者均患有缺血性心肌病（射血分数，29% ± 12%）。严重的 PET 缺陷大于致密的疤痕，分别为 63.0 ± 48.4 cm ²和 13.8 ± 33.1 cm ² ( P< 0.001)。同样，中度/重度 PET 缺陷 (≤70%) 大于异常电压 (≤1.5 mV) 的区域，分别为 105.1 ± 67.2 cm ²和 56.2 ± 62.6 cm ² ( P < 0.001)。双极电压分析（23,389 个映射点）显示，严重 PET 缺陷（n = 10,364；0.5 ± 0.3 mV）和中度 PET 缺陷（n = 5,243；1.5 ± 0.9 mV，P < 0.01）之间的电压降低，正常电压在正常之间PET 面积 (>70% 摄取) ( n = 7,782, 3.2 ± 1.3 mV, P < 0.001)。88% 的 VT 通道或出口部位（n = 44）代谢异常（重度 PET 缺陷，78%；中度 PET 缺陷，10%），而 12%（n = 6) 位于 PET 正常区域。45% ( n = 25) 的患者存在代谢通道 ( n = 26) ，平均长度和宽度分别为 17.6 ± 12.5 mm 和 10.3 ± 4.2 mm。代谢通道主要位于顶端或底部（86%），31% 包含 VT 通道或出口位点。在 59% 的病例（n = 33）中检测到代谢快速过渡区（¹⁸ F-FDG 示踪剂摄取/15 mm 变化 >50% ），共定位于 VT 通道或出口部位（15%）或这些部位附近（ 85%，12.8 ± 8.5 毫米）。21% 的患者出现代谢-电压不匹配，其中存在严重的 PET 缺陷，但电压表明心肌正常（n= 12)，其中 41% 的人窝藏 VT 通道或出口站点。结论：异常的¹⁸ F-FDG 摄取类别可以使用增量 3D 升压重建来检测。他们预测在大约 90% 的情况下，双极电压和 VT 通道或出口位置会降低。此外，功能成像允许检测缺血性 VT 基质内的新分子组织特征，例如代谢通道、快速过渡区和代谢-电压不匹配，证明基质内异质性，并为成像引导消融提供可能的靶点。