Multimodality imaging showed that any single modality significantly underestimated the total VT substrate area (76.0 cm2; P<0.001), highlighting regional heterogeneities in postischemic adaptation.
Observational (n=15)
Combining structural and functional imaging reveals regional heterogeneities in the postischemic VT substrate, suggesting that areas with both abnormal innervation and CMR scar may be prime targets for VT ablation.
p-value: p=<0.001
Postischemic adaptation results in characteristic myocardial structural and functional changes in the ventricular tachycardia (VT) substrate. The aim of this study was to compare myocardial structural and functional adaptations (late gadolinium enhancement/abnormal innervation) with detailed VT mapping data to identify regional heterogeneities in postischemic changes. Methods: Fifteen patients with ischemic cardiomyopathy and drug-refractory VT underwent late gadolinium enhancement cardiac MRI (CMR), 123 I-metaiodobenzylguanidine SPECT, and high-resolution bipolar voltage mapping to assess fibrosis (.3 SDs), abnormal innervation (,50% tracer uptake), and low-voltage area (,1.5 mV), respectively. Three-dimensional reconstructed CMR/ 123 I-metaiodobenzylguanidine models were coregistered for further comparison. Results: Postischemic structural and functional adaptations in all 3 categories were similar in size (reported as median quartile 1-quartile 3: CMR scar, 46.1 cm 2 33.1-86.9 cm 2 ; abnormal innervation, 47.8 cm 2 40.5-68.1 cm 2 ; and low-voltage area, 29.5 cm 2 24.5-102.6 cm 2 ; P . 0.05). However, any single modality underestimated the total VT substrate area defined as abnormal in at least 1 of the 3 modalities (76.0 cm 2 57.9-143.2 cm 2 ; P , 0.001). Within the total VT substrate area, regions abnormal in all 3 modalities were most common (25.2%). However, significant parts of the VT substrate had undergone heterogeneous adaptation (abnormal in ,3 modalities); the most common categories were "abnormal innervation only" (18.2%), "CMR scar plus abnormal innervation only" (14.9%), and "CMR scar only" (14.6%). All 14 VT channel/exit sites (0.88 0.74 mV) were localized to myocardium demonstrating CMR scar and abnormal innervation. This specific tissue category accounted for 68.3% of the CMR scar and 31.2% of the total abnormal postischemic VT substrate area. Conclusion: Structural and functional imaging demonstrated regional heterogeneities in the postischemic VT substrate not appreciated by any single modality alone. The coexistence of abnormal innervation and CMR scar may identify a particularly "proarrhythmic" adaptation and may represent a potential novel target for VT ablation.
Imanli et al. (Fri,) conducted a observational in Ischemic cardiomyopathy and drug-refractory ventricular tachycardia (n=15). Multimodality imaging (CMR, 123I-mIBG SPECT, and bipolar voltage mapping) vs. Single modality imaging was evaluated on Total VT substrate area defined as abnormal in at least 1 of the 3 modalities (p=<0.001). Multimodality imaging showed that any single modality significantly underestimated the total VT substrate area (76.0 cm2; P<0.001), highlighting regional heterogeneities in postischemic adaptation.