Department of Cardiology, Westmead Hospital, New South Wales, Australia (K.D.S., T.C., R.G.B., S.T., D.S., A.B., Y.K., C.-j.H., J.J.H.C., E.K., S.K.).
Westmead Applied Research Centre, The University of Sydney, New South Wales, Australia (K.D.S., T.C., R.G.B., C.D., S.T., A.B., Y.K., S.K.).
Circ Arrhythm Electrophysiol. 2024 Sep;17(9):e012922. doi: 10.1161/CIRCEP.124.012922. Epub 2024 Aug 28.
Cardiac magnetic resonance imaging (CMR)-defined ventricular scar and anatomic conduction channels (CMR-CCs) offer promise in delineating ventricular tachycardia substrate. No studies have validated channels with coregistered histology, nor have they ascertained the histological characteristics of deceleration zones (DZs) within these channels. We aimed to validate CMR scar and CMR-CCs with whole-heart histology and electroanatomic mapping in a postinfarction model.
Five sheep underwent anteroseptal infarction. CMR (116±20 days post infarct) was postprocessed using ADAS-3D, varying pixel intensity thresholds (5545, 6040, 6535, and 7030). DZs were identified by electroanatomic mapping (129±12 days post infarct). Explanted hearts were sectioned and stained with Picrosirius red, and whole-heart histopathologic shells were generated. Scar topography as well as percentage fibrosis, adiposity, and remaining viable myocardium within 3 mm histological biopsies and within CMR-CCs were determined.
Using the standard 6040 thresholding, CMR had 83.8% accuracy for identifying histological scar in the endocardium (κ, 0.666) and 61.4% in the epicardium (κ, 0.276). Thirty-seven CMR-CCs were identified by varying thresholding; 23 (62%) were unique. DZs colocalized to 19 of 23 (83%) CMR-CCs. Twenty (87%) CMR-CCs were histologically confirmed. Within-channel histological fibrosis did not differ by the presence of DZs (=0.242). Within-channel histological adiposity was significantly higher at sites with versus without DZs (24.1% versus 8.3%; <0.001).
Postprocessed CMR-derived scars and channels were validated by histology and electroanatomic mapping. Regions of CMR-CCs at sites of DZs had higher adiposity but similar fibrosis than regions without DZs, suggesting that lipomatous metaplasia may contribute to arrhythmogenicity of postinfarction scar.
心脏磁共振成像（CMR）定义的心室瘢痕和解剖传导通道（CMR-CC）在描绘室性心动过速基质方面具有广阔的前景。目前还没有研究通过与核心组织学相对比来验证这些通道，也没有确定这些通道内减速区（DZ）的组织学特征。我们旨在通过梗死模型中的全心组织学和电解剖标测来验证 CMR 瘢痕和 CMR-CC。
5 只绵羊接受前间隔梗死。CMR（梗死 116±20 天后）使用 ADAS-3D 进行后处理，改变像素强度阈值（5545、6040、6535 和 7030）。DZ 通过电解剖标测（梗死 129±12 天后）确定。取出的心脏切片，并用苦味酸天狼猩红染色，并生成全心病理壳。确定 3mm 组织学活检和 CMR-CC 内瘢痕的分布情况，以及纤维化、脂肪变性和剩余存活心肌的百分比。
使用标准的 6040 阈值，CMR 在心内膜（κ，0.666）和心外膜（κ，0.276）上识别组织学瘢痕的准确性分别为 83.8%和 61.4%。通过改变阈值确定了 37 个 CMR-CC，其中 23 个（62%）是唯一的。DZ 与 23 个（83%）中的 19 个 CMR-CC 共定位。20 个（87%）CMR-CC 通过组织学确认。通道内的组织学纤维化在有无 DZ 时没有差异（=0.242）。有 DZ 的通道内组织学脂肪含量明显高于无 DZ 的通道（24.1%比 8.3%；<0.001）。
经后处理的 CMR 衍生的瘢痕和通道通过组织学和电解剖标测得到验证。DZ 部位的 CMR-CC 内的区域脂肪含量较高，但纤维化程度与无 DZ 的区域相似，提示脂质性化生可能导致梗死后瘢痕的致心律失常性。
