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脂肪移植转位术(AGTP)对心肌梗死后瘢痕的电生理效应:致心律失常基质的多模态特征

Electrophysiological effects of adipose graft transposition procedure (AGTP) on the post-myocardial infarction scar: A multimodal characterization of arrhythmogenic substrate.

作者信息

Adeliño Raquel, Martínez-Falguera Daina, Curiel Carolina, Teis Albert, Marsal Roger, Rodríguez-Leor Oriol, Prat-Vidal Cristina, Fadeuilhe Edgar, Aranyó Júlia, Revuelta-López Elena, Sarrias Axel, Bazan Víctor, Andrés-Cordón Joan F, Roura Santiago, Villuendas Roger, Lupón Josep, Bayes-Genis Antoni, Gálvez-Montón Carolina, Bisbal Felipe

机构信息

ICREC Research Program, Germans Trias i Pujol Research Institute (IGTP), Barcelona, Spain.

Faculty of Medicine, University of Barcelona, Barcelona, Spain.

出版信息

Front Cardiovasc Med. 2022 Sep 20;9:983001. doi: 10.3389/fcvm.2022.983001. eCollection 2022.

DOI:10.3389/fcvm.2022.983001
PMID:36204562
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9530287/
Abstract

OBJECTIVE

To assess the arrhythmic safety profile of the adipose graft transposition procedure (AGTP) and its electrophysiological effects on post-myocardial infarction (MI) scar.

BACKGROUND

Myocardial repair is a promising treatment for patients with MI. The AGTP is a cardiac reparative therapy that reduces infarct size and improves cardiac function. The impact of AGTP on arrhythmogenesis has not been addressed.

METHODS

MI was induced in 20 swine. Contrast-enhanced magnetic resonance (ce-MRI), electrophysiological study (EPS), and left-ventricular endocardial high-density mapping were performed 15 days post-MI. Animals were randomized 1:1 to AGTP or sham-surgery group and monitored with ECG-Holter. Repeat EPS, endocardial mapping, and ce-MRI were performed 30 days post-intervention. Myocardial SERCA2, Connexin-43 (Cx43), Ryanodine receptor-2 (RyR2), and cardiac troponin-I (cTnI) gene and protein expression were evaluated.

RESULTS

The AGTP group showed a significant reduction of the total infarct scar, border zone and dense scar mass by ce-MRI ( = 0.04), and a decreased total scar and border zone area in bipolar voltage mapping ( < 0.001). AGTP treatment significantly reduced the area of very-slow conduction velocity (<0.2 m/s) ( = 0.002), the number of deceleration zones ( = 0.029), and the area of fractionated electrograms ( = 0.005). No differences were detected in number of induced or spontaneous ventricular arrhythmias at EPS and Holter-monitoring. SERCA2, Cx43, and RyR2 gene expression were decreased in the infarct core of AGTP-treated animals ( = 0.021, = 0.018, = 0.051, respectively).

CONCLUSION

AGTP is a safe reparative therapy in terms of arrhythmic risk and provides additional protective effect against adverse electrophysiological remodeling in ischemic heart disease.

摘要

目的

评估脂肪移植转位术(AGTP)的心律失常安全性及其对心肌梗死后(MI)瘢痕的电生理影响。

背景

心肌修复是MI患者一种有前景的治疗方法。AGTP是一种心脏修复疗法,可减小梗死面积并改善心脏功能。AGTP对心律失常发生的影响尚未得到探讨。

方法

对20头猪诱导MI。MI后15天进行对比增强磁共振成像(ce-MRI)、电生理研究(EPS)和左心室心内膜高密度标测。动物按1:1随机分为AGTP组或假手术组,并通过动态心电图监测。干预后30天重复进行EPS、心内膜标测和ce-MRI。评估心肌肌浆网钙ATP酶2(SERCA2)、连接蛋白43(Cx43)、兰尼碱受体2(RyR2)和心肌肌钙蛋白I(cTnI)的基因及蛋白表达。

结果

ce-MRI显示AGTP组总梗死瘢痕、边缘区和致密瘢痕质量显著减少(P = 0.04),双极电压标测中总瘢痕和边缘区面积减小(P < 0.001)。AGTP治疗显著减小了极慢传导速度(<0.2 m/s)区域面积(P = 0.002)、减速区数量(P = 0.029)和碎裂电图区域面积(P = 0.005)。在EPS和动态心电图监测中,诱发性或自发性室性心律失常数量未检测到差异。AGTP治疗动物梗死核心区SERCA2、Cx43和RyR2基因表达降低(分别为P = 0.021、P = 0.018和P = 0.051)。

结论

就心律失常风险而言,AGTP是一种安全的修复疗法,并为缺血性心脏病的不良电生理重塑提供额外保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/79caebd7a6a7/fcvm-09-983001-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/b638d1e14383/fcvm-09-983001-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/1bee4c559253/fcvm-09-983001-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/357edd420cc0/fcvm-09-983001-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/d526cf44103c/fcvm-09-983001-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/40cef280ba9f/fcvm-09-983001-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/aad7b817c248/fcvm-09-983001-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/79caebd7a6a7/fcvm-09-983001-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/b638d1e14383/fcvm-09-983001-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/1bee4c559253/fcvm-09-983001-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/357edd420cc0/fcvm-09-983001-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/d526cf44103c/fcvm-09-983001-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/40cef280ba9f/fcvm-09-983001-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/aad7b817c248/fcvm-09-983001-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8083/9530287/79caebd7a6a7/fcvm-09-983001-g007.jpg

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