AUTHOR=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 

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

JOURNAL=Frontiers in Cardiovascular Medicine

VOLUME=9

YEAR=2022

URL=https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2022.983001

DOI=10.3389/fcvm.2022.983001

ISSN=2297-055X

ABSTRACT=<sec><title>Objective</title><p>To assess the arrhythmic safety profile of the adipose graft transposition procedure (AGTP) and its electrophysiological effects on post-myocardial infarction (MI) scar.</p></sec><sec><title>Background</title><p>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.</p></sec><sec><title>Methods</title><p>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.</p></sec><sec><title>Results</title><p>The AGTP group showed a significant reduction of the total infarct scar, border zone and dense scar mass by ce-MRI (<italic>p</italic> = 0.04), and a decreased total scar and border zone area in bipolar voltage mapping (<italic>p</italic> &lt; 0.001). AGTP treatment significantly reduced the area of very-slow conduction velocity (&lt;0.2 m/s) (<italic>p</italic> = 0.002), the number of deceleration zones (<italic>p</italic> = 0.029), and the area of fractionated electrograms (<italic>p</italic> = 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 (<italic>p</italic> = 0.021, <italic>p</italic> = 0.018, <italic>p</italic> = 0.051, respectively).</p></sec><sec><title>Conclusion</title><p>AGTP is a safe reparative therapy in terms of arrhythmic risk and provides additional protective effect against adverse electrophysiological remodeling in ischemic heart disease.</p></sec>