Electrophysiological effects of adipose graft transposition procedure (AGTP) on the post-myocardial infarction scar: A multimodal characterization of arrhythmogenic substrate
Electrophysiological effects of adipose graft transposition procedure (AGTP) on the post-myocardial infarction scar: A multimodal characterization of arrhythmogenic substrate
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ObjectiveTo assess the arrhythmic safety profile of the adipose graft transposition procedure (AGTP) and its electrophysiological effects on post-myocardial infarction (MI) scar.BackgroundMyocardial repair is a promising treatment for patients with MI.The AGTP is a cardiac Lamps reparative therapy that reduces infarct size and improves cardiac function.
The impact of AGTP on arrhythmogenesis has not been addressed.MethodsMI 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.
ResultsThe AGTP group showed a significant reduction of the total infarct scar, border zone and dense scar mass by ce-MRI (p = 0.04), and a decreased total scar and border zone area in bipolar voltage mapping (p < 0.001).
AGTP Reclining Wheelchairs treatment significantly reduced the area of very-slow conduction velocity (<0.2 m/s) (p = 0.002), the number of deceleration zones (p = 0.
029), and the area of fractionated electrograms (p = 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 (p = 0.021, p = 0.018, p = 0.
051, respectively).ConclusionAGTP is a safe reparative therapy in terms of arrhythmic risk and provides additional protective effect against adverse electrophysiological remodeling in ischemic heart disease.