DOI: 10.1161/circ.148.suppl_1.18924 ISSN: 0009-7322

Abstract 18924: Structural and Electrical Remodeling Differences in Ischemia-Reperfusion versus Non-Reperfusion Myocardial Infarction

masahiro sekigawa, Jonathan Salas, David Callans, Francis E Marchlinski, Robert Gorman, Cory Tschabrunn
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Background: Structural and electrical remodeling following myocardial infarction (MI) can result in the development of arrhythmogenic substrate and ventricular tachycardia (VT). Various clinical factors such as reperfusion status, and occluded coronary distribution can impact the size of post-infarction scar.

Objective: To investigate the structural and electrical remodeling characteristics in 2 different porcine models of MI.

Methods: Fourteen swine underwent anterior infarction via 180min balloon occlusion followed by reperfusion (IR Group, n=7) or chronic total occlusion by embolizing the mid-LAD with a coil (CTO Group, n=7). Cardiac MRI and electroanatomic substrate mapping (Thermocool ST-SF) and high-resolution activation mapping (Pentaray 2-6-2mm) was performed in all subjects 8-9 weeks following infarction. Low bipolar voltage area (<1.5mV), very low bipolar voltage area (<0.5mV), and CMR LGE intensity volume reconstruction (inHeart Medical) were assessed. Programmed stimulation from the Ventricular apex was performed for VT inducibility assessment.

Results: The CTO group had more extensive low bipolar voltage area (CTO: 36±6cm 2 vs. IR: 23±12cm 2 , p=0.04) and dense low bipolar voltage areas (CTO: 20±7cm 2 vs. IR: 7±6cm 2 , p=0.01). LV EDV was similar (CTO: 122±14ml vs. IR: 136±38ml, np) and there was no significant difference in LVEF (CTO: 28±4% vs. IR: 26±4%, np) and CMR LGE scar volume (CTO: 12±3ml vs. IR: 12±4ml, np). Voltage mapping demonstrated clear significant differences in substrate size and LV Endocardial CMR LGE intensity was more homogeneous in the CTO group than the IR group (Figure). Monomorphic VT was inducible in all 14 subjects. A total of 19 VTs were induced in CTO group (range 1-4, TCL 241±33ms) and 12 in IR group (range 1-2, TCL 208±17ms).

Conclusions: Creation of a chronic infarct results in a significantly larger area of abnormal arrhythmogenic substrate than 180 minutes of ischemia-reperfusion.

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