A swine model of infarct-related reentrant ventricular tachycardia: Electroanatomic, magnetic resonance, and histopathological characterization

作者：Tschabrunn Cory M; Roujol Sebastien; Nezafat Reza; Faulkner Jones Beverly; Buxton Alfred E; Josephson Mark E; Anter Elad^*

来源：Heart Rhythm, 2016, 13(1): 262-273.

DOI：10.1016/j.hrthm.2015.07.030

• Myocardial infarction
• Mapping
• Ventricular tachycardia
• Ablation

BACKGROUND Human ventricular tachycardia (VT) after myocardial infarction usually occurs because of subendocardial reentrant circuits originating in scar tissue that borders surviving myocardial bundles. Several predinical large animal models have been used to further study postinfarct reentrant VT, but with varied experimental methodologies and limited evaluation of the underlying substrate or induced arrhythmia mechanism.
OBJECTIVE We aimed to develop and characterize a swine model of scar-related reentrant VT.
METHODS Thirty-five Yorkshire swine underwent 180-minute occlusion of the left anterior descending coronary artery. Thirtyone animals (89%) survived the 6-8-week survival period. These animals underwent cardiac magnetic resonance imaging followed by electrophysiology study, detailed electroan atomic mapping, and histopathological analysis.
RESULTS Left ventricular (LV) ejection fraction measured using CMR imaging was 36% - 6.6% with anteroseptal wall motion abnormality and late gadolinium enhancement across 12.5% - 4.10/o of the LV surface area. Low voltage measured using endocardial electroanatomic mapping encompassed 11.10/0 - 3.5% of the LV surface area (bipolar voltage <1.5 mV) with anterior, anteroseptal, and anterolateral involvement. Reentrant circuits mapped were largely determined by functional rather than fix anatomical barriers, consistent with "pseudo-block" due to anisotropic conduction. Sustained monomorphic VT was induced in 28 of 31 swine (90%) (67 VTs; 2.4 - 1.1; range 1-4) and characterized as reentry. VT circuits were subendocardial, with an arrhythmogenic substrate characterized by transmural anterior scar with varying degrees of fibrosis and myocardial fiber disarray on the septa l and lateral borders.
CONCLUSION This is a well-characterized swine model of scarrelated subendocardial reentrant VT. This model can serve as the basis for further investigation in the physiology and therapeutics of humanlike postinfarction reentrant VT.

• 出版日期2016-1