Transmural Mapping of Myocardial Refractoriness and Endocardial Dispersion of Repolarization in an Ovine Model of Chronic Myocardial Infarction

• Published in: Pacing and clinical electrophysiology 2009-07, Vol.32 (7), p.851-861
• Main Authors: POULIOPOULOS, JIM, THIAGALINGAM, ARAVINDA, EIPPER, VICKI E., CAMPBELL, CRAIG, ROSS, DAVID L., KOVOOR, PRAMESH
• Format: Article
• Language: English
• Subjects: Animals; Body Surface Potential Mapping - methods; Chronic Disease; conduction; Disease Models, Animal; dispersion; effective refractory period; Endocardium - physiopathology; fibrosis; Heart Conduction System - physiopathology; Humans; infarction; Myocardial Infarction - complications; Myocardial Infarction - diagnosis; Myocardial Infarction - physiopathology; repolarization; Sheep; Ventricular Dysfunction, Left - diagnosis; Ventricular Dysfunction, Left - etiology; Ventricular Dysfunction, Left - physiopathology
• ISSN: 0147-8389; 1540-8159
• DOI: 10.1111/j.1540-8159.2009.02399.x

Background: Myocardial refractoriness and repolarization is an important electrophysiological property that, when altered, increases the risk of arrhythmogenesis. These electrophysiological changes associated with chronic myocardial infarction (MI) have not been studied in detail. We assessed the influence of left ventricular (LV) scarring on local refractoriness, repolarization, and electrogram characteristics. Methods: MI was induced in five sheep by percutaneous left anterior descending artery occlusion for 3 hours. Mapping was performed at 19 ± 6 weeks post‐MI. A total of 20 quadripolar transmural needles were deployed at thoracotomy in the LV within and surrounding scar. Bipolar pacing was performed from each needle to assess the effective refractory period (ERP) of the subendocardium and subepicardium. The activation (AT) and repolarization (RT) times, and modified activation recovery interval (ARIm) were determined from endocardial unipolar electrograms recorded in sinus rhythm simultaneously from all needles. Scarring was quantified histologically and compared with electrophysiological characteristics. Results: Increased scarring corresponded with increased ERP (P < 0.01), decreased subendocardial electrogram amplitude (P < 0.001), and slope (P < 0.001). ERP did not differ between endocardium and epicardium (P > 0.05). The ARIm and RT were prolonged during early myocardial activation (P < 0.001). After adjusting for AT, the RT and ARIm were prolonged in areas of scarring (P < 0.001). After adjusting for electrogram amplitude, the ARIm was prolonged in dense scar (P < 0.05). Conclusions: We confirmed histologically that scarring contributes to prolongation of repolarization, increased refractoriness, and reductions in conduction and voltage post‐MI. Prolongation of repolarization may be further augmented when local activation is earliest or electrogram voltage is decreased within scar.