Electromechanical characterization of chronic myocardial infarction in the canine coronary occlusion model

• Published in: Circulation (New York, N.Y.) N.Y.), 1998-11, Vol.98 (19), p.2055-2064
• Main Authors: GEPSTEIN, L, GOLDIN, A, BEN-HAIM, S. A, LESSICK, J, HAYAM, G, SHPUN, S, SCHWARTZ, Y, HAKIM, G, SHOFTY, R, TURGEMAN, A, KIRSHENBAUM, D
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Biomechanical Phenomena; Cardiology. Vascular system; Chronic Disease; Coronary Disease - complications; Coronary heart disease; Dogs; Electrophysiology; Heart; Medical sciences; Myocardial Infarction - etiology; Myocardial Infarction - pathology; Myocardial Infarction - physiopathology
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.cir.98.19.2055

Defining the presence, extent, and nature of the dysfunctional myocardial tissue remains a cornerstone in diagnostic cardiology. A nonfluoroscopic, catheter-based mapping technique that can spatially associate endocardial mechanical and electrical data was used to quantify electromechanical changes in the canine chronic infarction model. We mapped the left ventricular (LV) electromechanical regional properties in 11 dogs with chronic infarction (4 weeks after LAD ligation) and 6 controls. By sampling the location of a special catheter throughout the cardiac cycle at multiple endocardial sites and simultaneously recording local electrograms from the catheter tip, the dynamic 3-dimensional electromechanical map of the LV was reconstructed. Average endocardial local shortening (LS, measured at end systole and normalized to end diastole) and intracardiac bipolar electrogram amplitude were quantified at 13 LV regions. Endocardial LS was significantly lower at the infarcted area (1.2+/-0.9% [mean+/-SEM], P