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(Circulation. 1998;98:2055-2064.)
© 1998 American Heart Association, Inc.
Basic Science Reports |
Electromechanical Characterization of Chronic Myocardial Infarction in the Canine Coronary Occlusion Model
From the Cardiovascular System Laboratory, The Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Correspondence to Lior Gepstein, MD, Cardiovascular System Laboratory, The Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Efron St, POB 9649, 31096 Haifa, Israel. E-mail mdlior{at}tx.technion.ac.il
Background—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.
Methods and Results—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<0.01) compared with the noninfarcted regions (7.2±1.1% to 13.5±1.5%) and with the same area in controls (15.5±1.2%, P<0.01). Average bipolar amplitude was also significantly lower at the infarcted zone (2.3±0.2 mV, P<0.01) compared with the same region in controls (10.3±1.3 mV) and with the noninfarcted regions (4.0±0.7 to 10.2±1.5 mV, P<0.01) in the infarcted group. In addition, the electrical maps could accurately delineate both the location and extent of the infarct, as demonstrated by the high correlation with pathology (Pearson's correlation coefficient=0.90) and by the precise identification of the infarct border.
Conclusions—Chronic myocardial infarcted tissue can be characterized and quantified by abnormal regional mechanical and electrical functions. The unique ability to assess the regional ventricular electromechanical properties in various myocardial disease states may become a powerful tool in both clinical and research cardiology.
Key Words: mechanics • myocardial infarction • electrophysiology • mapping
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