Preliminary animal and clinical experiences using an electromechanical endocardial mapping procedure to distinguish infarcted from healthy myocardium

• Published in: Circulation (New York, N.Y.) Vol. 98; no. 11; pp. 1116 - 1124
• Main Authors: KORNOWSKI, R, HONG, M. K, GEPSTEIN, L, GOLDSTEIN, S, ELLAHHAM, S, BEN-HAIM, S. A, LEON, M. B
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 15.09.1998; American Heart Association, Inc
• Subjects: Animals; Biological and medical sciences; Cardiology. Vascular system; Coronary heart disease; Diastole - physiology; Disease Models, Animal; Dogs; Echocardiography; Electrophysiology; Endocardium - diagnostic imaging; Endocardium - physiopathology; Heart; Humans; Ligation; Medical sciences; Myocardial Infarction - diagnostic imaging; Myocardial Infarction - physiopathology; Regression Analysis; Human; Electromechanics; Infarct; Device; Electrophysiology; Endocardium; Cardiovascular disease; Exploration; Coronary heart disease; Myocardial disease; Heart mapping; Animal; Myocardium; Technique
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.cir.98.11.1116

A catheter-based left ventricular (LV) endocardial mapping procedure using electromagnetic field energy for positioning of the catheter tip was designed to acquire simultaneous measurements of endocardial voltage potentials and myocardial contractility. We investigated such a mapping system to distinguish between infarcted and normal myocardium in an animal infarction model and in patients with coronary artery disease. Measurements of LV endocardial unipolar (UP) and bipolar (BP) voltages and local endocardial shortening were derived from dogs at baseline (n=12), at 24 hours (n=6), and at 3 weeks (n=6) after occlusion of the left anterior descending coronary artery. Also, 12 patients with prior myocardial infarction (MI) and 12 control patients underwent the LV endocardial mapping study for assessment of electromechanical function in infarcted versus healthy myocardial regions. In the canine model, a significant decrease in voltage potentials was noted in the MI zone at 24 hours (UP, 42. 8+/-9.6 to 29.1+/-12.2 mV, P=0.007; BP, 11.6+/-2.3 to 4.9+/-1.2 mV, P<0.0001) and at 3 weeks (UP, 41.0+/-8.9 to 13.9+/-3.9 mV, P<0.0001; BP, 11.2+/-2.8 to 2.4+/-0.4 mV, P<0.0001). No change in voltage was noted in zones remote from MI. In patients with prior MI, the average voltage was 7.2+/-2.7 mV (UP)/1.4+/-0.7 mV (BP) in MI regions, 17.8+/-4.6 mV (UP)/4.5+/-1.1 mV (BP) in healthy zones remote from MI, and 19.7+/-4.4 mV (UP)/5.8+/-1.0 mV (BP) in control patients without prior MI (P<0.001 for MI values versus remote zones or control patients). In the canine model and patients, local endocardial shortening was significantly impaired in MI zones compared with controls. These preliminary data suggest that infarcted myocardium could be accurately diagnosed and distinguished from healthy myocardium by a reduction in both electrical voltage and mechanical activity. Such a diagnostic electromechanical mapping study might be clinically useful for accurate assessment of myocardial function and viability.