Evaluation of Precordial Electrocardiographic Mapping as a Means of Assessing Changes in Myocardial Ischemic Injury

Precordial electrocardiographic mapping has been proposed as a method for evaluating the extent of myocardial injury in patients with acute myocardial infarction. To assess the relationship between direct measures of myocardial cell damage and findings obtained by precordial mapping, the left anterior descending coronary artery (LAD) was occluded in dogs instrumented for simultaneous recording of epicardial and precordial electrocardiograms. The sum in millivolts of ST-segment elevation recorded from 30 electrodes placed in a Silastic grid sutured to the epicardium (Epi∑ST) was compared to that recorded from 30 precordial electrodes (Pre∑ST). While ischemic injury was: 1) maintained constant with a fixed occlusion; 2) reduced by partial reperfusion; 3) increased by addition of a second occlusion; or 4) increased repeatedly by intermittent infusions of isoproterenol, Epi∑ST and Pre∑ST were always closely correlated in each of the 16 dogs studied: r = 0.92 ± 0.01 (sem). In seven control dogs, 30 minutes after coronary occlusion, Pre∑ST had fallen to 77.4 ± 6.6% of its value 15 minutes postocclusion. In seven experimental dogs, two branches of the LAD were occluded. Fifteen minutes after double occlusion, one occlusion was released; 30 min after the initial occlusion Pre∑ST had fallen significantly more than control, to 43.1 ± 13.1% of its value 15 minutes postocclusion. Simultaneously, epicardial sites in the reperfused area also showed normalization of ST segments and 24 hours later exhibited normal myocardial creatine phosphokinase activity and normal histologic appearance. During the same experiment, the mean precordial R wave voltage of sites with ST-segment elevations exceeding 0.15 mV 15 minutes following occlusion fell significantly (P < 0.05) more in the control group (from 1.14 ± 0.15 to 0.75 ± 0.06 mV) than in the reperfused group (from 1.06 ± 0.09 to 0.96 ± 0.17 mV) during the ensuing 45 minutes. Thus, more rapid normalization of Pre∑ST or preservation of precordial R wave voltage reflected the actual prevention of myocardial necrosis by reperfusion. These findings demonstrate the usefulness of precordial electrocardiographic mapping for evaluating changes in myocardial ischemic injury. Sites at which appearance of epicardial ST segment is not a reliable index of ischemic injury were associated with the development of intraventricular conduction blocks with Q to intrinsic deflection intervals exceeding 40 msec or QRS durations exceeding 65 msec; these changes were associated with precordial RSR′ configurations. Such sites, whether recorded from precordial or epicardial leads, should be excluded from ST-segment measurements used in the assessment of myocardial ischemia.