Electorcardiographic ST-segment analysis in the characterization of myocardial ischemia and infarction.
The ST segments of the electrocardiogram (ECG) become elevated within 20 to 30 seconds after the onset of acute coronary occlusion and, when persistent, such changes offer a possible indirect marker of the extent and severity of myocardial ischemic injury and of eventual cell death. When ST-segment elevation on the epicardial ECG is measured 15 minutes after an acute coronary occlusion in the dog, a general correlation exists with biochemical changes, regional myocardial blood flow, and myocardial electrolyte alterations measured at 15 minutes, although when an effort is made to correlate the degree of such alterations with the magnitude of the ST-segment change there is considerable scatter. On the other hand, when the ST-segment elevation at 15 minutes is correlated with myocardial blood flow, histologic changes, and creating phosphokinase (CPK) depletion 24 hours later, the correlation is good. Possible mechanisms underlying ST-segment elevation are discussed, and data are reviewed which indicate that the epicardial ECG my be relatively insentive to subendocardial injury; in the experimental setting this problem may be partially corrected by the use of intramyocardial ECG leads. The extension of direct epicardial ECG maps to precordial ST-segment mapping poses additional problems that include reduced sensitively, problems due to reciprocal changes in the ECG at the body surface, surface contact of the electrodes, pericarditis, and individual variability in the rate of spontaneous regression of ST-segment changes. Such mapping appears reliable only for infarctions of the anterior and lacteral wall. Further research is necessary on analysis of the QRS complex, and use of vector leads. Despite these problems experimental and clinical studies indicate that precordial electrocardiographic analysis may be useful for detecting acute changes in the severity of ischemic injury over relatively short periods of time (2 to 4 hours). This indirect measure clearly will require correlation with specific markers of ischemic damage, but with further improvements it seems likely that analysis of serial ECG changes will evolve into a valuable and reliable nonivasive clinical tool for characterizing myocardial ischemia and infarction.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003326:Coronary Circulation; D004285:Dogs; D004562:Electrocardiography; D007773:Lactates / Q000378:metabolism; D009203:Myocardial Infarction / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010496:Pericardium / Q000503:physiopathology; D010725:Phosphocreatine / Q000378:metabolism
D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate