Mechanism of inferior electrocardiographic ST-segment depression during acute anterior myocardial infarction in a baboon model.

Controversy exists concerning the mechanism of electrocardiographic (ECG) ST-segment depression in leads remote from an area of acute myocardial infarction. Thus, 13 baboons were studied during ligation of the distal third of the left anterior descending coronary artery. The morphologic pattern of the ECG limb leads in the supine baboons resembled that of an asthenic human and did not change when the chest was opened. The visually apparent infarct area of the distal anterior wall was confirmed by epicardial ECG mapping 30 minutes after ligation, and by tissue creatine kinase and histologic study at 24 hours. All 13 baboons had ST depression in leads III and aVF of 0.1 to 1.2 mV at 30 minutes, and 11 of 13 had similar changes in lead II. Also, all 13 baboons had ST elevation in lead aVL (n = 10) or aVR (n = 11), suggesting that the ST vector from the infarct area was directed away from the inferior leads. In no baboon did inferoposterior wall ventricular epicardial mapping show evidence of myocardial ischemia, and mean creatine kinase content from the infarct sites was markedly lower than that from posteroinferior sites (12.7 +/- 2.8 vs 20.6 +/- 2.1 IU/mg protein, p less than 0.01). In addition, the inferoposterior myocardium was normal histologically. In conclusion, acute myocardial infarction often results in reciprocal ST depression at sites distant from the area of acute necrosis and need not represent "ischemia at a distance."