Mechanism and diagnostic potential of reciprocal ECG changes induced by acute coronary artery occlusion in pigs

Abstract

Reciprocal ST-segment depression simulating additional subendocardial ischemia is commonly observed in ST-segment elevation myocardial infarction. To study the mechanism and characterization of the whole reciprocal electrocardiogram (ECG) patterns induced by acute coronary artery occlusion at different locations in the absence of additional subendocardial ischemia in pigs. Conventional 12-lead ECG and/or local extracellular epicardial, mid-myocardial, and endocardial electrograms were recorded during the acute occlusion of right coronary (RC) and left anterior descending (LAD) coronary arteries in the in situ (n = 9) or in the isolated perfused (n = 5) pig hearts. Mid-RC occlusion induced reciprocal ST-segment depression (-0.43 ± 0.14 mV; P<.01) and S-wave deepening (-0.74 ± 0.23 mV; P<.01) in anterior ECG leads. Mid-LAD occlusion induced reciprocal S-wave deepening (-0.43 ± 0.37 mV; P = .02) but not ST-segment depression in inferior leads. Proximal LAD induced reciprocal ST-segment depression (-0.21 ± 0.20 mV; P = .03) and S-wave deepening (-0.56 ± 0.58 mV; P = .04) in inferior leads. Reciprocal QRS widening was observed only during proximal LAD occlusion. Local extracellular recordings did not show significant reciprocal QRS and ST-segment changes. In the absence of additional subendocardial ischemia, acute coronary artery occlusion induces reciprocal ST-segment and S-wave changes in the 12-lead ECG that allow better differentiation between proximal and mid-LAD occlusion. Reciprocal ECG changes depend on conventional lead system design and not on the transmission of injury currents from the ischemic border zone to distant normal myocardium.