Epicardial and endocardial ST potential mapping in ischaemia

The electrocardiographic change associated with ischaemia is typically ST segment depression which is usually most prominent over the left chest wall. The position of the ST depression does not predict the ischaemic territories in the myocardium or the involved coronary arteries. To evaluate the source of ST depression, a sheep model of subendocardial ischaemia using partial coronary artery ligation coupled with atrial pacing was developed. Ischaemia was induced initially in either the left anterior descending coronary artery or the left circumflex coronary artery territory and subsequently in the territory of the other vessel. The ischaemic regions were documented by a fluorescent microsphere technique. During ischaemia potentials were mapped simultaneously from the endocardium and the epicardium. The distributions of epicardial potentials from either ischaemic source were very similar (0.77±0.14, P<0.0001), both showing ST depression on the free wall of the left ventricle, and no association between the ST depression and the ischaemic region. At the same time, the endocardial ST elevation was directly associated with the region of reduced blood flow. Insulating the heart from the surrounding tissue with plastic increased the magnitude of epicardial and endocardial ST and QRS potentials and decreased the potentials from limb leads, implying that the ST depression arises from current paths within the myocardium rather than external. Increasing the percent stenosis of a coronary artery increased epicardial ST depression at the lateral boundary and resulted in ST elevation starting from the ischaemic centre as ischaemia became transmural. These results suggest that the major source of ECG changes is the lateral boundary between ischaemic and normal territories. This postulate was supported by the spatial flow distributions which showed a sharp lateral flow change but a gradual transmural flow transition. In conclusion, ST segment depression can not distinguish an ischaemic region even from the epicardium. The ischaemic source does relate spatially to the endocardial ST change but not to the epicardial ST change. The current paths during subendocardial ischaemia must be in the myocardium and probably originate from the injury current which flows at the lateral boundary. These effects are not explained by conventional ECG theory but they do explain why body surface ST depression does not localise cardiac ischaemia in humans. The electric and pathophysiologic basis of remote ST depression occurring with ST elevation during acute myocardial infarction remains controversial. To explore the possible mechanism of such ST depression, different sizes of myocardial infarction were produced. The epicardial and endocardial ST potentials were measured and correlated with regional myocardial blood flow measured by fluorescent microspheres. Epicardial ST distributions showed that occluding a small vessel produced the expected ST elevation over the infarcting region with little ST depression over the noninfarcting region, whereas either the occlusion of the left anterior descending coronary artery or the left circumflex coronary artery resulted in a powerful electrical dipole with ST elevation over the infarcted region and ST depression over the noninfarcted region. Examination of fluorescent microsphere delivery into the tissues showed that with smaller infarcts the flow remained unchanged in the noninfarcted region (1.09±0.19 to 1.12±0.15, P>0.05). With large infarcts there was approximately a 30% flow reduction in the noninfarcted region which directly correlated to the perfusion pressure drop (r=0.82, P<0.001). These findings suggest that ST depression reflects extensive infarction and is associated with reduced perfusion of the noninfarcted myocardium. The reduced perfusion may have a significant reversible role in the poor prognosis of these patients.