whole_LiQin2005_thesis.pdf (14.01 MB)
Transmyocardial ST potential distributions in ischaemic heart disease
thesisposted on 2023-05-27, 15:09 authored by Li, Q
The origin of electrocardiographic ST segment depression in subendocardial ischaemia remains unclear. The location of ST depression does not enable the localization of an ischemic region. Previous studies showed that the current path was within the intramyocardium, and there was a current sink at the boundary of the ischaemic area which caused the ST depression on the epicardium. Thus, it is vital to explore the intramyocardial potential distributions during subendocardial ischaemia. Different subendocardial ischaemia animal models were produced in the present study as well as acute myocardial ischaemia model. (1) SUBENDOCARDIAL ISCHAEMIA MODEL The subendocardial ischaemia was produced by combining left atrium pacing with partial occlusion of the left anterior descending coronary artery (LAD) and/or the left circumflex coronary artery (LCX). ST potentials yvere collected simultaneously from epicardial, endocardial and three different layers of the intramyocardium of the left ventricular wall. Regional myocardial blood flow (RMBF) was also measured in the inner one-third, mid one-third and outer one-third of the left ventricular wall by fluorescent microspheres. The RMBF results showed that there was a decrease of endocardial RMBF in the ischaemic region during subendocardial ischaemia. In subendocardial ischaemia of alternate LAD or LCX areas, ST depression occurred on the epicardium, the distributions of the ST potential on the epicardium from either ischaemic region were very similar. At the same time, endocardial potentials showed ST elevation which was directly associated with the ischaemic area. In the intramyocardium, both ST elevation and ST depression occurred in different layers from the subendocardium to the subepicardium. Epicardial ST depression can not predict the ischaemic area, however, ST distribution patterns in different layers of intramyocardium during subendocardial ischaemia can be predicted from electrocardiographic theory. Thus, it is suggested that the intramyocardial electrical current path might be altered towards the epicardium. (2) SUBENDOCARDIAL ISCHAEMIA MODEL: TRANSITI,ON FROM MILD TO SEVERE DEGREE Further experiments were performed to transit ischaemia from mild degree to severe degree, and finally to full thickness ischaemia, in an attempt to explain how the intramyocardial electrical current path altered when spread towards the epicardium. ST potentials were also recorded simultaneously from epicardium, endocardium and three different layers of the left ventricular wall. By combining occlusion of the LAD or LCX by 30% and 70% of its original blood flow with left atrium pacing, mild and severe ischaemia were produced, full thickness ischaemia was produced by total occlusion of the LAD or LCX. Measurement of RMBF showed that RMBF in the inner one-third layer decreased, while RMBF in the mid and outer one-third layers remained unchanged in mild ischaemia. RMBF in every layer decreased in severe ischaemia in the ischaemic regions, with RMBF decreasing most in the inner one-third layer and least in the outer one-third layer. Although it was expected that, with 70% occlusion of the coronary artery, there would be an abrupt transition of RMBF between the mid and outer one-third layer of the left ventricular wall, the RMBF of the entire left ventricular wall was affected in the severe ischaemia. In the mild ischaemia group in either the LAD or LCX area, epicardial ST depression occurred after ischaemia and it was not related to the ischaemic region. Simultaneously recorded endocardial potentials showed ST elevation which was related to the ischaemic area. Intramyocardial ST potentials showed both ST elevation and ST depression in different layers of the LV wall, with ST elevation occurring in the ischaemic centre and ST depression occurring on the boundary of the ischaemic and non-ischaemic area. In severe subendocardial ischaemia of either the LAD or LCX area, both ST elevation and ST depression occurred on epicardium and different layers of intramyocardium, as in mild ischaemia, ST elevation appeare4 in ischaemic area, with the maximal magnitude occurring in the ischaemic centre; ST depression appeared in the non-ischaemic area, the magnitude of ST depressio!l decreased towards the ischaemic boundary. Endocardial ST elevation in severe ischaemia occurred in the ischaemic region. The different epicardial ST distribution between the mild and the severe ischaemic groups led to a postulate that the current path might breakthrough towards the epicardium during severe subendocardial ischaemia. When the ischaemia became full thickness, ST elevation appeared on the ischaemic area, and ST depression occurred on the non-ischaemic area in every layer of the left ventricle. However, the maximal ST elevation and ST depression occurred on the boundary of the ischaemic and the non-ischaemic regions. The ST distribution patterns between severe and full thickness ischaemia were totally different. (3) ACUTE MYOCARDIAL ISCHAEMIA MODEL Acute transmural ischaemia was developed by ligating either the LAD or the LCX. ST potentials and RMBF were recorded and measured in the same way as that in subendocardial ischaemia. After acute ischaemia, RMBF in different layers of the left ventricular wall in the ischaemic region decreased significantly, and RMBF in the inner and mid one-third layers in the non-ischaemic region also decreased. Similar ST potential distributions were obtained on different layers of the heart, i.e., ST elevation occurred on the acute ischaemic region while ST depression occurred on the non-ischaemic region. The highest magnitude of maximal and minimal ST potential occurred on the boundary of the ischaemic and the non-ischaemic areas. ST shift had a positive relationship with RMBF. However, ST depression did not relate to the corresponded RMBF decrease. The results supported that some basic balance between ST elevation and ST depression existed during ischaemia, the total current flowing out of the heart must flow back into the heart. The ST depression was also a part of the source.
Rights statementThesis (Ph.D.)--University of Tasmania, 2005. Includes bibliographical references