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Abstract & Commentary
By Michael H. Crawford, MD, Editor
Source: Noriega FJ, et al. Influence of the extent of coronary atherosclerotic disease on ST-segment changes induced by ST elevation myocardial infarction. Am J Cardiol 2014;113:757-764.
The early ECGs are the mainstay of predicting the culprit coronary artery in ST-segment elevation myocardial infarction (STEMI). However, in patients with multivessel coronary artery disease (CAD), other significant lesions may affect the accuracy of culprit artery prediction. Thus, these investigators from Spain reviewed the clinical records, ECGs, and acute angiograms of 289 patients with STEMI. Patients with left bundle branch block or ventricular-paced rhythm were excluded. On angiography, single vessel disease occurred in 149 patients (51%) and multivessel disease in 140. The patients were divided into three groups based on their culprit artery: 140 left anterior descending (LAD), 118 right coronary artery (RCA), and 31 left circumflex (LCx). With LAD occlusion, the overall pattern of ST segment changes was the same for single vessel and multivessel disease. However, only proximal LAD occlusion exhibited reciprocal ST depression in the inferior leads. With RCA occlusion, the ST segment pattern was similar for single and multivessel disease and included reciprocal ST depression in leads I, aVL, and V2, but in those with multivessel disease, ST depression often extended to leads V3-4. LCx occlusion resulted in ST elevation in the inferior leads and often V6 and reciprocal changes in V2-3 or even V4 in multivessel disease. In fact, ST elevation in V6 was highly predictive of LCx infarction. The authors concluded that patients with either single vessel or multivessel CAD have similar coronary artery-related ST changes on the admission ECG and that reciprocal changes in LAD occlusion patients predict a proximal culprit lesion.
Controversy has surrounded the interpretation of reciprocal ST segment changes on admission ECGs in patients with clear STEMI. Three major hypotheses have been advanced to explain them. The first is mirror ECG changes in opposing leads. This electrical phenomenon has been confirmed in animal studies where a single coronary is ligated and is supported by their study since reciprocal changes were present in both single vessel and multivessel disease patients in equal numbers in all three territories. Second is that reciprocal changes represent the ischemic zone around a large infarct that extends into adjacent leads. This study supports this hypothesis, especially in the LAD territory where proximal lesions exhibited reciprocal changes and more distal lesions did not. Presumably the proximal lesions subtended a larger infarct. Finally, there is the hypothesis of ischemia at a distance. This theory supposes that the occlusion of an artery may render an adjacent area with a significant coronary lesion ischemic when collaterals from the culprit vessel are lost. The data in this study did not support this theory as a major mechanism, but cannot totally exclude it either, since this level of analysis was not performed. However, the investigators conclude that reciprocal changes do not require the presence of multivessel disease.
Also of interest is that this study has added another criterion for distinguishing RCA from LCx occlusion as a cause of inferior lead ST elevation. ST elevation in V6 was 71% sensitive and 83% specific for LCx occlusion. Three other criteria have been proposed in previous studies that demonstrated similar accuracy: 1) ST elevation in lead III > II suggests RCA occlusion; 2) ST depression in lead I supports RCA occlusion; and 3) ST depression in leads V1, V2, and V3 summed divided by the ST elevation summed in leads II, III, and aVF is < 1, or the simpler ST depression in lead V3 divided by the ST elevation in lead III < 1 supports an RCA lesion.