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Introduction:Anterior wall ST elevation myocardial infarction (STEMI) is caused by occlusion of the left anterior descending (LAD) coronary artery. Proximal LAD occlusions are associated with larger infarcts and more complications. However, there is limited data demonstrating a relationship between ECG changes and the location of the LAD culprit lesion.Objective:To determine if patterns of ST elevations (STE)/depressions (STD) on the 12 lead ECG can predict if the culprit lesion in an anterior STEMI is in the proximal LAD.Methods:We performed a retrospective chart review of ECGs obtained from a database of patients diagnosed with myocardial infarction at Robert Wood Johnson University Hospital from January 2009 to December 2016. Lesions, defined as proximal or non-proximal with respect to the first diagonal of the LAD, were assigned according to the Bypass Angioplasty Revascularization Investigation (BARI) Protocol. Each lesion was assigned to one of the 4 ECG patterns described in Table 1. An analysis of variance was used to determine if the difference in ECG characteristics between groups was significant.Results:Of 447 ECGs denoted as anterior wall STEMIs, 227 met inclusion criteria. In total, 104 lesions were defined as proximal and 123 were non-proximal. There was a difference in the ECG pattern of proximal versus non-proximal culprits category (p = 0.006). Proximal culprit lesions were more likely to have STE in the precordial leads combined with STD in the inferior leads, whereas non-culprit lesions were more likely to have STE in the precordial leads without any STE or STD in the limb leads.Conclusions:In anterior STEMIs, proximal culprit lesions were more likely to exhibit ST elevations in precordial leads and ST depressions in inferior leads, compared to non-proximal culprit lesions, which were more likely to have ST elevations in only the precordial leads. Concomitant STE in lateral leads without inferior STD did not distinguish between the 2 groups.

Introduction:Inferior wall ST elevation MI (inf STEMI) may be caused by acute occlusion of the right coronary artery (RCA) or left circumflex artery (LCx). The ECG criteria of ST elevation (STE) in III greater than II with ST depression (STD) in aVL greater than I has been reported to predict RCA culprits; conversely, LCx culprits have been suggested to not satisfy these criteria.Objective:To evaluate the ECG criteria for predicting the culprit artery in inf STEMIs.Methods:We analyzed ECGs and coronary angiograms of 213 adult patients who presented to our institution from January 2009 to December 2013 with acute inf STEMI. ECGs were read by 2 investigators blinded to angiograms; likewise, coronary angiograms were read by 2 investigators blinded to ECGs. We recorded the coronary dominance (right, left, and co-dominant) and affected segments of the culprit lesions.Results:Of 213 patients with inf STEMI, 177 (83%) had RCA culprits and 36 (17%) had LCx culprits. The ECG criteria had 76% sensitivity, 69% specificity, 92% PPV, and 37% NPV for identifying the RCA versus LCx as the culprit. Dominance-stratified data is as shown (Table 1).Conclusion:We found that this commonly used ECG criteria for predicting culprit artery in inf STEMI had relatively low sensitivity, specificity, and NPV but excellent PPV. Our study highlights the importance of coronary circulation dominance in interpreting these results. The LCx is rarely the culprit unless it is a dominant or co-dominant vessel (27 out of 36). The excellent PPV is in large part due to the high prevalence of RCA culprits in inf STEMI. The low specificity is in part due to false positives from culprit dominant and co-dominant LCx (8 out of 11). The low NPV is a consequence of the low prevalence of LCx culprits in inf STEMI and the high number of false negatives. Nearly all false negatives (41 out of 42) are right dominant which demonstrates the limitations of these ECG criteria for identifying culprit artery in inf STEMI.