Findings from ECGs were first correlated with angiographic findings in patients presenting with STEMI by studies in the 1980s. In the setting of STEMI, the STE is present in the leads with positive electrodes overlying the infarcted region, and the STE distribution pattern can be used to predict the culprit vessel. The STE reflects an ischemia-induced injury current derived from the electrical voltage gradient at the boundary between the ischemic and normal myocardium.1
In the present case, the ECG showed dramatic STE in leads V1 through V3, which usually connotes anterior/anteroseptal infarction from proximal left anterior descending artery (LAD) occlusion.1 In contrast to our initial belief, the culprit vessel turned out to be the nondominant RCA, and there was no significant obstruction in the left coronary arteries. Emergency revascularization of the RCA by PCI led to resolution of chest pain and normalization of precordial ST-segment deviation on ECG. The precordial STE was believed to result from the right ventricle (RV) ischemic injury due to proximal occlusion of the nondominant RCA and RV branches.