A patient in their 50s, a current cigarette smoker with a history of hypertension but no known cardiac disease, presented with sudden-onset chest pain via emergency medical services (EMS). The patient was hypertensive with a systolic blood pressure of 220 mm Hg by EMS. On arrival at the emergency department, the patient was in acute distress due to ongoing chest pain. The patient was afebrile, heart rate was 72 bpm, respiration rate was 16 breaths per minute, and blood pressure was 153/97 mm Hg. The cardiopulmonary examination was overall unremarkable. The electrocardiograms (ECGs) obtained by EMS and in the emergency department showed ST-segment elevation (STE), up to 5 mm in amplitude, in leads V1 through V3 and horizontal/down sloping ST depression (STD) in leads V4 through V6. The diagnosis was STE myocardial infarction (STEMI). The patient was subsequently brought to the cardiac catheterization laboratory for emergency cardiac catheterization and coronary angiography as a code STEMI.
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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.
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CME Disclosure Statement: Unless noted, all individuals in control of content reported no relevant financial relationships. If applicable, all relevant financial relationships have been mitigated.
Corresponding Author: Ruihai Zhou, MSc, MD, RPVI, Division of Cardiology, Department of Medicine, University of North Carolina at Chapel Hill, 160 Dental Cir, Campus Box 7075, Chapel Hill, NC 27599-7075 (email@example.com).
Published Online: January 23, 2023. doi:10.1001/jamainternmed.2022.6088
Conflict of Interest Disclosures: None reported.
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