A 60-year-old male with a history of dyslipidemia and smoking habit presented to the emergency department with oppressive chest pain and diaphoresis, which had been persistent for 2 hours. When a 12-lead ECG was obtained, his pain was constant but less severe. The initial ECG is shown in Figure 1. Is the suspected diagnosis ST-segment elevation myocardial infarction or non–ST-segment elevation myocardial infarction? What is the culprit artery?

Figure 1. Initial 12-lead ECG at the emergency department.

Please turn the page to read the diagnosis.

The feature of the initial ECG was upsloping ST-segment depression at the J point continuing into positive symmetrical T waves in leads II, III, aVF, and V4 to 6, coupled with ST-segment elevation in lead aVR. The emergency physician did not recognize the ECG finding as an ST-segment elevation myocardial infarction equivalent and started initial treatment for non–ST-segment elevation myocardial infarction STEMI, including aspirin and intravenous administration of isosorbide dinitrate and unfractionated heparin. Although symptoms were getting better after the treatment, his pain did not disappear completely. At 10 hours after arrival, coronary angiography was performed, which revealed occlusion of the proximal site of the dominant right coronary artery (RCA) and Rentrop Grade 2 collateral flows from septal branches of the left anterior descending (LAD) artery. After stent implantation, his symptom completely disappeared (Figure 2).

Figure 2. Coronary angiography.A and B, Coronary angiography showed the occlusion of proximal site of right coronary artery (A), and percutaneous coronary intervention was performed (B). C, Coronary angiography after stent implantation revealed that right coronary artery was dominant.

Peak creatine kinase and creatine kinase-myocardial band levels were high (creatine kinase 4168 U/L, creatine kinase -MB 485U/L). It is surprising to note that, despite acute RCA total occlusion, significant ST-segment elevation was not documented during the early phase of myocardial infarction. However, ECG at 32 hours after arrival showed abnormal Q waves and negative T waves in leads II, III, and aVF (Figure 3). The enlarged initial ECG (leads II and aVR only) is shown in Figure 4. Cardiovascular magnetic resonance imaging was performed at 7 days after admission. Fat-saturated, T2-weighted images (Figure 5A) revealed the presence of inferoposterior wall edema, which was concordant with the presence of late gadolinium enhancement images (Figure 5B).

Figure 3. Although significant ST-segment elevation was not documented with repeated ECG evaluation during the early phase of myocardial infarction, abnormal Q waves and negative T waves were emerged in leads II, III, and aVF afterward.

Figure 4. Enlarged ECG in Figure 1 (leads II and aVR only). The features of ECG are upsloping ST-segment depression at the J point (large arrow) and symmetrical positive T wave (small arrow) in lead II. ST-segment elevation was observed in lead aVR (arrow head).

Figure 5. Cardiovascular MRI.A and B, Cardiovascular MRI at 7 days after admission showed high signal intensity on fat-saturated T2-weighted images (A) and the presence of late gadolinium enhancement (B), corresponding with acute transmural myocardial infarction of inferoposterior wall.

De Winter et al¹ reported similar findings of ECG as “a new ECG sign of proximal LAD occlusion.” The ECG pattern is seen in a minority (2%) of symptomatic LAD artery occlusion, which is upsloping ST-segment depression at the J point continuing into tall, prominent T waves in the precordial leads. This pattern has positive predictive values of 95% to 100% in the respective diagnostic studies.^2,3 The pathophysiological mechanisms of the ECG pattern have not been elucidated yet. Potential explanation is an anatomical variant of the Purkinje fibers with endocardial conduction delay. Another explanation might be that the absence of ST-segment elevation may be related to the lack of activation of sarcolemmal ATP-sensitive potassium channels by ischemic ATP depletion. Some authors postulated that collateral blood supply might protect the myocardium from transmural ischemia and prevent ST-segment elevation, and others advocated that the area of transmural ischemia was so large that no injury currents were generated toward the precordial leads but only directed upward to an aVR lead.

In the present case, the specific feature of ST-segment changes in the inferolateral leads is associated with the acute RCA total occlusion, which is similar in appearance to the de Winter¹ LAD pattern. Acute transmural myocardial infarction of the inferoposterior wall was confirmed by cardiovascular magnetic resonance. To our knowledge, there has been no report regarding RCA total occlusion with the feature of ECG similar to the de Winter¹ LAD pattern. Practitioners should recognize this new RCA obstruction pattern as ST-segment elevation myocardial infarction equivalent and need to perform emergent reperfusion therapy.

The authors thank Dr Masami Kosuge, Division of Cardiology, Yokohama City University Medical Center, for interpretation of the ECG findings.

None.

https://www.ahajournals.org/journal/circ