The abnormal ST-segment and T-wave morphology, now known as Wellens’ syndrome, was first described in the early 1980s [4]. In a study of 1,260 patients hospitalized for unstable angina between July 1980 and December 1985, 204 (16%) displayed this ECG pattern. After excluding patients with recent myocardial infarction and missing data, 180 patients were further analyzed. All had at least 50% stenosis in the proximal LAD, with 18% having total occlusion [6]. Another study showed Wellen’s syndrome has an incidence of 5.7% in patients with acute coronary syndrome [7]. Wellen’s syndrome is classified into type A or type B, which account for approximately 75% and 25% of the cases, respectively. Type A is characterized by a biphasic T-wave in leads V2 and V3, whereas type B is characterized by a deep T-wave inversion in the same leads. However, in both types these ECG changes can extend to involve any pericardial chest leads. In addition, the criteria require a history of angina, the absence of precordial Q waves, and normal or slightly elevated cardiac biomarkers [8]. The pathophysiological mechanisms of the ECG pattern have not been elucidated yet. The Wellens’ ECG pattern was originally related to atherosclerotic subocclusion of the LAD, it was subsequently observed in other conditions characterized by a reversible left ventricular dysfunction (stunned myocardium) or myocardial edema, by either ischemic or nonischemic causes, including takotsubo syndrome and intracranial bleeding [9,10,11,12,13].

Surprisingly, despite severe ostial stenosis of the LM, typical Wellen’s syndrome type B was documented. Patients with an ACS due to LM culprit are at high risk of in-hospital mortality and at continued mortality risk post hospital discharge [14, 15]. This patient was successfully treated with PCI. His symptoms resolved following stent implantation. After the reperfusion therapy, the ECG showed resolution of the T-wave inversions in the V2 and V3 leads, indicating there was resolution of the Wellen’s pattern. The patient’s coronary angiograph revealed a dominant right coronary artery and a small left circumflex artery. Myocardial ischemia of the anterior left ventricular wall may explain the patient’s ECG pattern, which is reflected in the characteristic T-wave changes. In LM disease, transient ischemia followed by reperfusion may produce these characteristic T-wave changes in the anterior wall leads.

Hu H et al. first reported that Wellen’s ECG pattern caused by LM terminal bifurcation lesions involving the ostium of LAD and left circumflex coronary artery, with 95% and 90% stenosis, respectively [16]. However, to our knowledge, there are no reports regarding severe ostial stenosis of LM with ECG features similar to Wellen’s type B pattern.

The clinical implications of recognizing atypical presentations of Wellen’s syndrome are significant. Delayed diagnosis or misinterpretation of the ECG findings could lead to missed opportunities for timely intervention. As demonstrated by De Zwaan et al., 75% of patients with Wellen’s syndrome developed extensive anterior wall myocardial infarction only weeks after admission [4]. Once Wellen’s syndrome is identified in patients with suspected acute coronary syndrome, an urgent or even emergent invasive strategy is recommended [1, 4, 9]. If there is significant proximal LAD occlusion, PCI or coronary bypass surgery should be performed to prevent extensive anterior myocardial infarction. LM stenosis can be particularly hazardous due to the extensive myocardial territory it supplies. Although rare, this condition should be considered when the corresponding ECG pattern is observed. Prompt recognition and management of such cases are essential to avoid misdiagnosis and prevent fatal outcomes.