Abstract Background Wellens syndrome, also known as "left anterior descending coronary syndrome," is characterized by the appearance of T–wave changes recorded on the ECG and it is an ECG manifestation of critical proximal left anterior descending artery stenosis. Case Report A 65–year–old man from Bangladesh with a history of chronic ischemic heart disease and trivessel coronary artery disease following surgical revascularization (CABG 2007). Recent admission for NSTEMI (June 2022) with unchanged coronary angiography compared to the previous one. Comorbidities include peripheral arterial disease, type II diabetes with organ damage, and COPD with recent exacerbations. Last myocardial scintigraphy (2021) was positive for inducible myocardial ischemia in the posterolateral region. Admission due to fever, productive cough, and severe chest pain. Initial instrumental assessments revealed ST–segment alterations in inferior leads and V1–V2 with negative/isodiphasic T–waves, not present in previous ECG tracings. A slight troponin elevation with ischemic curve (101 → 303 → 277 → 155 pg/dl, normal range < 50 pg/dl) led to the diagnosis of NSTEMI. Echocardiogram showed concentric remodeling of the left ventricle with normal global systolic function and hypokinesia of the mid–basal inferior wall (noted). Additionally, chest CT revealed pulmonary consolidations in the right middle lobe and upper left lobe, prompting antibiotic therapy and bronchodilator inhalation. Arterial blood gas analysis: pH 7.45, pO2 83, Lactate 0.8, HCO3– 24, P/F 360. Coronary angiography showed an unchanged picture compared to the previous one (patent AMIS and AMID, good run–off in native branches, no distal stenosis at the anastomosis). Clinical symptoms, inflammatory indices, and myocardial damage markers clinically improved during hospitalization. Discharged after optimization of anti–ischemic therapy with DAPT and diagnosis of NSTEMI. However, ECG abnormalities persisted at discharge (negative T–waves in DI–aVL–V1–V2). Post–discharge cardiac MRI was requested. Conclusions Diagnostic hypotheses include, primarily, a possible type II myocardial infarction due to an ongoing pneumonia (although hypoxia/hypovolemia/hypotension sufficient to cause MI was never documented during hospitalization), MINOCA, or microcirculatory disease (functional tests such as iFR/FFR, ACh, IMR were not performed during coronary angiography), or a possible myocarditic outcome (pending MRI).