A 77-year-old male was admitted with COVID-19 requiring intubation, prone positioning and treatment for bilateral segmental pulmonary embolism. Medical history consisted of type 2 diabetes and stable chronic lymphocytic leukaemia. Two weeks after intubation, he developed electrocardiographic changes with deeply inverted T waves in leads V2 to V4 (figure 1). Electrolytes were normal. Cardiac biomarkers were significantly elevated. The day after, a transthoracic echocardiography showed moderate left ventricular dysfunction with anterior wall akinesia and normal right ventricular function. The patient was treated conservatively with a beta blocker and clopidogrel on top of unfractionated heparin. Four days later he went into cardiac arrest due to ventricular fibrillation for which cardiopulmonary resuscitation and defibrillation were performed with return of spontaneous circulation. Coronary angiogram demonstrated significant stenosis of the distal left main coronary artery and proximal left anterior descending artery (LAD), for which a bifurcation stenting procedure was performed successfully. Triple anticoagulation therapy was started. Despite a negative fluid balance with loop diuretics in the days after coronary intervention, progression of hypoxaemia persisted and the patient died after the transition of the treatment goals from cure to comfort.

Wellens’ syndrome, also known as LAD coronary syndrome, is a clinical syndrome specific for critical stenosis of the LAD. It was first described by De Zwaan et al. in 1982 in patients with unstable angina, of which 75% developed anterior wall myocardial infarction weeks after admission.[1] Electrocardiographic changes can beclassified in two types. Type A is characterised by biphasic terminal negative T waves in leads V2 and V3 and occurs in approximately 25% of cases (figure 2). Type B is characterised by deeply inverted T waves in leads V2 and V3 and occurs in approximately 75% of cases.