A 79-year-old man underwent TAVI with a self-expanding transcatheter heart valve (Acurate Neo, Size L, Boston Scientific, Ecublens, Switzerland) due to severe symptomatic aortic valve stenosis in March 2018. He was discharged on dual antiplatelet therapy (DAPT) including clopidogrel 75 mg/day for 6 months and aspirin 100 mg/day indefinitely. Before TAVI, coronary artery disease was excluded by invasive coronary angiography (). Seven months later, the patient woke up at night time because of sudden intense angina pectoris at rest ceasing spontaneously after approximately 2 h. The next morning, the patient called emergency medical services and he was admitted to the chest pain unit. The patient was asymptomatic at the time of presentation. On physical examination, his vital signs were stable and cardiac, pulmonary and abdominal examination was unremarkable. The 12-lead electrocardiogram (ECG) did not show any abnormalities. However, cardiac biomarkers were significantly elevated. His initial high-sensitivity cardiac troponin T was 386 ng/L and rose to 590 ng/L after 3 h (normal value < 14 ng/L). D-dimer levels were slightly increased to 1.42 mg/L (normal value < 1.28 mg/L, age-adjusted cut-off 0.79 mg/L). White blood cell count as well as C-reactive protein were within normal range. No left ventricular regional wall motion abnormalities were detected by transthoracic echocardiography. Suspecting a non-ST-elevation acute coronary syndrome, initial treatment comprised intravenous administration of 5000 IU unfractionated heparin and 500 mg aspirin. Early invasive coronary angiography was performed, but no coronary occlusion could be detected (). Having excluded a vessel occlusion as the reason for the acute chest pain, pulmonary embolism and aortic dissection were considered as differential diagnosis. Both were finally ruled out by multidetector computed tomography (CT). However, the CT scan indicated thrombosis of the prosthetic aortic valve. A dedicated cardiac CT scan confirmed thrombosis of both right and non-coronary leaflets (). By means of cardiac magnetic resonance imaging (MRI), two acute transmural myocardial infarction lesions in the midventricular and apical inferior wall were detected ( and ). Left ventricular ejection fraction measured by transthoracic echocardiography was normal and mean aortic pressure gradient had not changed significantly since the last routine control 3 months after prosthetic valve implantation (Pmean 9 mmHg). A 24-h Holter ECG monitoring revealed no cardiac arrhythmias and intracardiac thrombi were excluded by transoesophageal echocardiography. Because of these findings, therapeutic anticoagulation with unfractionated heparin was started during the hospital stay. Finally, the patient was discharged in a good clinical condition on phenprocoumon [target international normalized ratio (INR) 2–3]. Antiplatelet therapy with aspirin was consequently stopped. A follow-up visit after 8 weeks with repetition of a CT scan was recommended. However, the patient did not attend planned follow-up. After contacting the patients’ relatives, we found out that the patient had died from an unknown cause 2 months after the described clinical event. Further investigations including inquiry of the general practitioner did not contribute to any explanation for the cause of death.