Dear Editor, Severe aortic stenosis is associated with significant morbidity and mortality if untreated. The transcatheter aortic valve implantation(TAVI) is now feasable and effective gold standart treatment option in patients with severe aortic valve stenosis (AS) and associated with similar rate of major adverse events compared to the surgery [1][2][3][4][5][6][7][8]. The relation between aortic stenosis and gastrointestinal angiodysplasia was known as Heyde's Syndrome since 1958. High fluid shear stress through the narrowed valve is thought to be the underlying mechanism leads to the mechanical disruption of the large von Willebrand factor multimers. Aortic valve replacement either surgical or with TAVI seems to reduce gastrointestinal bleeding in approximately 80% in patients with Heyde syndrome in whom gastrointestinal bleeding is associated with intestinal angiodysplasia due to acquired von Willebrand's disease (type 2A) and aortic valve stenosis. The patients especially with atrial fibrillation who need anticoagulant therapy may have bleeding risk despite aortic valve replacement [9][10][11][12][13][14][15][16][17][18][19][20]. We report a case of patient presenting with a massive intestinal bleeding originating from intestinal angiodysplasia after percutaneous aortic valve replacement.Herein, we report a case of a 76-year-old man with massive gastrointestinal bleeding after successful TAVI procedure due to the triple therapy(acetylsalicylic acid-100 mg, clopidogrel-75 mg and apixaban -2x2.5 mg). The patient was admitted to our hospital because of severe and symptomatic coronary artery [left anterior descending artery(LAD)] and aortic valve stenosis. The patient had also hypertension, diabetes, chronic atrial fibrillation, dyspnea(functional class II-III) and syncope on his medical history. On physical examination, the arterial blood pressure was 110/70 mm Hg, the pulse was 76 bpm and irregular. There was a 3/6 systolic murmur on the right sternal border radiating to the right side of the neck. The peripheral arterial pulses were weak. There was high voltage criteria and atrial fibrillation on his surface electrocardiography. There was significant and calcific stenosis on LAD with coronary angiography and computed tomography angiography (Fig.1). On thoracic echocardiography, there were severe left ventricular hypertrophy, severe left ventricular dysfunction and global hypokinesia and left ventricular ejection fraction(LVEF) was 26%. Aortic valve was severely calcific and aortic valve area was 0,6 cm2. Aortic valve maximal/mean pressure gradient: 47/30 mm. In order to detect the severity of the