HS syndrome is characterized by aortic stenosis and GI angiodysplasia1. The pathophysiology of this syndrome involves not only increased number of angiodysplasias but higher risk of bleeding from them. The physiological link between angiodysplasia and aortic stenosis is unclear but hypo-oxygenation of intestinal mucosa, possibly related to cholesterol emboli with resultant vasodilatation, has been hypothesized among many others2. Bleeding from angiodysplasias appears related to the high shear stress across the stenotic aortic valve, leading to acquired von Willebrand’s disease (Type 2AvWF disease) and coagulopathy2.
Cessation of bleeding following SAVR or TAVR with gradual disappearance of angiodysplasia has been reported, in some cases despite long-term anticoagulant therapy3,4. GIB may cease in 95% of cases following AVR vs 5% in cases undergoing laparotomy with or without bowel resection. In patients who have undergone SAVR, aortic valve restenosis usually leads to the recurrence of GI bleeding which resolves after redo surgery.
- Heyde EC. Gastrointestinal bleeding in aortic stenosis. N Engl J Med 1958;259:196.
- Kapila A, Chhabra L, Khanna A. Valvular aortic stenosis causing angiodysplasia and acquired von Willebrand’s disease: Heyde’s syndrome. BMJ Case Rep 2014 doi:10.1136/bcr-2013-201890.
- Abi-akar R, El-rassi I, Karam N et al. Treatment of Heyde’s syndrome by aortic valve replacement. Curr Cardiol Rev 2011; 7:47–49.
- Pyxaras, SA, Santangelo S. Perkan A et al. Reversal of angiodysplasia-derived anemia after transcatheter aortic valve implantation. J Cardiol Cases 2012; 5: e128–e131.
Contributed by Biqi Zhang, medical student, Harvard Medical School