Continuous-Flow Left Ventricular Assist Device–Related Gastrointestinal Bleeding

Left Ventricular Assist Devices (LVADS): History, Clinical Application and Complications

“…GI bleeding rates in LVAD patients ranges from 10–61% 31)32)33)34). A metanalysis of 1,697 patients showed a GI bleeding rate of 23% 35). The most common etiology of GI bleeding in LVAD patients is arteriovenous malformations or angiodysplasia which occur in 29% of LVAD patients 35).…”

“…A metanalysis of 1,697 patients showed a GI bleeding rate of 23% 35). The most common etiology of GI bleeding in LVAD patients is arteriovenous malformations or angiodysplasia which occur in 29% of LVAD patients 35). It is thought that the CF in the second and third generation LVADs may contribute to the development of angiodysplasias.…”

“…It is thought that the CF in the second and third generation LVADs may contribute to the development of angiodysplasias. The most common location of GI bleeding in these patients is the upper GI tract (48%) of patients 35). The pathophysiology of GI angiodysplasia in CF LVAD patients is incompletely understood but there is evidence that the hypoxia-inducible factor (HIF)-1α/angiopeptin pathway may be involved 36)37).…”

“…Another option for medical therapy is digoxin which inhibits HIF-1α synthesis 40). Although the incidence of GI bleeding is higher in recipients of second and third generation LVADs compare to the first generation pulsatile LVADs, mortality from GI bleeds is actually lower in recipients of the newer, CF LVADs compared to the pulsatile LVADs (20.9% vs. 43.7%, respectively) 35). From the DT clinical trial comparing HeartMate II to HeartMate I, there was no difference in GI bleeding episodes that required transfusions or surgery.…”

Interplay of pump design elements and bleeding predilection—Mechanisms for a forward momentum

“…2 To illustrate the magnitude of the issue, gastrointestinal bleeding occurs in approximately 33% of the patients with an LVAD implantation, 1 and the etiology is complex, as well as multifactorial. 3 While the use of anti-coagulation and anti-thrombotic therapy probably plays a major role, the use of these agents cannot explain all the bleeding events and other mechanisms, such as the development of mucosal angiodysplasias specifically associated with continuous flow (arteriovenous malformations), remain essential. 4 The interference with a natural coagulation system disturbed by a blood-device interface and shear stress-dependent damage to coagulation proteins, in particular the degradation of high molecular forms of von Willebrand factor (HMvWF), has been previously corroborated as a contributor to bleeding risk in this patient population.…”