Distal Anastomotic Intimal Hyperplasia: Histocytomorphology, Pathophysiology, Etiology, and Prevention

Abstract

The ubiquitous relationship of late graft occlusion, particularly the nonautogenous bypasses and distal anastomotic intimal hyperplasia (DAIH), has been extensively investigated. After having established the specific location of DAIH in human autogenous, biologic and prosthetic late graft occlusion, canine models were designed to elucidate the role of compliance mismatch between graft and the host artery and the configuration of the distal end to side versus end to end anastomosis using autogenous artery. DAIH occurred in all end to side anastomosis but not in side matching end to end anastomosis. Compliance mismatched is not the cause of DAIH development, but it enhances the pathogenesis. Further study using pharmacologic agents to modulate the activities of vascular myoblasts was successful in attenuating DAIH development and progression. Since DAIH occurs through a cascade of events initiated by endothelial lifting of the overlapping processes at the gap junction to allow blood borne elements to enter the subendothelial space, then incites myoblast proliferation and matrix synthesis leading to DAIH formation at the heel and toe where oscillatory flow exists. Control of myoblast activity is needed on a permanent basis to prevent DAIH development and progression. Cessation of treatment allows resurgence of DAIH biogenesis. Direct regulation of vascular myoblast activity preclude the need of inhibiting other source of stimuli that increases as our knowledge of the subject grows. Without the participation of myoblast, there will be no DAIH irrespective of the potency and numbers of enzymatic, hormonal, or mechanical inciting factors.