Inflammatory cytokines and experimental arterial and vein grafts

Abstract

Ten years after surgery, only 40% of the saphenous coronary artery bypass grafts have a normal appearance. 1 Myointimal hyperplasia and atherosclerosis are unusual in the internal thoracic artery. A systematic review has shown better patency rates for the radial artery. 2 The aim of our study was to determine the release of several inflammatory cytokines from experimental arterial and vein grafts. Increased production of inflammatory cytokines by vein grafts might lead to higher incidence of occlusive changes.

Commentary: Veins grafts reversibly adapt to the arterial circulation

“…All these are essential when thinking about the Law of Laplace and the adaptive changes that the veins underwent and whether this model accurately replicates clinical conditions. Second, Sterpetti and colleagues 3 demonstrate an increase in cytokine levels with vein grafts in the arterial circulation, but the mechanism of action for vein graft hyperplasia they propose of increased cytokine release leading to a chronic inflammatory state and progression of myointimal hyperplasia in turn leading to graft occlusion is a tenuous and unsubstantiated conclusion to make from this study.…”

“…In this edition of the Journal , Sterpetti and colleagues 3 investigate whether the release of inflammatory cytokines in vein grafts leads to their lower patency rate relative to arterial grafts in CABG. In a rat model, a segment of vena cava was anastomosed to the abdominal aorta, mimicking the conditions of SVG to coronary anastomosis.…”

“…The findings of this animal model are certainly intriguing and of great interest. but Sterpetti and colleagues 3 fall short of providing meaningful mechanisms of action or clinically applicability. First, what are the details of this model, and does it really replicate the clinical conditions of SVGs used in CABG?…”

Commentary: Born vein, you cannot die artery!

“…[4][5][6] More recently, inflammation has been advocated to be responsible for vein graft disease because interleukin1b inhibition with canakinumab was able to target inflammation in vein graft disease. 6 The study by Sterpetti and colleagues 7 provides further confirmation that a vein graft inserted into an arterial circulation remodels, increasing the internal diameter and the thickness of the wall as adaptive mechanism to higher internal pressure and larger quantities of blood. Inflammatory mediators are at the basis of this adaptive morphological change, leading SVG from a hyperplastic reaction to a true atherosclerotic plaque formation.…”