Commentary: Veins grafts reversibly adapt to the arterial circulation.

Alison F. Ward, MD (left), and Richard Lee, MD, MBA (right)

Vein grafts reversibly adapt to the arterial circulation, potentially from release of cytokines. Clinical relevance of these findings is limited by the unknown mechanism of action of these changes.

See Article page 48.

Coronary artery bypass grafting (CABG) is the criterion standard for treatment of complex multivessel coronary artery disease, but its long-term success and survival benefit to the patient depend on graft patency. Saphenous vein grafts (SVGs) are commonly used for multivessel CABG, but they have a patency rate of only 50% at 10 years., Is the poor patency rate of SVGs due to harvesting technique, anastomotic factors, or the vascular biology of the conduit itself?

In this edition of the Journal, Sterpetti and colleagues 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 vein was then explanted and anastomosed to the iliac vein. Vein grafts implanted into the arterial circulation increased in both diameter and wall thickness; once reimplanted into the venous circulation, these changes disappeared completely. Cytokine analysis paralleled these findings, with increased release from the venous conduits implanted in the arterial circulation but not from those placed in the venous circulation. In contrast, arterial grafts did not demonstrate any morphologic or cytokine level changes.

The findings of this animal model are certainly intriguing and of great interest. but Sterpetti and colleagues 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? The specifics of the experimental design are difficult to tease out—the wall thickness and diameters of the grafts, the pressure conditions of the arterial and venous circulations, and the flows within the grafts. 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 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.

The goal of research is to answer questions that will guide us toward improving care for our patients. Although this study sheds light on the morphologic changes that vein grafts undergo, its reversibility, and its correlation with cytokine levels, we gain little understanding of the mechanism of action of vein hyperplasia on which to intervene and improve patient outcomes.