Abstract
BackgroundMore than 50% of aortocoronary saphenous vein grafts are occluded 10 years after surgery. Intimal hyperplasia is the initial critical step in the progression toward occlusion. Internal mammary veins, which are physiologically prone to less hydrostatic pressure, may undergo an accelerated progression to intimal hyperplasia and thus be suitable for investigation of the mechanisms of aortocoronary vein graft disease.MethodsSix minipigs underwent aortocoronary bypass grafting using standard cardiopulmonary bypass and cardioplegic arrest. Mammary vein were grafted in a reversed manner from ascending aorta to left anterior descending coronary artery (LAD). The proximal LAD was ligated, rendering the anterior left ventricle vein graft-dependent. Minipigs were killed after 4 weeks, and vein grafts were harvested. Histological and immunohistological investigation were performed with respect to morphometric analysis, endothelial damage/dysfunction (v-Willebrand-factor (vWF)), smooth muscle cells (α-smooth actin) and proliferation rate (proliferation marker Ki 67).ResultsMean intimal area of vein grafts was increased compared to ungrafted mammary veins. Intimal hyperplasia in vein grafts was characterized by massive accumulation of smooth muscle cells with a high proliferation rate and endothelial perturbation. Significant (p = 0.001) intimal hyperplasia of the grafted mammary vein compared to the ungrafted mammary vein was found. These changes were absent in ungrafted mammary veins.ConclusionThe present study demonstrates a pig model of aortocoronary vein graft intimal hyperplasia which is characterized by an accelerated progression within internal mammary veins. The model is suitable to investigate the pathophysiology of aortocoronary vein graft intimal hyperplasia as well as therapeutic approaches.
Highlights
The saphenous vein is still a conduit of choice for coronary artery bypass grafting
The histological changes associated with vein graft failure are defined as intimal hyperplasia
We found an accelerated intimal hyperplasia in vein grafts after four weeks indicated by morphometric analysis, endothelial damage/dysfunction markers, and proliferation of smooth muscle cells
Summary
The saphenous vein is still a conduit of choice for coronary artery bypass grafting. Following arterializations, vein grafts undergo immediate injury like ischemia and wall stress. The histological changes associated with vein graft failure are defined as intimal hyperplasia. They include acute thrombosis or early medial and intimal thickening that may be focally progressive. Further reason is late artheroma formation, which is the most important cause of failure beyond five years after implantation [1]. This vein graft failure is result of progressive thickening of the intima and media acting over the first months and slow process of atherosclerosis over years [2]. Internal mammary veins, which are physiologically prone to less hydrostatic pressure, may undergo an accelerated progression to intimal hyperplasia and be suitable for investigation of the mechanisms of aortocoronary vein graft disease
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