Abstract
Bypass surgery is one of the most frequently used strategies to revascularize tissues downstream occlusive atherosclerotic lesions. For venous bypass surgery the great saphenous vein is the most commonly used vessel. Unfortunately, graft efficacy is low due to the development of vascular inflammation, intimal hyperplasia and accelerated atherosclerosis. Moreover, failure of grafts leads to significant adverse outcomes and even mortality. The last couple of decades not much has changed in the treatment of vein graft disease (VGD). However, insight is the cellular and molecular mechanisms of VGD has increased. In this review, we discuss the latest insights on VGD and the role of inflammation in this. We discuss vein graft pathophysiology including hemodynamic changes, the role of vessel wall constitutions and vascular remodeling. We show that profound systemic and local inflammatory responses, including inflammation of the perivascular fat, involve both the innate and adaptive immune system.
Highlights
Occlusive atherosclerotic disease is a leading cause of mortality and morbidity worldwide
Overexpression of tissue inhibitors of matrix metalloproteinase (MMP) (TIMP) 1, 2, and 3 in vein graft models in various experimental animals resulted in intimal hyperplasia formation due to reduced smooth muscle cells (SMCs) migration and proliferation and inhibition of MMP activity as well as reduced infiltration and migration of inflammatory cells [84,85,86,87,88]
A third protein was constructed by combining the three constructs resulting in TIMP1.amino terminal fragment (ATF).bovine pancreas trypsin inhibitor (BPTI) that was capable of inhibiting both plasmin and MMP activity at the cell surface, which effectively reduced vein graft intimal hyperplasia and outward remodeling [97]
Summary
Specialty section: This article was submitted to Atherosclerosis and Vascular Medicine, a section of the journal Frontiers in Cardiovascular Medicine. For venous bypass surgery the great saphenous vein is the most commonly used vessel. Graft efficacy is low due to the development of vascular inflammation, intimal hyperplasia and accelerated atherosclerosis. The last couple of decades not much has changed in the treatment of vein graft disease (VGD). Insight is the cellular and molecular mechanisms of VGD has increased. We discuss the latest insights on VGD and the role of inflammation in this. We discuss vein graft pathophysiology including hemodynamic changes, the role of vessel wall constitutions and vascular remodeling. We show that profound systemic and local inflammatory responses, including inflammation of the perivascular fat, involve both the innate and adaptive immune system
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