Abstract

Introduction. Migration of the smooth muscle cells (SMCs) to the tunica media in the saphenous vein (SV) transplants is facilitated by matrix metalloproteinases (MMPs). The aim of this study was to identify any associations between expression of MMP-2 or endogenous tissue inhibitors (TIMP-2 and TIMP-3) in the SV segments and late failure of the SV grafts. Methods. Two hundred consecutive patients with a mean age of 63.1 ± 8.9 years who underwent primary isolated venous CABG were examined. Patients were retrospectively split into two subgroups, with the SV graft disease (SVGD (+); n = 47) or without it (SVGD (−); n = 153). In the SV segments, immunohistochemical analysis of the expression of the MMP-2, TIMP-2, and -3 was performed. Results. In the SVGD (+) patients, tissue expression of MMP-2 was stronger, whereas that of both TIMPs was weaker than in the SVGD (−) patients. In majority of the SV segments obtained from the SVGD (−) individuals, a balance in MMP and TIMP expressions was found, whereas an upregulation of MMP-2 expression was usually noted in the SVGD (+) subjects. Conclusion. The strong expression of MMP-2 accompanied by reduced immunostaining of both TIMPs is associated with the development of the SV graft disease and unfavorable CABG outcomes.

Highlights

  • Migration of the smooth muscle cells (SMCs) to the tunica media in the saphenous vein (SV) transplants is facilitated by matrix metalloproteinases (MMPs)

  • multidetector spiral computed tomography angiography (MSCT) revealed occluded SV grafts, and these findings were confirmed in the coronary angiography

  • The follow-up coronary angiography revealed failure of the grafts in 31 study participants who manifested an exacerbation of angina and in 5 subjects without any symptoms of the progression of coronary artery disease (CAD)

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Summary

Introduction

Migration of the smooth muscle cells (SMCs) to the tunica media in the saphenous vein (SV) transplants is facilitated by matrix metalloproteinases (MMPs). The strong expression of MMP-2 accompanied by reduced immunostaining of both TIMPs is associated with the development of the SV graft disease and unfavorable CABG outcomes. The interposition of the SV segments into the arterial system during coronary artery bypass grafting (CABG) initiates a series of biological events within the venous wall [5]. They are thought as adaptation to the high arterial stretch forces and wall shear stresses [6]. Transformation of the venous smooth muscle cells (vSMCs) from contractile to synthetic and the abnormal proliferation and migration of these cells from the tunica media to the tunica intima through internal elastic lamina are key events in the development of neointima [6, 10]. Before migration of vSMCs, the surrounding extracellular matrix (ECM) must be initially degraded by the matrix

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