Long-term histological and immunohistochemical findings in human venous aorto-coronary bypass grafts

Author:

Ribichini Flavio1,Pugno Francesco2,Ferrero Valeria1,Wijns William3,Vacca Giovanni4,Vassanelli Corrado1,Virmani Renu5

Affiliation:

1. Division of Cardiology, Department of Biomedical Sciences and Surgery, University of Verona, 37126 Verona, Italy

2. Laboratory of Human Pathology, Ospedale Cottolengo, Torino, Torino 10100, Italy

3. Cardiovascular Center Aalst, OLV Hospital, 9300 Aalst, Belgium

4. Department of Clinical and Experimental Medicine, University of Piemonte Orientale, Novara 28100, Italy

5. CVPath, International Registry of Pathology, Gaithersburg, MA 20878, U.S.A.

Abstract

The aim of the present study was to analyse the long-term histology and immunohistochemistry of the plaque composition and cellular infiltration of SVGs (saphenous vein grafts) containing metallic stents. Percutaneous interventions in SVGs have a worse long-term clinical outcome compared with stenting of coronary arteries. Whether the pathological features of old degenerated SVGs condition the efficacy of drug-eluting stents is also unknown. Histology and immunohistochemistry of seven SVGs in the coronary circulation containing 12 metallic stents implanted 5 to 61 months before retrieval were analysed in patients undergoing a second aorto-coronary bypass surgery at a mean time of 11±6 years. The pathology of the old SVGs showed an important thrombotic and necrotic composition of the plaque, with plaque protrusion through the stent wires and a fragile media layer that could easily be damaged by stent placement with subsequent neointimal proliferation; indeed, stents with medial fracture had significantly greater mean neointimal thickness than those without (1.37±0.68 compared with 0.81±0.47 mm2; P<0.02). Neointimal inflammatory cell density correlated with increased neointimal thickness in patent vessels (r2=0.43, P<0.001). Immunostaining showed the total absence of ERs (oestrogen receptors), a poor cellular proliferative state as indicated by the presence of the Ki-67 marker, and persistent inflammation close to the stent wires as revealed by KP-1 and ACE (angiotensin-converting enzyme) immunostaining in most inflammatory cells in contact with the metal. These pathological findings may contribute to the more severe progression of disease and worse clinical outcome observed after conventional stented angioplasty of SVGs and might also interfere with the efficacy of drug-eluting stents in this specific atherosclerotic milieu.

Publisher

Portland Press Ltd.

Subject

General Medicine

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