Cath Lab Digest

Abstract

Following the introduction of percutaneous angioplasty (PTA), arterial stents emerged as a tool for preventing the acute arterial wall recoil and chronic restenosis associated with PTA. The use of stents has grown considerably in the last decade. There is a wide spectrum of clinical applications for the use of stents in the arterial vascular system, but every vascular territory demands specific stent adaptations such as resistance to kink and fracture in the femoropopliteal segment or high radial force in aortic ostial lesions. This article discusses the different types of bare-metal stent models and how their characteristics influence endothelialization as well as their potential impact on clinical practice.

Key words: stent, atherosclerosis, endothelium, restenosis

VASCULAR DISEASE MANAGEMENT 2010;7:E95–E102

Introduction

In 1964 Charles Dotter introduced the concept of arterial remodeling and in 1974 Andreas Gruentzig performed the first peripheral human balloon angioplasty. Later, physicians started to recognize the limitations of angioplasty and stents were introduced with the objective of tacking down dissection flaps and providing mechanical support of recoiling lesions. In 1991, the U.S. Food and Drug Administration approved for the first time the use of the Palmaz stent for the treatment of atherosclerotic obstructive disease. Since then, the use of stents in the treatment of atherosclerotic obstructive lesions has widely spread, although significant limitations still remain.

Restenosis is one of the most prevalent complications of stenting. Restenosis is the process of luminal narrowing in an atherosclerotic artery after endovascular interventions and has been found to occur in 20–50% of stented vessels.¹ Restenosis is the arterial wall healing response to mechanical injury and has long been attributed to neointimal proliferation,² thrombosis³ and negative remodeling.⁴ However, there is now increasing evidence for the role of inflammation in vascular healing and in the development of restenosis. Vascular injury, de-endothelialization, platelet and leukocyte interactions and expression of autocrine and paracrine inflammatory mediators (cytokines such as interleukin-1 and tumor necrosis factor), which are triggered following stent implantation, orchestrate an inflammatory response that leads to smooth-cell proliferation, potential neointimal growth and subsequent restenosis. Stents may be implanted at sites of advanced macrophage-rich atheromatous lesions. Stent implantation induces a vascular inflammatory response that also contributes to restenosis.

Recently, the use of immunosuppressive drug-eluting stents (DES) has provided very promising results in the treatment of restenosis, although they inhibit endothelialization, arresting the healing process of the vessel walls after vascular injury caused by stent implantation, which may translate into adverse clinical events.⁵

Different stent models have distinct rates of in-stent restenosis; the vascular injury caused by stent placement determines the risk and degree of restenosis.⁶ The degree of vascular injury and subsequent restenosis appears to depend on the depth of strut penetration during stent implantation.⁷

This article discusses several bare-metal stent (BMS) models and how stent characteristics affect endothelialization and in-stent restenosis and their implications in clinical practice.

Types of Stents

Stents are implantable devices that can be classified according to design or geometry (mesh structure, coil, slotted tube, modular or custom design), delivery system and mechanism of expansion (self-expanding or balloon-mounted), and composition (stainless steel, cobalt-based alloy, tantalum, nitinol, etc). Additional stent characteristics include strut thickness and shape, metal-to-artery ratio, method of stent cleaning and polishing, corrosion resistance, durability, open area-to-metal surface ratio, sharpness of the end of the stent, fracture resistance, kinkability, biocompatibility and long-term clinical outcomes.