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1.  INTRODUCTION

Options for the surgical treatment of cardiovascular diseases include implantable cardiovascular devices such as stents, the total artificial heart, vascular grafts, heart valves, and ventricular assist devices. Still, cardiovascular devices implanted in the human body have been shown to bee associated with complications indicating the need of improving their biocompatibility. Biocompatibility has been defined as "the ability of a material to perform with an appropriate host response in a specific application” (1). Cardiovascular devices, such as the left ventricular assist device, have been shown to be associated with thromboembolism, bleeding, and infection, which are characteristics of poor biocompatibility (2). Activation of the coagulation cascade caused by the artificial surfaces of such cardiovascular devices has been shown to cause thromboembolic events (3).

To improve the biocompatibility of implantable cardiovascular devices whose artificial surfaces will be contacting the blood stream, endothelial cells might be an optimal lining since they naturally occur in human blood vessels at the blood-contacting surface. Endothelial cells secrete--among others factors--chemotactic, growth, and nonthrombogenic factors such as prostacyclin and nitric oxide (NO).

Bordenave et al.suggested the seeding of endothelial cells onto vascular grafts because this metabolically active endothelial lining plays a major role in preventing in vivo blood thrombosis and because vascular grafts implanted into humans do not form an endothelial monolayer spontaneously (4).


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Nikolaychik et al. have tested endothelial cell monolayers under dynamic conditions inside a beating ventricular prosthesis in vitro with the goal of producing a permanent biocompatible artificial cardiac prosthesis (5). They have measured an endothelial cell loss of 35% indicating denudation of the endothelial cell lining.

Scott-Burden et al., investigated smooth muscle cells genetically engineered with endothelial-Nitric Oxides Synthase seeded on the surfaces of left ventricular assist devices and implanted in a calf for 24 hours (6). Genetically engineered smooth muscle cells have been shown to secrete Nitric Oxide and to provide an adherent, nonthrombogenic autologous cell lining.

There are drawbacks, however, to using either endothelial cells or smooth muscle cells to line cardiovascular devices. Neither cell type is abundantly available nor easily accessible, harvested, and isolated. Moreover, endothelial cells have been observed to slough off easily from artificial surfaces (2). The process of harvesting, isolating, and cultivating both endothelial cells and smooth muscle cells from autologous vessels is invasive and time-consuming.

In contrast, auricular chondrocytes are abundant, readily accessible, and able to be easily and efficiently harvested. One potential source of chondroctyes, auricular cartilage, can be harvested by a minimally invasive technique that preserves cell viability, decreases surgical time, and postoperative complications (7).

In vivo, chondrocytes are naturally nourished by diffusion and produce substantial amounts of extracellular matrix components (8). Therefore, cultured chondrocytes may be more likely to remain viable and adherent to artificial surfaces.


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We investigated in vitro the isolation and culture of auricular cartilage as a more efficient, less invasive means of obtaining autologous tissue for lining the luminal surfaces of implantable left ventricular assist devices (LVAD’s) and in vivo the adherence of cultured auricular cartilage cells (chondrocytes) to the luminal surfaces of a LVAD in a calf model.


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