Biomedical Engineering Reference
In-Depth Information
10
Biomaterials in cardiac restoration therapy
D. SELIKTAR and K. SHAPIRA-SCHWEITZER,
Technion - Israel Institute of Technology, Israel
Abstract
: In this chapter we will cover the use of biomaterials for cardiac
restoration, including acellular biomaterial therapies, non-injectable
biomaterials and injectable biomaterials. The chapter fi rst reviews the
use of biomaterials alone to stabilize the cardiac wall geometry and
prevent cardiac remodeling. Next we will cover the two distinct
categories of biomaterial-based cardiac cell therapies: a tissue
engineered cardiac patch that attempts to create a tissue analog
in vitro
which is to be sutured directly onto the infracted myocardium, and an
injectable biomaterial/cell graft which is focused on the use of liquid-to-
solid hydrogels as cell carriers that increase the cell survival and improve
the overall contractility of the infarcted myocardium.
Key words
: cardiac cell therapy, injectable biomaterials, hydrogel, cardiac
patch.
10.1 Introduction
Nearly 2400 Americans die of cardiovascular-related diseases (CVD) each
day - an average of one death every 37 seconds. CVD claims approximately
as many lives each year as cancer and diabetes mellitus combined.
1
Although
there have been signifi cant improvements in cardiac medicine, the optimal
solution for the failing heart remains heart transplantation. Unfortunately,
there is a signifi cant shortage of donors - in 2007 there were close to 3000
heart patients on the transplant waiting list in the United States alone.
There are many more who are not considered to be candidates for heart
transplantation but could benefi t from a cardiac restoration therapy that
can rejuvenate part of the heart muscle immediately following a heart
attack and myocardial infarction (MI).
2
MI is a progressive process starting with an occlusion and a reduction of
the coronary blood supply that leads to myocardial ischemia and the immi-
nent death of cardiac cells (i.e. cardiomyocytes). A tissue repair process is
initiated at the onset of MI, immediately following the loss of the cardio-
myocyte population in the injured tissue. Several events occur during this
repair process, including the invasion of infl ammatory cells into the infract
area and the increased activity of matrix metalloproteinase (MMPs) at the
site of infl ammation. Collagen degradation is subsequently increased, and
this is accompanied by additional cell loss, wall thinning and ventricular
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