Coronary-Artery Stent

The use of percutaneously introduced
prosthetic devices to maintain the luminal
integrity of diseased blood vessels
was proposed by Dotter and Judkins in
1964 (2), well before the introduction of
coronary angioplasty by Gruntzig et al
1997.(3)
Palmaz et al introduced the use of balloon-
mounted stents (as used in coronary
arteries today) in peripheral arteries
in 1985.(4)
Schatz et al subsequently modified the
palmaz-stent, which led to the development
of the first commercially successful
stent, the palmaz-schatz stent.(5)
One such device was a metal tube or"
Scaffold" that was inserted. Puel and
Sigwart were the first to implant a stent
in humans after balloon angioplasty in
March 1986.
Sigwart and colleagues were also the
first to describe the use of this stent in
1987 for emergency vessel closure during
balloon angioplasty.(6)
In 1994 the first Palmaz-Schatz stent
was approved for use in the United
States.(7)
Over the next decade, several generations
of bare metal stents were developed,
with each succeeding one being
more flexible and easier to deliver to
narrowing.(7)
Early observation trials highlighted
problems associated with the use of
stents, in particular, a high incidence of
subacute occlusion, despite aggressive
anticoagulation regimens that prolonged
hospital stays and that were difficult
to control and occasionally led to
serious events.(1)
In 1993 two important randomized trialscompared the Palmaz-schatz stent with
angioplasty, establishing the elective
placement of coronary stents as a standard
treatment. (BENESTENT,
STRESS)
Although the implantation of an intracoronary
stent prevents the acute recoil
and post-injury arterial shrinkage associated
with balloon angioplasty, it
increases the risk of subacute thrombosis
(3.7 percent of patients, a value higher
than that seen with balloon angioplasty
alone) and, more importantly,
replaces the atherosclerotic coronary
disease with the more severe iatrogenic
condition of in-stent neointimal hyperplasia,
that is, the growth of scar tissue
inside the stent through the cell-cycle
pathway, and as a result, the proliferation
and migration of vascular smoothmuscle
cells.(1) This in-stent restenosis
occurs in about 25% of cases of bare
metal implantation, typically at six
months, necessitating a repeat procedure.(
7) A recent meta-analysis of 29
published, randomized studies involving
9918 patients and comparing balloon
angioplasty with routine coronary
stenting with bare stents confirmed that
stenting reduces restenosis and repeat
intervention, but dose not reduce mortality
or MI.(8)
Once a role for elective stent implantation
was established, the next goal was
to overcome the compplications of subacute
thrombosis and neointimal hyperplasia
through pharmacologic and physical
means.
Various biologically inert surfaces coatings,
such as carbon, platinum, phosphorylcholine,
and gold, have beenapplied to stainless-steel stents in an attempt to reduce
thrombosis and restenosis, but the effectiveness of
these strategies has not been proven in clinical trials.
Significat reduction of stent thrombosis with heparincoated
stents has been reported from a single center
study.(9)