Angioplasty and Stents
Individuals with coronary artery disease (blocked arteries supplying the heart
muscle) were initially treated with medications. The development of bypass
surgery in the 1970s was the first mechanical correction for this disease which
lead to improvement in both symptoms, and depending upon the anatomy of the
patient, improved longevity.
Patients longed for a less invasive correction of this problem which lead to the
development of coronary balloon angioplasty by Dr. Andreas Gruntzig in
Switzerland in 1977. The principle behind this procedure was simple: an
uninflated balloon catheter was inserted into a blocked coronary artery, the
balloon was inflated and the blockage was crushed into the wall of the artery
(figure 1).
Angioplasty unfortunately was fraught with hazards. Abrupt vessel closure due to
blood clot formation or tearing of the inside of the artery (known as a
dissection) led to heart attacks and frequently required urgent bypass surgery.
Since arteries are muscular, the artery would expand with the balloon inflation
and then returned to its previous size over the upcoming weeks (due to elastic
recoil) with no significant improvement in symptoms. Nevertheless, for many
individuals this procedure worked extremely well in alleviating their symptoms.
Stents were developed to address the issues of dissection and elastic recoil in
the 1990s. Stents act as a scaffolding proping the artery open and preventing
recoil. They also stabilized the inner blood vessel wall and helped to prevent
(and were also used to treat) dissections (figures 2 and 3). The need for urgent
bypass surgery began to decrease.
Stents presented their own unique problems. The body formed scar tissue on the
stents leading to narrowing of the stented area (a problem known as restenosis).
The original stents were quite stiff and difficult to insert due to the
curvature of the coronary arteries. Blood clot formation on the stents
themselves led to heart attacks.
In 1999, the medication Clopidogrel was approved by the FDA and became the
mainstay to prevent blood clot formation on stents. Combined with Aspirin, the
two drugs also led to a significant reduction in the restenosis rate from
approximately 40-50% down to 25%. The advent of newer stent designs and
materials in the early 2000s lead to a further reduction down to 15-20%. The use
of anticancer drugs to prevent tissue in-growth into the stents (drug-eluting
stents) lead to a reduction of in-stent stenosis down to 6-8% which is where
things are today.
See our Patient Brochure Page.
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