2. What is a Stent?
A small tubular mesh usually made of
either stainless steel or Nitinol.
Inserted into stenotic arteries to keep the
lumen patent often used after PTCA.
Used at various sites including the
coronary, renal, carotid and femoral
arteries.
Non-arterial uses e.g. in bronchus,
trachea, ureter, bile duct.
5. History
The concept of vascular stents is
accredited to Charles Dotter in 1969, who
implanted stainless steel coils in canine
peripheral arteries.
Not followed up in humans because of
haemodynamically significant narrowing.
Not in clinical practice until 1980s.
Market leader is the Palmaz stent
designed by Julio Palmaz in 1985.
Initially, 18 grafts placed in canine vessels, with
patency rates approaching 80% at 35 weeks.
6. Motivation for development-
Blood Thrombosis
A formation of blood clot inside a blood
vessel, obstructing the flow of blood.
Likely to lead to cardiac infraction, may result
in death.
8. Smoking, high BP, toxins etc cause damage to the
vascular endothelium.
LDL and fibrin pass through and collect in the sub-
endothelium.
Monocytes adhere to the damaged endothelium,
migrate to the sub-endothelial space and engulf
LDL – FOAM CELLS.
SMC migration and CT formation.
Two main types of plaque:
Atheromatous (athere: gruel, oma: tumour(
Fibrous (like atheroma but with connective tissue cap(
9. CVD statistics
Heart and circulatory disease is the UK's
biggest killer.
In 2001, cardiovascular disease caused
40% of deaths in the UK, and killed over
245,000 people.
Coronary heart disease causes over
120,000 deaths a year in the UK:
approximately one in four deaths in men
and one in six deaths in women.
12. PTCA
Minimally invasive procedure
Percutaneous access either in the brachial or
femoral arteries.
A guide wire is advanced to the stenotic
region.
A balloon is advanced along the wire and
inflated/deflated several times to fracture the
plaque and open the lumen.
13.
14.
15. Angioplasty and other coronary intervention procedures, 1991-2000, UK
Number of Tot al angioplast y and Rat e per Annual % Success Mort alit y
int ervent ion cent res ot her coronary million increase (% ) (% )
int ervent ion procedures
1991 52 9,933 174 86 0.48
1992 52 11,575 203 16.5 88 0.71
1993 53 12,937 227 11.8 89 0.59
1994 54 14,624 256 13.0 90 0.60
1995 54 17,344 304 18.6 89 0.69
1996 53 20,511 359 18.1 90 0.72
1997 58 22,902 402 11.7 92 0.89
1998 61 24,899 437 8.7 92 0.80
1999 63 28,133 494 13.0 90 0.61
2000 66 33,652 590 20.0 92 0.70
Source: British Cardiovascular Intervention Society (2002) htpp://www.bcis.org.uk
16. Complications of PTCA
Plaque rupture, may lead to:
Thrombus formation
Intimal flap
Arterial rupture
Acute closure
Sub-optimal result
Restenosis
Requires further intervention to make vessel
patent
17.
18. Stenting vs. PTCA
Prevents acute closure
Tacks back intimal flaps
Less restenosis:
30–50%restenosis with PTCA (coronary arteries(.
Coronary stents are associated with fewer
repeat revascularisation procedures
Rates of death and MI are low and are
not significantly different between stents
and PTA.
20. Mechanism of Restenosis
shear stress
Intimal Hyperplasia
lumen
shear stress
If baseline shear stress not restored – continuing
intimal hyperplasia and RESTENOSIS
21. Factors Which Contribute to In-
stent Restenosis
Thrombus/platelet/fibrin adherence to stent
struts.
Metabolic disorder/smoking/atherogenic
diet.
Small lumen diameter.
Stress concentration at end of stent.
Flow disturbance within stented region.
23. Previous flow studies
of Palmaz stents
Peacock et al. (1995) used hot
film probe distal to stent;
found flow disturbance under
mild exercise conditions.
Berry et al. (1997) performed
dye injection flow visualization
and found significant flow
disturbance within and distal to
stent; stagnation near struts.
End systole
Diastole
Flow
24. Effects of compliance mismatch
Axial Position
Compliance
Abrupt Compliance
mismatch creates:
Pressure Wave Reflections
Flow instability
Wall Stress concentration
25. Improving Vascular Stents (1(
Thrombus
Anticoagulants
Heparin – systemically or coated on stent.
Inhibition of the GP IIb-IIIa receptor:
Prevents platelet aggregation.
Available as Abciximab.
Associated with incidence of MI.
PTFE coated stents.
27. Improving Vascular Stents (2(
Small diameter artery
Combination of local and systemic medication
and covered stents.
Intimal hyperplasia
Brachytherapy:
Use of ionising radiation to stop cellular proliferation.
Delivery: Radioactive stents, catheter radiation.
10%restenosis but may cause necrosis.
Anti-proliferative agents e.g. rapamycin
(Sirolimus(
28. Improving Vascular Stents (3(
Mechanical and flow disturbances:
Compliance Matching Stent (CMS(
This stent is rigid in the middle and becomes more
compliant near its ends.
This compliance is achieved by parabolic and
cantilevered struts.
The middle struts are straighter, providing some
resistance to recoil and support for the
atherosclerotic plaque.
29. Compliance Matching StentCompliance Matching Stent
Parabolic and canti-
levered struts cause
ends to be most
compliant.
Straighter struts in
middle provide stiff
support for plaque.
Transition in between.
30. Compliance Matching Stent
The gradual change from rigid to compliant
with the CMS reduces stress concentration at
the stent edges.
The geometry of this stent also fosters more
laminar flow through the stent.
Less flow disturbance means less intimal
hyperplasia.
37. Normal Stent vs. CMS
Normal Stent
Flow disruption
Disturbed shear stress
Intimal hyperplasia
No return to baseline
shear
RESTENOSIS
CMS
More laminar flow
Less disturbed shear
stress
Less intimal hyperplasia
Return to baseline shear
PATENT LUMEN
38. My PhD Project
Involves in vivo testing of the CES.
Comparison with SMART stent:
Amount of intimal hyperplasia.
Effects on flow and pressure waves.
Quantifying effect of “overstretch”.
In vivo sites – carotid and iliac arteries.
