Vascular stents


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  • 25% mortality of pts with mediastinitis
  • However, any potential differences may be masked by the crossover to stents after poor results (such as dissection) immediately after PTA.
  • Vascular stents

    2. 2. What is a Stent? A small tubular mesh usually made ofeither stainless steel or Nitinol. Inserted into stenotic arteries to keep thelumen patent often used after PTCA. Used at various sites including thecoronary, renal, carotid and femoralarteries. Non-arterial uses e.g. in bronchus,trachea, ureter, bile duct.
    3. 3. Current stent designsPalmaz, the market leader
    4. 4. Palmaz “Corinthian” Iliacartery stentGianturco-Roubin II Stent
    5. 5. HistoryThe concept of vascular stents isaccredited to Charles Dotter in 1969, whoimplanted stainless steel coils in canineperipheral arteries.Not followed up in humans because ofhaemodynamically significant narrowing.Not in clinical practice until 1980s.Market leader is the Palmaz stentdesigned by Julio Palmaz in 1985.Initially, 18 grafts placed in canine vessels, withpatency rates approaching 80% at 35 weeks.
    6. 6. Motivation for development-Blood Thrombosis A formation of blood clot inside a bloodvessel, obstructing the flow of blood. Likely to lead to cardiac infraction, may resultin death.
    7. 7. Thrombus in Human Coronary Artery
    8. 8. Smoking, high BP, toxins etc cause damage to thevascular 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 engulfLDL – 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. 9. CVD statisticsHeart and circulatory disease is the UKsbiggest killer. In 2001, cardiovascular disease caused40% of deaths in the UK, and killed over245,000 people.Coronary heart disease causes over120,000 deaths a year in the UK:approximately one in four deaths in menand one in six deaths in women.
    10. 10. Revascularisation techniquesCoronary Artery Bypass Graft (CABG(Percutaneous Transluminal CoronaryAngioplasty (PTCA(Stents
    11. 11. CABGMajor surgeryComplicationsStrokeMediastinitis (1-4%(Renal dysfunction (8%(
    12. 12. PTCAMinimally invasive procedurePercutaneous access either in the brachial orfemoral arteries.A guide wire is advanced to the stenoticregion.A balloon is advanced along the wire andinflated/deflated several times to fracture theplaque and open the lumen.
    13. 13. Angioplasty and other coronary intervention procedures, 1991-2000, UKNumber of Tot al angioplast y and Rat e per Annual % Success Mort alit yint ervent ion cent res ot her coronary million increase (% ) (% )int ervent ion procedures1991 52 9,933 174 86 0.481992 52 11,575 203 16.5 88 0.711993 53 12,937 227 11.8 89 0.591994 54 14,624 256 13.0 90 0.601995 54 17,344 304 18.6 89 0.691996 53 20,511 359 18.1 90 0.721997 58 22,902 402 11.7 92 0.891998 61 24,899 437 8.7 92 0.801999 63 28,133 494 13.0 90 0.612000 66 33,652 590 20.0 92 0.70Source: British Cardiovascular Intervention Society (2002) htpp://
    14. 14. 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 vesselpatent
    15. 15. Stenting vs. PTCAPrevents acute closureTacks back intimal flapsLess restenosis:30–50%restenosis with PTCA (coronary arteries(.Coronary stents are associated with fewerrepeat revascularisation proceduresRates of death and MI are low and arenot significantly different between stentsand PTA.
    16. 16. Stent FailureRestenosis20-30%
    17. 17. Mechanism of Restenosisshear stressIntimal Hyperplasia lumen shear stressIf baseline shear stress not restored – continuingintimal hyperplasia and RESTENOSIS
    18. 18. Factors Which Contribute to In-stent RestenosisThrombus/platelet/fibrin adherence to stentstruts.Metabolic disorder/smoking/atherogenicdiet.Small lumen diameter.Stress concentration at end of stent.Flow disturbance within stented region.
    19. 19. Thrombus in Human Coronary Artery
    20. 20. Previous flow studiesof Palmaz stentsPeacock et al. (1995) used hotfilm probe distal to stent;found flow disturbance undermild exercise conditions.Berry et al. (1997) performeddye injection flow visualizationand found significant flowdisturbance within and distal tostent; stagnation near struts.End systoleDiastoleFlow
    21. 21. Effects of compliance mismatchAxial PositionComplianceAbrupt Compliancemismatch creates:Pressure Wave ReflectionsFlow instabilityWall Stress concentration
    22. 22. 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.
    23. 23. Intimal hyperplasia instented Canine iliac artery.After insertion of stentplus PTFE graftmaterial.
    24. 24. Improving Vascular Stents (2(Small diameter arteryCombination of local and systemic medicationand 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(
    25. 25. Improving Vascular Stents (3(Mechanical and flow disturbances:Compliance Matching Stent (CMS(This stent is rigid in the middle and becomes morecompliant near its ends.This compliance is achieved by parabolic andcantilevered struts.The middle struts are straighter, providing someresistance to recoil and support for theatherosclerotic plaque.
    26. 26. Compliance Matching StentCompliance Matching StentParabolic and canti-levered struts causeends to be mostcompliant.Straighter struts inmiddle provide stiffsupport for plaque.Transition in between.
    27. 27. Compliance Matching StentThe gradual change from rigid to compliantwith the CMS reduces stress concentration atthe stent edges.The geometry of this stent also fosters morelaminar flow through the stent.Less flow disturbance means less intimalhyperplasia.
    28. 28. Compliance TestingString apparatusFinite Element Analysis
    29. 29. Compliance Test (string apparatus)-101234560 1 2 3 4 5Load (N)Deformation(mm)Slope = 1.87Slope = 0.77Slope = -0.01Slope = -0.02Deflection
    30. 30. 00.510 6 12 18 24 30 36 42Axial Position (mm)NormalizedComplianceCMSPalmazIn Vitro Diameter Compliance Measurements
    31. 31. End systoleDiastoleFlow
    32. 32. 1.21.44-011.35-011.25-011.16-011.06-019.70-028.76-027.82-026.89-025.93-024.99-024.05-023.11-022.17-021.23-022.91-03
    33. 33. Palmaz CMS6 week post implantation
    34. 34. Normal Stent vs. CMSNormal StentFlow disruptionDisturbed shear stressIntimal hyperplasiaNo return to baselineshearRESTENOSISCMSMore laminar flowLess disturbed shearstressLess intimal hyperplasiaReturn to baseline shearPATENT LUMEN
    35. 35. 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.
    36. 36. Stents used in study
    37. 37. Pig femoral artery, overstretched by 25% and stented– 1 month after procedure.