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Intimal hyperplasia

Basci science Intimal hyperplasia

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Intimal hyperplasia

  1. 1. F2 Parach Sirisriro 1st April 2019 INTIMAL HYPERPLASIA
  2. 2. REFERENCE Textbook 1. Rutherford's Vascular Surgery and Endovascular Therapy 9th edition , Chapter 47, 589-601.e 2. Vascular and Endovascular Surgery: A Companion to Specialist Surgical Practice, 6th Edition , Chapter 7, 83-101.e
  3. 3. OUTLINE • RESPONSE OF THE ARTERY TO INJURY - Hemodynamics - Systemic Vascular Diseases - Intravascular Bare Metal Stents - Intravascular Drug-Eluting Stents - Intravascular Drug-Eluting Balloons • RESPONSE OF VEIN TO INJURY • HEALING RESPONSE OF THE PROSTHETIC GRAFT • INTIMAL HYPERPLASIA AND DIALYSIS ACCESS • CONCLUSION
  4. 4. DEFINITION • The abnormal migration and proliferation of vascular smooth muscle cells with the associated deposition of extracellular connective tissue matrix • followed by remodeling of this new tissue 1. Rutherford's Vascular Surgery and Endovascular Therapy 9th edition , Chapter 47, 589-601.e
  5. 5. STAGE OF INTIMAL HYPERPLASIA 1. Rutherford's Vascular Surgery and Endovascular Therapy 9th edition , Chapter 47, 589-601.e
  6. 6. Pathophysiology intimal Hyperplasia • Platelets accumulate on denuded region • Endothelial cells proliferate • SMCs also proliferate and migrate into intima, causing intimal thickening 1. Rutherford's Vascular Surgery and Endovascular Therapy 9th edition , Chapter 47, 589-601.e
  7. 7. Pathophysiology Intimal Hyperplasia
  8. 8. Pathophysiology Intimal Hyperplasia Conde Cath & Cardiovasc Int. 2003;60:236
  9. 9. Pathophysiology Intimal Hyperplasia Conde Cath & Cardiovasc Int. 2003;60:236
  10. 10. Pathophysiology Intimal Hyperplasia Conde Cath & Cardiovasc Int. 2003;60:236
  11. 11. Pathophysiology Intimal Hyperplasia
  12. 12. Pathophysiology Intimal Hyperplasia • Factors from platelets, leukocytes, smooth muscle cells, and extracellular matrix interact and regulate the process of intimal hyperplasia, making each step a potential therapeutic target
  13. 13. Pathophysiology Intimal Hyperplasia
  16. 16. Hemodynamics - Changes in hemodynamic parameters  affect the arterial structure of both normal and diseased vessels. - Blood flow (closely associated with shear stress) is associated with the formation of intimal hyperplasia In an experimental study, Hehrlein confirmed that reduced vascular runoff after angioplasty results in the increased development of intimal hyperplasia
  17. 17. Systemic Vascular Diseases - Exposure to cigarette smoke increases the development of experimental intimal hyperplasia by two fold. - Cholesterol reduction therapies with statins have been shown in some studies to reduce the development of restenosis - Diabetes is a predictor for restenosis. - Restenotic plaques in diabetic patients is composed of atherosclerotic plaque . - This might suggest that recoil/remodeling may be predominant.
  19. 19. - After balloon angioplasty, there is thrombus formation, intimal hyperplasia development, elastic recoil, and negative remodeling. - In contrast, after stent placement, elastic recoil and negative remodeling are eliminated and thrombus formation followed by intimal hyperplasia development are the main contributors to “Instent restenosis” CONSEQUENCE AND CURE OF ANGIOPLASTY
  20. 20. Mechanism of Instent restenosis • A stent is generally used if – the result of balloon angioplasty is technically unsatisfactory – if there is arterial occlusion, immediate elastic recoil, dissection, or restenosis • Four categories of in-stent restenosis have been defined: (1) focal (≤10-mm length) (2) diffuse (>10-mm length) (3) proliferative (>10-mm length and extending outside the stent) (4) occlusion
  21. 21. Mechanism of Instent restenosis
  22. 22. Mechanism of Instent restenosis
  23. 23. Mechanism of Drug-eluting stents
  24. 24. Intravascular Drug-Eluting Stents PaclitaxelSirolimus
  25. 25. Intravascular Drug-Eluting Balloons
  26. 26. The chief benefit cited for DEBs is -Avoidance of additional metal and polymer barriers, which may disrupt or hinder vascular healing -DEB-treated vessels show - delayed vascular healing characterized by dose-dependent increases in fibrin deposition, - delayed re-endothelialization, - lower number of neointimal cells, - increased medial VSMC loss Intravascular Drug-Eluting Balloons
  28. 28. Healing response of prosthesis graft
  29. 29. Intimal Hyperplasia and Dialysis Access - AVBG : The anastomoses appear to be the areas of maximal intimal hyperplasia as a result of surgical trauma and the presence of flow disturbance. - The majority of stenoses occur at the venous anastomoses and within 1 cm of the anastomosis AVF : Five anatomic stenotic lesions in arteriovenous fistula grafts have been categorized: stenosis in the draining vein proximal to the venous anastomosis (36%), stenosis in the central vein (24%), stenosis at the venous anastomosis (25%), stenosis at the arterial anastomosis (11%), and intragraft hyperplasia (4%).
  30. 30. Treatment Vascular reconstruction • Principal way to salvage failing grafts • Based on assumption that renewed or continued intimal thickening is unlikely • With regular follow-up, stenoses in vein grafts may be discovered prior to graft thrombosis • If these lesions are reconstructed in time, long-term outcome is generally good
  31. 31. Conclusion Intimal hyperplasia Intimal hyperplasia is a complex response to injury. Vascular reconstruction is effective in salvage of vein grafts if performed in time Antiplatelet agents are effective if given at or within a short time of surgery Development of effective therapy requires an understanding of the underlying pathophysiology.