Print this page10. Response of the Arterial Wall to Injury and Intimal Hyperplasia
General considerations
- Degrees of vascular injury.
- General characteristics of intimal hyperplasia (including its differentiation from restenosis).
Types of injury resulting in intimal hyperplasia
- Angioplasty, stenting, endarterectomy.
- Vein grafting.
- Prosthetic grafting.
The three-wave model of intimal hyperplasia
- Medial smooth muscle cell proliferation (including the role of platelet-derived growth factor, basic fibroblast growth factor and angiotensin II).
- Smooth muscle cell migration (including the role of extracellular matrix, platelets, migratory factors and the endothelium).
- Intimal expansion (including the regulation of the extent of intimal hyperplasia).
Prospects for control of intimal hyperplasia
- Surgical technique.
- Promoting endothelialization.
- Pharmacologic control of smooth muscle cell activity (including systemic and local drug delivery techniques).
- Brachytherapy.
- Strategies for the future (including antibodies to growth factors, antisense nucleotides, gene therapy etc).
References
Newby AC, Zaltsman AB. Molecular mechanisms in intimal hyperplasia. J Pathol 2000;190:300-309.
The underlying causes of intimal hyperplasia are migration and proliferation of vascular smooth muscle cells provoked by injury, inflammation, and stretch. This review discusses, at a molecular level, both the final common pathways leading to smooth muscle migration and proliferation and their (patho)-physiological triggers. It emphasizes the key roles played by growth factors and extracellular matrix-degrading metalloproteinases, which act in concert to remodel the extracellular matrix and permit cell migration and proliferation.
Purcell C, Tennant M, McGeachie J. Neo-intimal hyperplasia in vascular grafts and its implications for autologous arterial grafting. Ann R Coll Surg Engl 1997;79:164-168.
In this article the structure and development of neointimal hyperplasia in vascular grafts, both venous and arterial, are reviewed briefly. The clinical outcomes of various arterial grafts that are now being used, including the radial, the internal mammary and the gastroepiploic arteries, as well as the underlying cell biology of their adaptation to the grafted environment are also reviewed.
Davies MG, Hagen PO . Pathobiology of intimal hyperplasia. Br J Surg 1994;81:1254-1269.
Intimal hyperplasia may be defined as the abnormal migration and proliferation of vascular smooth muscle cells with associated deposition of extracellular connective tissue matrix. In this article, the pathology of intimal hyperplasia is reviewed with particular attention to its physiology, pharmacology, cell biology and molecular biology.
Neville RF, Sidawy AN. Myointimal hyperplasia: basic science and clinical considerations. Semin Vasc Surg 1998;11:142-148.
The development of the intimal hyperplasia at the outflow anastomosis of a prosthetic bypass or in autogenous saphenous vein bypass placed in the arterial system is responsible for most bypass failures. This article reviews current knowledge on the pathogenesis of myointimal hyperplasia and addresses possible therapeutic considerations for the future.
Tennant M, Dilley RJ, McGeachie JK, Prendergast FJ. Histogenesis of arterial intimal hyperplasia and atherosclerosis. Aust N Z J Surg 1990;60:79-85.
This article briefly reviews the histological evidence for the genesis of intimal hyperplasia and atherosclerosis in arteries. It concentrates upon the origin, structure, behaviour and interactions of vascular smooth muscle cells in the intimal (subendothelial) layer.