from acute thrombosis to chronic fibrosis begins with invasion of neutrophils followed by monocytes and macrophages, with subsequent development of myofibroblasts and thickening of the interstitial matrix in the post-thrombotic vein. Substantially more detailed work in the inflammatory pathway has been done, with a particular emphasis on metalloproteinase 9, which appears to have a regulatory function in post-thrombotic vein biomechanics.1 Knowledge of the inflammatory pathway represents a potential area for medical and interventional prevention of post- thrombotic syndrome after acute DVT.


The venous revolution


Where we are and where we’re going By David S. Shin, MD; Frederic Bertino, MD; Ramsey A. Al-Hakim, MD; Ronald S. Winokur, MD, FSIR; Kush R. Desai, MD, FSIR; and Jeffrey Forris Beecham Chick, MD, MPH


Bertino F


rom a basic science perspective, a number of questions remain unanswered regarding deep veins. Venous disease is a cause of morbidity and mortality for patients of all ages, though the past several years have shown marked progress in research and approval of techniques and devices used for the treatment of venous disease. Major areas of research potential


1999


Percutaneous delivery of pancreatic islet cells to the liver for transplantation to treat diabetes is first used.


Endovenous laser ablation to treat varicose veins and venous disease is introduced.


include the inflammatory pathway from acute deep venous thrombosis (DVT) to chronic fibrosis, and venous wall biomechanics and flow dynamics in the normal and disease states.


New and emerging research The inflammatory process of DVT to fibrosis has been an area of active research in recent years. The pathway


2000


The first results indicating success of uterine fibroid embolization are published.


Within the current body of literature, the understanding of venous wall biomechanics and luminal flow dynamics in the normal and post-thrombotic state is in its infancy. The normal and post-thrombotic veins have been described in animal models and human studies, with the latter demonstrating a predominance of type I collagen, which increases wall stiffness.2


Venous


intervention with the application of radial force by stent placement shows exaggeration of the Poisson effect in veins compared to arteries. This biomechanical phenomenon is due to the relatively lower inherent elasticity of veins and is even further amplified in the post-thrombotic vein wall with increased stiffness. The Poisson effect may limit the overall lumen gain achievable by application of radial force. Understanding these vein wall biomechanics provides a segue into enhanced research on vein flow dynamics, predominantly via computational modeling.


Currently, the understanding of normal venous flow is poor and the quantitation


2001


Kyphoplasty becomes a more accessible therapy option.


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