1 – INFLAMMATION AND THE PATHOPHYSIOLOGY OF CHRONIC VENOUS DISEASE: MOLECULAR MECHANISMS

Publisher Summary This chapter discusses the inflammation and the Pathophysiology of chronic venous disease. The inflammatory cascade serves a lifetime as a repair mechanism that leads after removal of injured tissue to formation of new tissue. This cascade leads to return of basic organ functions or may just end up in the formation of a connective tissue (i.e., a scar). After removal of cell debris during resolution of inflammation, macrophages generate new growth factors, fibroblast and other connective tissue cells migrate and differentiate, new blood vessels grow, and new tissue is generated. Likely, there is an important role for stem cells that determine what particular functions the new tissue will be able to carry out. While in many cases venous disease leads eventually to resolution of the inflammation, we are concerned with cases that have recurrent inflammation without definitive resolution. The lack of a resolution of inflammation indicates that the stimulus that activates the inflammatory cascade remains active and has not been brought under control. There are numerous ways to induce cell activation in the circulation and trigger an inflammatory cascade. Another mechanical stimulus that controls the inflammatory and thrombotic phenotype is fluid shear stress.