Abstract
While recent developments have allowed greater insight into the vascular pathobiology and intimal hyperplasia, very few of these advances have led to improved clinical care of hemodialysis vascular accesses. Indeed the most common procedure for the treatment of access stenosis and thrombosis is the same model for the creation and study of intimal hyperplasia. The evolution of our understanding of vascular thrombosis is reviewed with a current concept that includes a dynamic interplay of the biophysics, chemistry and biology of the blood vessel with the blood and its constituents. Implications for possible future interventions based on these novel concepts are offered, and the significance of improving our understanding of the pathobiology is emphasized.
Copyright (c) 2010 S. Karger AG, Basel.
MeSH terms
-
Angiotensin-Converting Enzyme Inhibitors / therapeutic use
-
Anticoagulants / adverse effects
-
Anticoagulants / therapeutic use
-
Arteriovenous Shunt, Surgical / adverse effects*
-
Calcium Channel Blockers / therapeutic use
-
Catheters, Indwelling / adverse effects*
-
Cell Movement / drug effects
-
Constriction, Pathologic
-
Drug-Eluting Stents
-
Endothelium, Vascular / injuries
-
Epoprostenol / physiology
-
Equipment Failure
-
Forecasting
-
Hemorheology
-
Humans
-
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use
-
Hyperplasia
-
Models, Cardiovascular
-
Nitric Oxide / physiology
-
Pentoxifylline / therapeutic use
-
Randomized Controlled Trials as Topic
-
Renal Dialysis / methods*
-
Sepsis / etiology
-
Sepsis / prevention & control
-
Thrombosis / etiology
-
Thrombosis / physiopathology
-
Thrombosis / prevention & control
-
Tunica Intima / pathology
-
Vasodilation
Substances
-
Angiotensin-Converting Enzyme Inhibitors
-
Anticoagulants
-
Calcium Channel Blockers
-
Hydroxymethylglutaryl-CoA Reductase Inhibitors
-
Nitric Oxide
-
Epoprostenol
-
Pentoxifylline