Abstract

Arteriovenous fistula (AVF) remains the vascular access of choice in hemodialysis but generates cardiovascular constraints. Its creation immediately induces an increase in cardiac output. Increased venous return and subsequent volume overload lead to biventricular remodeling, and eventually to dysfunction. High-output heart failure (HOHF) caused by high-flow AVF is a recognized but not strictly defined clinical entity, based on the combination of hypervolemia with an elevated cardiac output. A Qa greater than 2 L/min is a risk factor for HOHF, particularly in susceptible patients. The most used flow reduction procedure is post-anastomotic vein caliber reduction by a banding technique, relieving symptoms and partially reversing previously induced structural abnormalities, but the benefit often remains limited in time.

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