Plication Of A High-flow Arteriovenous Fistula Resulting In Improvement Of High-output Heart Failure

Abstract

<h3>Introduction</h3> High-output heart failure (HOF) is characterized by a state of congestion resulting from high cardiac output (CO) and decreased systemic vascular resistance (SVR). Arteriovenous fistulae (AVF) are durable vascular access used for renal replacement therapy (RRT). They are an important and perhaps under-recognized etiology of HOF. We present a case where plication of a high-flow AVF resulted in clinical improvement of HOF. <h3>Case Presentation</h3> A 54-year-old woman with end-stage renal disease underwent renal transplant eighteen years ago after receiving RRT through an AVF for eleven months. Currently, she has developed chronic renal allograft dysfunction and congestive heart failure. Her baseline ejection fraction (EF) and estimated glomerular filtration rate (eGFR) were 50-55% and 25-30 mL/min/1.7m². On this hospital admission, she had marked volume overload (20 kg over her dry weight), poor response to continuous rate infusion bumetanide, and newly depressed EF of 25-30%. Right heart catheterization showed elevated CO (9.8 L/min) and elevated filling pressures (right atrial pressure 17 mmHg; pulmonary capillary wedge pressure 27 mmHg). Doppler ultrasound of the AVF measured its flow to be 4.9 L/min. Temporary occlusion of the AVF resulted in a 35% decrease in CO and 21% increase in SVR, suggesting HOF due to AVF. Due to ongoing concern for renal allograft failure, the decision was made to plicate the AVF to preserve its potential future use in RRT. A 10cm length of the AVF was plicated. Repeat echocardiography ten days after plication revealed recovery of EF to baseline. Following the plication, her response to diuresis improved and she eventually achieved euvolemia over a period of three weeks. She was discharged home on oral bumetanide 3mg twice daily. <h3>Conclusion</h3> AVF-related HOF is associated with detrimental ventricular remodeling that may be reversed with attenuation of the shunt. In our case, plication was used in a novel manner to preserve AVF function. There are no guidelines that suggest how AVF should be managed following renal transplant. Further work in this field may be useful in exploring the role of plication in the management of HOF.