HFSA ePoster Library

Outcomes With Impella 5.0 And 5.5 In Cardiogenic Shock
HFSA ePoster Library. Azobou Tonleu F. 09/10/21; 343420; 191
Franck Azobou Tonleu
Franck Azobou Tonleu
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Abstract
Discussion Forum (0)
Introduction: 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.
Case Presentation: 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.
Conclusion: 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.
Table 1: Hemodynamic and Echocardiographic Findings
AVF Not OccludedAVF Occluded
Cardiac Output
7.7 L/min5.1 L/min
Cardiac Index4.1 L/min/m22.7 L/min/m2
Central Venous Pressure
18 mmHg18 mmHg
Systemic Vascular Resistance1058 dynes/s/cm-51280 dynes/s/cm-5
BEFORE PLICATIONAFTER PLICATION
Left Ventricular Ejection Fraction25-30%55-60%
Left Ventricular Posterior Wall Dimension1.4 cm1.3 cm
Left Ventricular Internal Diameter (end diastole) 6.1 cm6.1 cm
Tricuspid  Annular Plane Systolic Excursion
2.4 cm2.3 cm
Right Atrial Volume
126 mL142 mL
Left Atrial Volume
112 mL121 mL
Aortic Valve Maximum Velocity1.6 m/s2.0 m/s
Right Ventricular Systolic Pressure44 mmHg63 mmHg
Right Atrial Pressure15 mmHg15 mmHg

Introduction: 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.
Case Presentation: 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.
Conclusion: 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.
Table 1: Hemodynamic and Echocardiographic Findings
AVF Not OccludedAVF Occluded
Cardiac Output
7.7 L/min5.1 L/min
Cardiac Index4.1 L/min/m22.7 L/min/m2
Central Venous Pressure
18 mmHg18 mmHg
Systemic Vascular Resistance1058 dynes/s/cm-51280 dynes/s/cm-5
BEFORE PLICATIONAFTER PLICATION
Left Ventricular Ejection Fraction25-30%55-60%
Left Ventricular Posterior Wall Dimension1.4 cm1.3 cm
Left Ventricular Internal Diameter (end diastole) 6.1 cm6.1 cm
Tricuspid  Annular Plane Systolic Excursion
2.4 cm2.3 cm
Right Atrial Volume
126 mL142 mL
Left Atrial Volume
112 mL121 mL
Aortic Valve Maximum Velocity1.6 m/s2.0 m/s
Right Ventricular Systolic Pressure44 mmHg63 mmHg
Right Atrial Pressure15 mmHg15 mmHg

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