Why do arteriovenous (AV) fistulas cause heart failure?

From the Guidelines

Arteriovenous fistulas cause heart failure because they create an abnormal connection between arteries and veins, leading to increased cardiac workload and eventual heart chamber dilation and remodeling, as supported by the most recent study 1.

Key Points

• Arteriovenous fistulas bypass the capillary network, creating a low-resistance pathway for blood to return to the heart more quickly and in larger volumes than normal.
• This increased venous return forces the heart to pump more blood with each beat and at a faster rate, leading to persistent volume overload and cardiac strain.
• The heart muscle initially compensates by thickening, but eventually fails, leading to decreased contractility, reduced ejection fraction, and high-output heart failure.
• Large fistulas or multiple fistulas pose the greatest risk, as the amount of blood shunted correlates with the severity of cardiac strain.
• Treatment typically involves closing the fistula through surgical or endovascular techniques to eliminate the abnormal blood flow and reduce cardiac workload, with the goal of improving morbidity, mortality, and quality of life outcomes.

Evidence-Based Recommendation

Based on the most recent study 1, closing the arteriovenous fistula through surgical or endovascular techniques is the recommended treatment to eliminate the abnormal blood flow and reduce cardiac workload, thereby improving outcomes in patients with heart failure due to arteriovenous fistulas. This approach prioritizes reducing morbidity, mortality, and improving quality of life, and is supported by the latest evidence in the field.

From the Research

Mechanisms of Heart Failure in Arteriovenous Fistulas

• Arteriovenous fistulas (AVFs) can cause heart failure due to increased cardiac output, leading to congestive heart failure 2.
• The development of heart failure is associated with increased activity of vasoconstrictor neurohormonal systems, such as the renin-angiotensin system (RAS), sympathetic nervous system (SNS), endothelin system, and arginine vasopressin (AVP) 2.
• Compensatory activation of systemic and vasodilating systems, including atrial natriuretic peptide (ANP) and nitric oxide (NO), occurs in response to the increased cardiac output 2.

Hemodynamic Effects of Arteriovenous Fistulas

• High-output cardiac failure can occur as a rare complication of high-output arteriovenous fistulas 3.
• The hemodynamic effects of a fistula include increased preload, leading to increased cardiac output, which can result in cardiac hypertrophy and eventual heart failure 4.
• Routine access flow monitoring can demonstrate blood flows (Qa) >2000 mL/min in patients with high-output heart failure 4.

Diagnostic Criteria for High-Flow Arteriovenous Fistulas

• There are currently no universally accepted criteria defining a high-flow fistula, but a Qa value ≥2000 mL/min is often used as a definition 5.
• Indexation of AVF blood flow for height2.7 may provide a more accurate definition of high-flow fistula, with a Qa ≥603 mL/min/m2.7 detecting the occurrence of high-output cardiac failure with good accuracy 5.
• Echocardiographic evaluation can reveal alterations in left ventricular mass, diastolic volume, and atrial volume, as well as diastolic dysfunction, in patients with high-flow AVFs 6, 5.

Treatment and Management

• Treatment of high-output heart failure secondary to arteriovenous fistula should be directed at correcting the underlying problem by surgical banding or ligation of the fistula 4.
• The use of angiotensin converting enzyme (ACE) inhibitors and/or angiotensin II (ATII) blockers may be beneficial in the management of patients with large AVFs 2.