From the Guidelines
Arteriovenous fistulas cause heart failure primarily through hemodynamic overload, leading to high-output cardiac failure as a result of increased venous return and volume overload of the heart. This is evident in patients with liver arteriovenous fistulas, where transarterial embolization has been used to treat high-output cardiac failure, although with significant complications and caution advised 1. The formation of an abnormal connection between an artery and vein creates a low-resistance pathway, allowing blood to bypass the capillary network and flow directly from the high-pressure arterial system to the low-pressure venous system.
- Key factors contributing to the development of heart failure in this context include:
- Increased venous return to the heart
- Volume overload of the right heart chambers
- Cardiac chamber dilation and heart muscle hypertrophy
- Increased workload on the heart, leading to decreased cardiac efficiency
- The severity of heart failure caused by arteriovenous fistulas depends on the size and location of the fistula, with larger and more proximal fistulas having more significant hemodynamic effects, as seen in cases where orthotopic liver transplantation has been proposed as a definitive curative option for hepatic vascular malformations in hereditary hemorrhagic telangiectasia 1.
- Treatment of arteriovenous fistulas to prevent or manage heart failure typically involves closing the fistula through surgical or endovascular techniques, such as transarterial embolization, to eliminate the abnormal blood flow and allow the heart to recover, although the choice of treatment should be made with caution due to potential complications 1.
From the Research
Mechanisms of Heart Failure in Arteriovenous Fistulas
- Arteriovenous fistulas (AVFs) can lead to heart failure due to increased cardiac output, which may result in the development of congestive heart failure 2.
- The increased cardiac output is associated with enhanced activities 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.
Clinical Presentation and Diagnosis
- Patients with high-output heart failure secondary to AVF may present with symptoms such as tachycardia, elevated pulse pressure, hyperkinetic precordium, and jugular venous distension 3.
- Echocardiogram may reveal either a low or high left ventricular ejection fraction, and right-heart catheterization demonstrates an elevated cardiac output with a low to normal systemic vascular resistance 3.
- Routine access flow monitoring should demonstrate blood flows (Qa) >2000 mL/min in patients with high-output heart failure secondary to AVF 3.
Treatment and Management
- Treatment of high-output heart failure secondary to AVF should be directed at correcting the underlying problem by surgical banding or ligation of the fistula 3.
- The use of angiotensin-converting enzyme (ACE) inhibitors and/or angiotensin II (ATII) blockers may be beneficial in the management of patients with large AVF 2.
- ACE inhibitors have been shown to reduce morbidity and mortality in patients with heart failure, and their use is recommended in the routine management of patients with heart failure 4.
Cardiovascular Risk
- AVFs can add to the already high burden of cardiovascular risk in patients with advanced kidney disease, including by promoting water and salt retention, and by inducing or worsening left ventricular hypertrophy 5.
- There is increasing evidence that a fistula can increase cardiac risk, particularly in patients with high-flow fistulas 6, 5.
- Systematic transthoracic echocardiography evaluation with measurement of global longitudinal strain (GLS) should be proposed for all patients with Qa >2250 mL/min or Qa/CO >33% to detect those at higher risk of cardiac impact of the AVF 6.