Case Presentation: We report here a case of high output heart failure (HOHF), a rare but potential complication of Arteriovenous fistula (AVF) in a post-renal transplant patient.A 60-year-old male with end-stage renal disease and subsequent renal transplant 3 months ago presented with exertional dyspnea, worsening anasarca, and weight gain of 20 pounds. The patient also reported new-onset pain at the site of his right upper extremity (RUE) AVF. Physical exam revealed a positive thrill noted over the RUE AVF and pitting edema in both lower extremities. Significant laboratory findings were potassium of 5.0 mmol/L, an elevated creatinine of 1.65 mg/dL, and BNP of 70 pg/mL. Chest x-ray showed bilateral perihilar interstitial prominence. Transthoracic echocardiography (TTE) showed normal left ventricular (LV) size with mild wall hypertrophy and LV ejection fraction of 55-60%. Right ventricular systolic pressure was elevated at 43 mm Hg. A vascular ultrasound of the right upper extremity revealed an elevated anastomotic velocity of 735 cm/second with turbulent flow, suggestive of a high-output fistula, without evidence of thrombosis. Ventilation-perfusion (V/Q) imaging was equivocal for chronic thromboembolic pulmonary hypertension (CTEPH). Right heart catheterization delineated the cause of pulmonary hypertension as Group 2, secondary to high-output heart failure attributed to the arteriovenous fistula. The shunt study showed systemic saturations in the superior vena cava consistent with mixing from the fistula.Treatment with diuretics transiently helped alleviate his dyspnea but worsened his renal function. The patient underwent a successful excision of the RUE AVF aneurysm with ligation of the fistula. Postoperatively, the patient’s edema and dyspnea began to improve. Marked improvement in clinical and renal function was noted in the next few weeks. Repeat TTE revealed a significant reduction in right ventricular systolic pressure to 23 mm Hg.
Discussion: While AVFs are crucial for hemodialysis (HD), they can also precipitate cardiovascular complications. High access flow is linked with HOHF, and significant correlations exist between access flow and cardiac output, underscoring the need for careful management (1, 2). This is demonstrated by RHC with elevated cardiac output, with low to normal systemic vascular resistance in such cases (3). HOHF is therefore a rare complication of AVFs in renal transplant patients (4). Many authors believe that this rare etiology is often overlooked in patients with renal disease and new onset- heart failure since these patients have other risk factors to explain their cardiac deterioration (5). In addition, the presence of AVF is considered an independent risk factor for PH. Despite this knowledge, the incidence of banding of AVF due to new onset heart failure is only 2.8% (6). A definitive diagnosis was established through RHC, which delineated the AVF’s hemodynamic impact. Improvement in clinical symptoms and renal function following the ligation of the AVF explained the significant hemodynamic strain exerted by the AVF, affirming the diagnostic and therapeutic importance (7).
Conclusions: This case highlights the importance of considering AVF as a rare but important etiology of new-onset high-output heart failure in patients with renal disease. It also emphasizes the need for vigilance in post-transplant care, ensuring that AVFs do not evolve from vascular access points to contributors of cardiac dysfunction.