A HIGH–PRESSURE MYSTERY: UNVEILING THE BODY‘S HIDDEN SHORTCUT

Abstract An arteriovenous fistula (AVF) is an abnormal connection between an artery and a vein, bypassing the capillary network. Acquired AVFs are most commonly caused by trauma or surgery and are typically located in peripheral sites. At the cardiac level, AVFs may induce a high–output state, potentially leading to heart failure. Management of complications involves optimizing medical therapy and considering surgical intervention. With timely treatment, the prognosis is generally favorable. However, untreated AVFs can result in severe outcomes, including heart failure, pulmonary hypertension, and death. Case Report: A 58–year–old male, with a history of trauma from a war device explosion, underwent right femoral vascular repair. In 2011, he developed native aortic valve endocarditis, necessitating replacement with a 25 mm St. Jude bileaflet mechanical prosthesis and tricuspid valve repair via the De Vega technique. Post–discharge echocardiography revealed left ventricular dilation, mildly reduced ejection fraction (45%), and transprosthetic gradients of 55 mmHg (maximum) and 33 mmHg (mean). No follow–up cardiac evaluations were recorded. In 2024, the patient underwent evaluation for a sub–renal abdominal aortic aneurysm. Preoperative cardiac assessments revealed high transprosthetic gradients, severe tricuspid regurgitation, and echocardiographic findings of pulmonary hypertension. He was referred to a High–Specialty Center for further investigation. Transthoracic echocardiography at our facility demonstrated findings consistent with a high–output state: elevated transprosthetic velocities (Vmax 3.9 m/s, mean gradient 41 mmHg), increased LVOT and transprosthetic velocity–time integrals (31.2 cm and 82 cm, respectively), and biventricular and biatrial dilation (Figure 1) with preserved systolic function. Transesophageal echocardiography confirmed proper mobility of prosthetic discs with no adherent formations (Figure 2). Right heart catheterization showed post–capillary pulmonary hypertension and increased pulmonary artery saturation. Oximetry revealed a significant step–up in saturation, with a Qp/Qs ratio of 1.4, suggesting an extracardiac shunt. CT angiography identified a right femoral AVF (Figure 3) as the likely cause of the high–output state, pulmonary hypertension, and chamber dilation. Secondary causes, including sepsis, hyperthyroidism, and anemia, were excluded. The patient was referred for corrective surgery.Figure 1 Figure 2 Figure 3