L. Laquian1, Y. He1, S. Berceli1,2 1University Of Florida,Division Of Vascular And Endovascular Surgery,Gainesville, FL, USA 2Malcom Randall Veterans Affairs Medical Center,Gainesville, FL, USA
Introduction: Chronic inflammation and hemodynamic changes are major components of the altered physiology in hemodialysis (HD) patients. Parallel studies in our laboratory have identified significant changes in leukocyte biology and their genomic profile in association with arteriovenous fistula (AVF) creation. The purpose of this study is to characterize the changes in blood flow and wall shear stress (WSS) associated with AVFs. We hypothesize that increased WSS and turbulence associated with AVFs act as a driving force for the altered biology in HD patients.
Methods: Utilizing vessel dimension and blood flow data compiled from the literature, normal systemic circulation was modeled and then adapted for left brachiocephalic AVF creation using postoperative values. For each vascular segment, transit time, peak WSS, and peak Reynolds number (as an indicator of turbulent flow) were calculated. Fraction of circulation time spent at high WSS (>40 dyn/cm2) and turbulent flow (Reynolds number >4000) was computed in normal and AVF models.
Results: Increased flow after AVF creation results in elevated peak WSS and Reynolds number in the subclavian and brachial arteries. Peak WSS in the left subclavian artery increases by more than seven fold from 32 dyn/cm2 preoperatively to 232 dyn/cm2 after AVF creation. Left brachial artery peak WSS increases from 46.0 dyn/cm2 to 209.5 dyn/cm2 after AVF placement. Overall, high peak WSS in normal upper extremity circulation occurs for 9.5% of circulation time but does not exceed 50 dyn/cm2 (Fig 1A). After AVF creation, 13.5% of circulation time is spent at high WSS, with 7.4% of circulation time spent at over 200 dyn/cm2. With an AVF, subclavian artery flow turns turbulent as Reynolds number increases from 1309 in normal circulation to 9366. Peak Reynolds number in the brachial artery increases from 660 to 3008 after AVF, reflecting more disordered and chaotic flow. In normal circulation, 2.5% circulation time is spent at turbulent flow, while an AVF increases circulation time at turbulent flow to 13.9% (Fig 1B).
Conclusion: AVF creation leads to elevated WSS and more turbulent flow compared to normal circulation. Furthermore, the time spent at high WSS and turbulent flow increases after AVF placement. Ongoing studies have been initiated to investigate the influence of this increased exposure time to higher WSS and turbulent flow on circulating immune cell phenotype and their role in the chronic inflammatory state that characterizes the typical HD patient.
