Hemodynamic changes in the cephalic vein of patients with hemodialysis arteriovenous fistula

Albayrak, Ramazan; Yüksel, Şeref; Çölbay, Mehmet; Değirmenci, Bumin; Acartürk, Gürsel; Haktanır, Alpay; Karaman, Ozcan

doi:10.1002/jcu.20307

Cited by 29 publications

(28 citation statements)

References 17 publications

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“…Blood flow in the cephalic vein is normally approximately 28 ± 14 ml/min [35]. Successful radial-cephalic AVF have flow rates averaging between 600–1000 ml/min with higher peak flows in the larger diameter brachial-cephalic AVF.…”

Section: Mechanisms Contributing To Avf Maturation and Failurementioning

confidence: 99%

Future research directions to improve fistula maturation and reduce access failure

Patel

Hänisch

et al. 2016

Seminars in Vascular Surgery

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With the increasing prevalence of end stage renal disease there is a growing need for hemodialysis. Arteriovenous fistulae (AVF) are the preferred type of vascular access for hemodialysis but maturation and failure continue to present significant barriers to successful fistula use. AVF maturation integrates outward remodeling with vessel wall thickening in response to drastic hemodynamic changes, in the setting of uremia, systemic inflammation, oxidative stress and preexistent vascular pathology. AVF can fail due to both failure to mature adequately to support hemodialysis, as well as development of neointimal hyperplasia (NIH) that narrows the AVF lumen, typically near the fistula anastomosis. Failure due to NIH involves vascular cell activation and migration and extracellular matrix remodeling with complex interactions of growth factors, adhesion molecules, inflammatory mediators, and chemokines, all of which result in maladaptive remodeling. Different strategies have been proposed to prevent and treat AVF failure, based on current understanding of the modes and pathology of access failure; these approaches range from appropriate patient selection and use of alternative surgical strategies for fistula creation, to the use of novel interventional techniques or drugs to treat failing fistulae. Effective treatments to prevent or treat AVF failure requires a multidisciplinary approach involving nephrologists, vascular surgeons and interventional radiologists, allowing careful patient selection and the use of tailored systemic or localized interventions to improve patient-specific outcomes. This review provides contemporary information on the underlying mechanisms of AVF maturation and failure and discusses the broad spectrum of options that can be tailored for specific therapy.

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Section: Mechanisms Contributing To Avf Maturation and Failurementioning

confidence: 99%

Future research directions to improve fistula maturation and reduce access failure

Patel

Hänisch

et al. 2016

Seminars in Vascular Surgery

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show abstract

“…34 Studies evaluating successful radial-cephalic AVF reveal normal flow rates averaging between 600–1000 ml/min, with many individual AVF exposed to even higher peak flows, and this magnitude of flow increases substantially in the larger diameter brachial-cephalic AVF (Table 2). Dixon et al reported that 90% of forearm AVF have flow between 500–2000 ml/min, whereas 90% of upper arm AVF have flow between 500–3000 ml/min.…”

Section: Flow and Pressurementioning

confidence: 99%

Vein graft adaptation and fistula maturation in the arterial environment

Chen

Wong

et al. 2014

Journal of Surgical Research

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Veins are exposed to the arterial environment during two common surgical procedures, creation of vein grafts and arteriovenous fistulae (AVF). In both cases veins adapt to the arterial environment that is characterized by different hemodynamic conditions and increased oxygen tension compared to the venous environment. Successful venous adaptation to the arterial environment is critical for long term success of the vein graft or AVF, and in both cases is generally characterized by venous dilation and wall thickening. However, AVF are exposed to a high flow, high shear stress, low pressure arterial environment, and adapt mainly via outward dilation with less intimal thickening. Vein grafts are exposed to a moderate flow, moderate shear stress, high pressure arterial environment, and adapt mainly via increased wall thickening with less outward dilation. We review the data that describe these differences, as well as the underlying molecular mechanisms that mediate these processes. Despite extensive research, there are few differences in the molecular pathways that regulate cell proliferation and migration or matrix synthesis, secretion, or degradation currently identified between vein graft adaptation and AVF maturation that account for the different types of venous adaptation to arterial environments.

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“…Cephalic vein flow rate is normally 28 ml/min for a vein diameter of 2.3 mm [14]. In order to keep the Reynolds number (Re) in our enlarged model of 5 mm diameter similar to its physiological value, the flow rate was adjusted to 60 ml/min (Re = 73).…”

Section: Boundary Conditionsmentioning

confidence: 99%

“…The 3D geometry and the meshing were designed using GAMBIT (Fluent Inc.). While the cephalic vein diameter usually ranges from 1.9 -3.9 mm, reaching from 1mm to over 6 mm in actual measurements [14,18,19], we chose a 5 mm inner diameter and 85 mm long straight tube section to make it compatible with the in vitro model in our laboratory. A 16 gauge (1.3 mm inner diameter, 1.7 mm outer diameter) catheter was placed inside the vein with an entrance orientation of 30˚ relative to the vein symmetry axis.…”

Section: Geometry and Computational Meshingmentioning

confidence: 99%

Biomechanical aspects of catheter-related thrombophlebitis

Rotman

Shav²,

Raz³

et al. 2013

JBiSE

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Short peripheral catheters (SPCs) are the most common intravenous devices used in medical practice. Short peripheral catheter thrombophlebitis (SPCT) is the most frequent complication associated with SPCs, causing discomfort and usually leading to removal of the catheter and insertion of a new one at a different site. The aim of this research was to explore whether biomechanical factors, in addition to biochemical factors, also play a role in the formation of thrombophlebitis. Hence, two of the biomechanical aspects of SPCT were investigated: the physical pressure load exerted by the SPC on the endothelial monolayer, and disturbances in the flow patterns due to the SPC. Endothelial activation was studied by subjecting human umbilical vein endothelial cells (HUVEC) to a weight load of SPC pieces and measuring the release profile of von-Willebrand Factor (vWF) over time, using ELISA. vWF release was chosen as the measure for endothelial activation since it was the major component of the Weibel-Palade Bodies (WPBs), which underwent exocytosis by endothelial cells during activation. Flow patterns were analyzed on a 3D computational fluid dynamics (CFD) model of a brachiocephalic vein with SPC. vWF release profiles were significantly higher in the HUVECs subjected to the load, indicating HUVEC activation. CFD simulations demonstrated a decrease in flow velocities along the catheter body, between the catheter and the vein, due to an enlarged boundary layer. Results indicate that the contact region between the SPC body and the vein wall can be partially responsible for SPCT development, and inflammatory and coagulatory processes initiated by stimulated endothelial cells may be amplified due to disturbed blood flow.

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Hemodynamic changes in the cephalic vein of patients with hemodialysis arteriovenous fistula

Abstract: The increase in cross-sectional area and flow volume of the cephalic vein is larger in patients with brachiocephalic fistulas than in those with radiocephalic fistulas; however, flow velocities and waveform parameters are not different.

Cited by 29 publications

References 17 publications

Future research directions to improve fistula maturation and reduce access failure

Future research directions to improve fistula maturation and reduce access failure

Vein graft adaptation and fistula maturation in the arterial environment

Biomechanical aspects of catheter-related thrombophlebitis

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