Haemodynamics of angioaccess venous anastomoses

Haemodynamics of angioaccess venous anastomoses

Haemodynamics anastomoses M.C.S. Shu* and N.H.C. of angioaccess venous Hwang** “Medtronic Inc., Minneapolis, MN 55432 and ‘Department Memphis Sta...

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Haemodynamics anastomoses M.C.S.

Shu* and N.H.C.

of angioaccess

venous

Hwang**

“Medtronic Inc., Minneapolis, MN 55432 and ‘Department Memphis State University, Memphis, TN 38152, USA Received

March

1990, accepted

October

of Biomedical

Engineering,

1!~90

ABSTRACT A largepercentage of arteriovenous haemodialysis angioaccess loop gra@s (2 VLG) fail within the first year afier surgeery, the occlusive lesions being found predominantly at the venous anastomosis site. This paper presents a detailed flow dynamic study of the AL&G system using three elastic, transparent bench-topJlow models, which were based on the geometry of silicone rubber casts obtained at &#erent timesborn a chronic animal model. Each model thus represented a diJSerent stage of the lesion development. Flow visualimtion and laser Doppler anemometer surveys of the flow field confirmed that the hydrodynamic factors favour lesion development near the stagnation point opposite the anastomotic toe, where the momentum of the impinging jet stream, combined with the oscillating wall shear stress generated in the vicinity of the stagnation point, acts in both directions. The accumulation of tracer particles in the region offlow separation is believed to be a combined contribution from the hydraulic forces and the inward motion of the vessel wall. As these hydrodynamic factors are enhanced upon firther development of the occlusive lesion, a vicious cycle may be firmed. Keywords: Doppler

Haemodialysis angioaccess mapping, wall shear stress

graft,

arteriovenous

INTRODUCTION Vascular stenosis (VS) is responsible for the late failure of various types of arterial substitutes’-” and anastomoses. In usually occurs at the graft-host synthetic substitutes, it is frequently observed at distal anastomoses’. Factors related to the development of VS include haemodynamic stresses in the anastomotic region’, mismatch of mechanical properties”, distensibility between the host vessel and the graft7, and low velocity or high frequency flows. Graft diameter and turbulent flow at the anastomotic region also attributes to uneven distributions of pressure and shear on the endothelia and subendothelial stresses myocytes, which may also incite stenosis!‘. To understand better the anastomotic flow field, we adapted an end-to-side arteriovenous haemodialysis angioaccess loop graft (AVLG) as the haemorrheologic model; AVLG is a surgically implanted conduit that facilitates haemodialysis in patients with chronic renal failure. The surgically implanted AVLG is anastomosed by one end to a host artery and by the other end to a vein to create a fistula conduit which brings high pressure arterial blood flow into an otherwise slow flowing vein. Abnormal haemodynamic characteristics are created and perhaps exaggerated by the haemodynamic changes introduced during haemodialysis procedures. Thus, the construction of the AVLG system leads to changes in Correspondence

and reprint requests to: Prof. Ned H. C. Hwang

0 I!)!)1 Butterworth-Heinemann Ol_(l-~51!25/!)1/021O~i-IO

conduit.

occlusive

lesions,

flow

visualization,

laser

both pressure and flow in the host vein to which the graft is anastomosed. Since thickening of the intima is one of the typical reactions associated with the elevated intravascular pressure found in larger arteries’“. ‘I, it is conceivable that a similar reaction may occur at the venous anastomosis of the AVLG system. Early studies revealed marked thrombus formation and intimal hyperplasia in the venous anastomotic region”. To assess the haemorrheologic contribution to thrombosis and VS development, the AVLG system provides an ideal model with a well-defined flow field in which the distributions of flow, wall shear stress and structure of turbulence could be investigated in details. Based on the data of an earlier animal study, we designed an in vitro bench-top flow model to study the detailed flow dynamics of the AVLG system. Most of the in vitro vascular dynamic models reported in the literature used rigid, conduits, either using one-to-one or enlarged scales 1J--‘x. However, it is speculated that the wall motions may significantly alter the flow field inside blood vesselsl+2I, and thus may invalidate many conclusions that were derived from the rigid flow model studies. Recently, several studies using elastic transparent flow models have been reported 22-26. We have developed an elastic transparent flow model to mimic the venous anastomosis of AVLG; its construction was based on room temperature vulcanizing (RTV) silicone rubber casts obtained from AVLG implanted in dogsz7. Of particular interest were the haemodynamic characteristics of three AVLG flow models with different area

for RES J, Biomed.

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Haemodynamics of venous ana.stomosis: M.C.S. Shu and N.H.C. Hwang

Figure 2 Three selected RTV silicone rubber casts representing different degrees of area reduction (AR) that occurred in the vicinity of venous anastomoses. Left: cast with slight AR (model B, 90%); Middle: cast with moderate AR (model C, 58%); Right: cast with significant AR (model D, 48%). PA = Proximal artery; PV = proximal vein; G = graft Figure 1 View of a femoral-femoral dog’s hind leg

looped

graft implanted

in the

reductions (AR), namely light (l), moderate (m) and significant (s), in the venous anastomotic regions. The consequences of pulsatility and wall motions upon flow features in the three flow models were compared under identical input flow conditions. MATERIALS

AND METHODS

Expanded polytetrafluoroethylene (el’TFE) loop grafts were implanted bilaterally between the femoral artery and the femoral vein in mongrel dogs (of average weight 30 kg) to mimic the AVLG system created between the brachial artery and the cephalic vein in patients. The standard AVLG configuration used in this study was a 6 mm diameter, 25 cm long aft with both ends bevelled to 4.5” (anastomotic loop angle $ (Figure 7). The dogs were reoperated upon at different times for haemodynamic and pathophysiological studies. These detailed surgical procedures and in vivo studies have been reported elsewhere”‘“7. To acquire the luminal geometry of the AVLG system in situ, RTV silicone rubber was injected under physiological pressure to fill the AVLG system up to a distance of approximately 5 cm from both ends of the anastomoses. The cast was obtained after a 24h curing period in situ. Three RTV casts with different stages of stenoses were chosen for the present study. The time course of the implantation was not considered for the three casts chosen, since the implantation period and the stenotic growth in the AVLG system were not necessarily correlated in the animal experiment series. The area ratio defined as &/AD was employed to quantify AR, where Ad was the narrowest cross-sectional area and An was the estimated cross-sectional area of its host vein based on the outside diameter measured during implantation. Figure 2 shows the three selected casts: cast B (light AR), cast C (moderate AR) and cast D (significant AR). The ratios of &/Ao were 90, 58 and 48% for casts B, C and D, respectively. The geometrical configurations of all the animal casts indicated uniformly that AR always occurred

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circumferentially near the venous anastomotic toe, and grew primarily toward the downstream direction in the host vein. The three selected RTV casts were used to fabricate elastic transparent Silastic flow models. On average, five Silastic models were made from each RTV cast. Due to the modelling tolerance, one was selected as the flow model, based on the dynamic compliance (defined below). The matched compliance should duplicate the in vivo flow pattern inside the in vitro flow model. The flow model fabrication techniques have been presented elsewhere”“, ‘s. The diameter changes in the flow models were measured by an ultrasonic dimension gauge. A simple dynamic compliance”” was then calculated: Ds-Dd Cdyn

=

Dd(Ps -

=pd)

AD &AZ’

where D is the vessel diameter and P is the intravascular pressure. (The subscripts s and d represent, respectively, the systolic and the diastolic values.) The values calculated from measured data for the model artery and the model vein were O.O56/AP, and O.O23/AP,, respectively. The in vitro AVLG system was constructed by connecting the arterial anastomosis model and the venous anastomosis model with a 6mm PTFE GorTex loop graft (Gore Inc, Flagstaff, AZ, USA). The experimental flow loop used in this study is shown schematically in Figure 3. The loop system consisted of a constant head storage tank which provided inlet fluid to the model; a pulsatile wave duplicator; and a preload system which consisted of an adjustable linear resistor and an adjustable compliance unit to tune the arterial inlet flow waveforms. The box containing the flow model was installed immediately downstream of the compliance unit. An afterload system was provided at the distal artery and the distal vein to tune the arterial and venous flow waveforms. A pulse duplicator provided the arterial pulse pressure waveforms to the proximal (heart side) artery. The pressure waveforms proximal and distal

Haemo+amics _

Honeycomb

-_

Adjustable flow

laminated

resistor

Adjustable JF

-

compliance

AF_

unit

Electromagnetic meter Pressure

9.L

flow

probe transducer

‘\ ser A

___--!

L_

Figure

3

_.

Schematic

~~__

_~~_

of the

__

in vitro flow-loop

system

to the anastomoses in the model artery and vein were monitored simultaneously by four physiological pressure transducers (Model P23 ID, Gould Inc., Medical Product Division, Oxnard, CA 93030). The flow waveforms at the same positions were also monitored by electromagnetic flowmeter (EMF) probes (Ze eda SWD-4, 1937 2fith Ave East, Seattle, WA 98112 P. The preload and afterload to the AVLG system were tuned until waveforms comparable with those of the in uivo measurements were obtained. The testing fluid first passed a honeycomb flow laminator before it reached the proximal artery to ensure stable inlet flow to the AVLG system. The blood analogue fluid used was a solution of 32.7% glycerol in distilled water with a small amount of CaC12 added to match the refractive indices of the Silastic vessel and the container box”‘,“‘. The analogue fluid has a dynamic viscosity of 3.62 x lo-’ dyne s cm-> and density of 1.1 gem-~’ at room temperature. The average Reynolds number and Womersley number for the graft flow were 900 and 4.7, respectively. Figure 4 shows a set of typical pressure and flow waveforms which were obtained from a AVLG flow

FPA

FPA

FDV

Figure 4 Typical pressure and flow waveforms at proximal artery (PA), proximal vein (PV), and distal vein (DV) at a heart rate of 70 bpm. The interactive phase relationship of PA uerxzu PV and PA uer5u.s DV is indicated by arranging them vertically. Points a, b, c and d indicate the flow phase angles at 45”, W”, l35”, and 225”, respectively

of venous anastomosis: M.C.S Shu and N.H.C. Hujaq

model system at the proximal (heart side) artery, the proximal (heart side) vein and the distal (foot side) vein, respectively. The input pressure waveform at the proximal artery usually consisted of high frequency components at the end of the systolic phase. These high frequency components were damped out after they travelled through an A--V fistula graft. Thus, smooth pressure waveforms at the proximal vein and distal vein were obtained, as shown in Figure 4. Before carrying out the detailed flow field survey, flow visualization was made to obtain general information about the flow field. Pulsatile hydrogen bubbles were generated at the upstream end of the proximal artery using a 6V DC square wave. The hydrogen bubbles were synchronized with the pulse frequency of the AVLG system. Four platinum wires (O.OXmm) were stretched across the diameter of the model inlet as the cathode. The cathode wires were arranged in parallel with 0.5 mm spacings between. A 15 mW He-Ne laser with a wavelength = 632.8nm (visible red) was used as the light source. The laser beam was enlarged by a microscope lens (X 20). A 50pm pin-hole located at the front side of the lens was used to filter the laser light. The filtered laser beam was then projected on a cylindrical lens. A light plane generated by the cylindrical lens was used to illuminate the flow field. The distance between the cylindrical lens and the flow field can be adjusted to provide greater detail in the flow patterns of the illuminated plane. Flow visualization was made usin a high-speed movie camera (Locam model 003 10003 ‘i with 16mm colour movie film (Kodak 72.50, ASA 400). To facilitate laser Doppler anemometer (LDA) measurements, the flow model was mounted on a motorized two-dimensional transverse table which had an accuracy of 16pm per dial division in both X and Y directions. The movement of the transverse table was controlled by a Cremenco Z80D microcomputer. The movement in the Z direction was manually adjusted by micrometers. The LDA used in the experiment was a TST (Thermal Systems, Inc., St. Paul, MN 5.5164) Model 1090 tracker system with Bragg cells. Using an achromat focusing lens of 120 mm focal length, the elliptical measuring volume has major and minor axes of 0.4mm and 0.75 mm, respectively. The elliptical measuring volume consists of 64 fringes, spaced 1.38pm apart. Velocity surveys were made at seven different sections in the venous and arterial host vessels in the flow models. The sections were spaced 7mm (approximately one diameter) apart. The survey was taken across the diameter at each section, as shown in Figure 5. At each cross-section surveyed, the starting position at the wall was manually adjusted to the upper side of the arterial wall and at the lower side of the venous wall. The ‘at the wall’ locations were determined without flow in the loop. Near the wall, the first three sampling points along the diameter were spaced lOOpurn from each other, and the fourth sampling point was 400pm from the third. For all the remaining points along the same diameter until near the opposite wall 800pm spacings were maintained. At this time, the same measuring procedure was

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Haemodynamics of venous anastomosis: M.C.S. Shu and N.H.C. Hwang

Toe

‘\

_

Since the voltages of the velocit signals were increased by a frequency shifter to B istinguish positive from negative flow, the velocity data needed to be corrected before proceeding with data analysis. These velocity signals resulting from the function of a frequency shifter were corrected by a constant value recorded during the data acquisition period. The constant value varied with the location of the data acquisition. The true velocity signals obtained at each point could be expressed as:

i

j = 1,2, . . ., k

T

where j indicates the surveyed point at each crosssection, k is the number of measured points at each section, C, is the constant frequency shift value of the jth point surveyed, T is the period of a cycle and N is the number of ensembling cycles. The pressure waveform at the proximal artery was used as a time trigger to identify the beginning of a cycle. The digitized velocity signals were ‘ensemble averaged’ for 30 cycles of continuous pulses at each measuring point. The wall shear stress distribution was calculated from the slope of the measured velocity profiles ‘at the wall’. Since the wall motion at each crosssection surveyed was recorded simultaneously with the velocity profiles, the distance dri(t) between the vessel wall and the nearest point to the wall is a function of time. Thus we have:

lT&&&;eel . . :. . :, ;

b.c/

6

5

7,

,

4

3

2

,-B

10

Figure 5 Cross-sections where LDA velocity distribution surveys were made in the flow models: a, model B; b, model C; c, model D. The distance between two neighbouring sections was approximately one diameter of the proximal vein. B = Lower side, T = upper side

where i=O, 1, . . ., 6, and ,u is the viscosity testing fluid.

of the

RESULTS repeated from the opposite wall. Certain overlap of the positions surveyed was necessary to check the consistency of the measurements. To assess the value of wall shear rate, the distensible host vessel was instrumented with ultrasonic dimension gauges to measure changes in the segment diamete?“. Two crystals were glued to the external surface on the opposite sides of the flow model and aligned along the diameter. The velocity signals, pressure signals and the ultrasonic dimension gauge signals were simultaneously recorded on a magnetic analogue tape using a FM record (Hewlett-Packard Model 3968A, band-width O-10 kHz) at a tape speed of 19.05mms-‘. The signals were recorded for a minimum of 2 min at each sampling point and later played back for digitization using a PDP 1 l/23 digital computer (16 bits per word) at a sampling rate of 2500 oints s-‘. According to the Nyquist criterion for signa P processing, this would guarantee a frequency response of 1000 Hz in the flow measurement. The digitized data were processed on a Micro Vax 3.4 computer. Wall movement as a function of time was calculated from the variation of the recorded ultrasonic signal.

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The AVLG system provided a well-defined flow field by shunting high momentum arterial blood into an otherwise slow-flowing vein through a looped graft conduit of constant diameter. Flow in the venous anastomotic region remained pulsatile in all three models studied. Flow visualization was performed in the median plane including the graft branch. Velocity distributions were obtained at different cross-sections as shown in Figure 5. The wall shear stresses were calculated from the velocity profiles at each crosssection surveyed. Results of the measurement are presented at eight different phase angles in a cardiac cycle. This study focused mainly on the flow characteristics in the venous anastomotic region. Flow visualization Flow visualizations were made to obtain the.general flow patterns at the venous anastomosis in all three flow models. The use of laser sheet light and hydrogen bubbles as tracers in the transparent elastic flow model allowed clear vision of the flow field and the effect of the vessel wall motion on the local flow patterns.

Figure 6 Typical flow patterns at the venous anastomosis of model B showed a strong r = reattachment point, s = stagnation point

anastomosesof: a, model B; b, model C; and d, model D. The cross-sectional axial

vortex.

C = Circulation

Figure 611-c shows the typical flow patterns inside the venous anastomoses of models B, C and D, respectively. Figure 6d presents a cross-sectional view of the flow activity near the anastomosis of model B including both the graft and the host vein. All the pictures were taken at the same systolic phase. The analysis of high speed movie film indicated that the jet stream from the graft conduit impinged on the opposite wall of the host vein. The strength of the jet stream oscillated in harmony with cardiac phase angles. The hydrogen bubble streaks in Figure 6a indicate that most of the entering flow was directed toward the heart in the proximal vein along the opposite wall of the anastomosis. Heavy hydrogen bubble concentration was observed near the stagnation region at the opposite wall of the anastomotic toe. Due to the sudden change in the flow area at the anastomosis, a large region of boundary layer separation was observed immediately downstream from the toe of the anastomosis. Frame-by-frame analysis indicated that bubble motion inside this region was slow and three-dimensional as shown in Figure 6d. The hydrogen bubbles tended to accumulate also in this region. The reattachment point of the separation region in systolic phase was found further downstream from the toe. Boundary layer separation was also observed at the heel of the anastomosis. The flow inside the distal vein was slow and dominated by a large spiral vortex along the axis of the distal vein. The results of flow visualization also indicated that the stagnation point as well as the reattachment point of the flow separation region oscillated slightly around their original locations generated in the early

region,

d = distal

vein,

g = graft

conduit,

view at the distal p = proximal vein,

systolic phase. These observations agreed well with our earlier findingP. The entering jet was always found to impinge directly on the site of maximum AR. The AR in model C was found to be located at the stagnation region as shown in Figure 6a. Hydrogen bubble concentration was also observed in this region. The hydrogen bubble streaks in the picture indicated that the velocity skewed toward the lower side after passing the stenotic region. The AR extended outward from the anastomosis in both directions of the host vein, as can be seen in Figure 6c when compared with that in Figure 6a and b. Since the AR formed a narrow passage, the boundary layer separation region at the toe was dramatically reduced and it seems to have been pushed further upstream. Boundary reattachment occurred inside the stenotic section. Flow was high in this narrow section due to reduction of the cross-sectional area. A diverging tube flow occurred in the proximal vein immediately after the narrow segment, creating a small separation zone circumferentially. Figure 6c shows a large vortex formation below the anastomotic heel. This vortex vanished during the diastolic phase. Phasic velocity

profiles

The results from the LDA velocity measurement are displayed in Figures 7-9. The velocity profile was smoothed out by curve-fitting the LDA data points. The profiles are displayed by dividin a cardiac cycle into eight equal phase angles (4,5” ‘7 . To facilitate discussions, the same data are also presented at the

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Haemodynamics of venous anastomosti:M.C.S. Shu and N.H.C. Hwang

BV3

BV5

.rl

BV6

BV4

I

Diameter

(mm1

Diameter

(mm)

Figure 7 Phasic velocity profiles at different diametric sections for model B. The origin of the coordinates is placed at the lower (B) side (as defined in Figure 5). The label at the right upper corner of each graph indicates the cross-section where velocity was measured, e.g. BV,(g) = model B with velocity measured at section 1 in the graft conduit

5

Diameter

(mm)

Diameter

(mm)

Diameter

(mm)

(mm)

Figure 8 Phasic velocity profiles at different diametric sections for model C. The origin of the coordinates is placed at the lower (B) side (as defined in F’rgare 5). The label at the right upper corner of each graph indicates the cross-section where velocity was measured, e.g. CV,(dv) = model C with velocity measured at section 1 in the distal vein

108 J. Biomed. Eng. 1991, Vol. 13, March

Diameter

Figure 9 Phasic velocity profiles at different diametric sections for model D. The origin of the coordinates is placed at the lower (B) side (as defined in F’zgure 5). The label at the right upper corner of each graph indicates the cross-section where velocity was measurd, e.g. DV, = model D with velocity measured at section 2

Figure 10 Velocity distributions in the AVLG system of models B, C and D at four different phase angles (see Figure 4)

ffaemo+amics

various sections surveyed, at four different phase angles (Figure 70). The origins of the coordinates in Figures 7-9 coincide with the lower side of the flow model. Since each flow model was a distensible replica of the actual animal vasculature, the luminal geometry was not that of a uniform conduit. Significant velocity variation along the axial direction was noticed. As the wall boundary was moving in and out (indicated by the arrow) during each pulse cycle, the ‘at the wall velocity’ sampling point is indicated by the broken lines. Solid lines are used near the walls for the velocity profiles in G, since the graft conduit was coated with plastic Glaze (Deep Flex Plastic, Inc., Murfreesboro, TN 37133) to match the nondistensibility of the Gore-Tex graft and no radial movement of the wall occurred there. Near parabolic velocity profiles were found at section BV, in the graft conduit before reaching the venous anastomosis. The maximum velocity at the peak systolic phase was approximately 60cms-‘, where the velocit at the diastolic phase was approxiY mately 36 cm s- . Through a cardiac cycle, the velocity profiles remained approximately parabolic and their magnitudes varied according to the respective phase angles. The velocity profiles became skewed when flow moved further into section BVP. In the host vein, velocity is defined as positive in the direction toward the heart and negative in the direction toward the foot. The velocity profiles in section BV2 represent the velocities both in the graft conduit and in the distal vein. Near parabolic velocity profiles were recorded in the former even though they were slightly skewed toward the lower side. This is comparable with the observations made in the flow visualization study. Since section BV2 included the venous anastomotic heel, retrograde flow (toward the foot) occurred in the distal vein during systole, even though its magnitude was small compared with the flow in the graft conduit. The retrograde flow appeared only during peak systole, while forward flow occurred during most of the heart cycle. Flow visualization at the site of anastomosis also demonstrated the same pattern throughout a cardiac cycle. Further downstream in the distal vein, the velocities at sections BV, and BV” were lower and oscillatory. In section BV3, a significant reverse flow was measured near the lower side of the flow model. Because the impinging jet stream from the graft conduit was suddenly broadened in this region, a strong reverse flow was observed near the lower side of the flow model. The maximum reverse flow in section BV~< was found to reach 20 cm s-‘. Further downstream, in section BV.1, the velocity profiles skewed toward the upper wall of the venous conduit. The velocity near the lower wall changed from a negative value in section BV3 to a positive one in section BV4. The stagnation point of the impinging jet on the lower wall was located between section BV_3 and BV4. A recirculation region was found at the upper wall of section BVS. The same flow phenomenon at this region was also indicated in flow visualization. The velocity peak skewed toward the lower side in this section. The flow velocity at the upper side of section BV(;, downstream from section BV.5,

ofvenousarmstomosis:

M.C.S. Shu and N.H.C. Hwang

remained positive throughout the cardiac cycle. The high velocity core in this section stayed near the lower wall, even though the velocity near the upper wall also increased. Similar velocity distributions were observed in model C, which represents a minor lesion development in the vicinity of the ana$tomotic toe on its opposite wall of the host vein. In section CV,(G), near-parabolic velocity profiles were obtained. The flow in section CV2 may be categorized into positive and negative portions at different locations. The flow in the distal vein of model C was as slow as that of model B. A large reverse flow region was also observed near the lower side of section CV:$. The skewed velocity profiles at sections CVi, CV,; and CV(; in this model were found to have patterns similar to those observed in model B. Model D represents a significant AR downstream from the venous anastomotic toe. Stronger retrograde flow was seen in the distal vein of this model. A larger reverse flow region also occurred at the lower side of section DV:( near the stagnation region. Velocity at the lower side of section DVJ was much larger than that of sections BVI and CV1. In section DV5, no reverse flow was seen at either side of the host vein but rather a near-parabolic velocity profile with high peak velocity was observed. The velocity profile in section DV,i was skewed toward the lower side, while slower velocity was found near the upper wall at this section. The velocity profiles at the arterial sides of the three AVLG flow models are depicted in Fi we 8. Only four phase angles (45”,
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Haemodynamics of venous anastomosix h4.C.S. Shu and N.H.C. Hwang

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C Figure 11 Wall shear stress distributions at the upper and lower sides of: a, model B; b, model C; and c, model D are presented phase angles (shear stress values at sections 0 and 1 were obtained from the distal veins)

downstream of the jet stream impingement, may be related to the tissue reaction in this region. WSS at both the upper and lower waIIs of model C are also shown in Figure 77. The magnitudes of WSS at the upper wall of model C are found to be larger generally than those in model B. The high WSS near the anastomotic toe extended beyond the toe into the constricted region during the peak systolic phase (90”). Further AR development resulted in much

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as a function

of

smaller WSS at the lower wall of section 3 and 4 as compared with that of model B. The increased WSS at the u er wall in this region was thought to be responsi KPe for the accelerated development of AR into the downstream direction in the proximal vein. It is interesting to note that WSS at the lower wall of sections .5 and 6 had high values even during the diastolic phase. As the flow skewed to the lower side, high WSS were expected during the diastolic period.

Haemodynamics

Figure 12 models

Distribution of wall shear stress along the vessel walls of B, C and D at four different phase angles

Model D demonstrated a near zero WSS at the upstream of the anastomotic toe. The WSS value increased rapidly immediately past the toe. The highest WSS was found downstream of AR. The excessively high WSS observed in this region further enhanced the theory of shear-induced tissue reactions. The absolute value of the WSS along the venous walls of all three models is shown in Figure 72. Lower WSS were observed in the distal vein of all three models. High WSS always occurred at the narrow section in the host vein, as expected. The geometrical changes among the three models significantly altered the distribution of WSS, as shown in Figure 12. The development of VS in the host vein created a near zero WSS zone at the hoop of model D. This phenomenon however was not expected. Careful comparison made with the three models seems to indicate that the VS develops in the downstream direction in the host vein. DISCUSSION Haemodialysis AVLG failure after 30 days is most commonly related to the development of a stenotic lesion”OJi. The stenosis is most commonly located near the venous anastomosis”‘. Stenosis at the arterial anastomosis is rarely foundsi. This paper presents a detailed observation of the flow phenomena at the venous anastomosis. Flow pulsatility existed throughout the AVLG system

ofvenous anastomosis:

M.C.S. Shu and N.H.C. Hwang

although its magnitude attenuated along the graft conduit. Boundary layer separation occurred at both the toe and the heel of the venous anastomosis. Flow recirculation regions were clearly identified downstream of the toe and the heel. This study also showed that the hydrogen bubble tracers accumulated around the stagnation region, and in the separation region near the toe during the systolic phase. Bubble accumulation in the stagnation region seems to indicate that bubbles are trapped close to the wall by the force developed in the impinging jet. The accumulation at the separation region was thought to be a combined contribution from the boundary separation and the inward motion of the wall. At the early systolic phase, fresh bubbles were found trapped inside the separation region. Many of the bubbles were washed away during the diastolic phase. The trapped bubbles left from the previous cycle were observed to mix with fresh bubbles that arrived with the jet stream. Local pressure was expected to increase due to the sudden decrease of flow in the region, and the inward motion of the wall might enhance the chance for the bubbles inside the region to make contact with the wall. The surgical construction of the venous anastomosis creates an inner tension and stress mismatch at the toe”‘. Venous compliance at this site is reduced. A small ‘dead’ flow zone is formed immediately downstream from the toe and is located immediately upstream of the recirculation region. Comparatively low shear rates and limited convective mass exchange may provide hydrodynamic conditions for lysed platelets and red blood cells to aggregate. The momentum created by the oscillatory impinging jet transfers into a hydraulic force acting on the endothelial layer of the host vein. In the meantime, WSS generated at the vicinity of the stagnation point act in opposite directions. Under the combined action of the impinging force and the oscillating WSS, the endothelial cells may be elongated along the shear stress direction”” and the endothelial layer in the vicinity of the stagnation region can be injured. In addition, the jet stream may transport lysed platelets or other thrombotic agents from the upstream end to the stagnation region. Genesis of vascular lesion may take place when the activated blood elements are brought into contact with the damaged endothelial layer. Blasberg et al. ” have shown that even maximally activated platelets do not seem to adhere to walls, unless transportation toward the wall is provided by hydrodynamic forces. We found that the hydrodynamic conditions favour lesion development at the stagnation point opposite the venous anastomotic toe and at the boundary separation point near the venous anastomotic toe. The lesion development at these regions was also found by other groups”~‘. The lesion seems to develop circumferentially, instead of starting along the anastomotic surgical ring as suggested by early studies which claimed that the compliance mismatch at the surgical ring might stimulate the growth of the lesion along the rin$“,“‘. Compliance mismatch along the anastomotic surgical ring between the graft and the host vein did not seem to be a major factor in stimulating the lesion at the venous anastomosis in this study.

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Haemodynamics

ofvenousanastomosis: M.C.S.

Shuand N.H.C. Hwang

We incorporated most of the physiological conditions, i.e. pulsatile flow and compliance characteristics, in a human body. It provides some insight into the complex flow features which may occur clinically at a distal anastomosis. However, future studies should include the visco-elastic property of the vessel wall and a non-Newtonian fluid in an in vitro investigation.

ACKNOWLEDGEMENTS The RTV silicone rubber casts used in this experiment were obtained from animal models developed under the National Institutes of Health grant HL 33089. The animal surgery was performed in the Experimental Surgery Laboratory, Baylor College of Medicine, by Drs J.A. Lafuente, R.K. Chen and Z.R. Gao under the supervision of Prof. G.P. Noon. Thanks are also due to Dr C. Hita, F. Polick and R. Malmauskas. REFERENCES 1. Karayannacos P, Hostetler J, Bond MG, Kakos G, Williams R, Kilman J, Vasko J. Late failure in vein grafts. Ann Surg 1978; 87: 183-8. 2. Ross R, Glomset JA. Atherosclerosis and the arterial smooth muscle cell. Science 1973; 180: 1332-9. 3 Soyer T, Lempinen M, Cooper P, Norton L, Eiseman B. A new venous prosthesis. Surgery 1972; 72: 864-8. 4. Guillon PJ, Levenson SH, Kester RC. The complications of arteriovenous grafts for vascular access. Br J&erg 1980; 67: 517-21. 5 Imparato AM, Baumann FG, Pearson J, Kim GE, Davidson T, Ibrahim I, Nathan I. Electron microscopic studies of experimentally produced fibromuscular arterial lesions. Surg Gynecol Obstet 1974; 139: 407-.504. WM, Megerman J, Hasson JE. L’Italien G, 6. Abbott Warnock DF. Effect of compliance mismatch on vascular graft patency. J Vast Surg 1987; 5: 37682. 7. Clark RE, Apostolou S, Kardos JL. Mismatch of mechanical properties as a cause of arterial prosthesis thrombosis. Surg Forum 1976; 27: 208-10. 8. Berguer R, Higgins RF, Reddy DJ. Intimal hyperplasia: An experimental study. Arch Surg 1980; 115: 332-5. 9. Sottiurai VS, Yao JST, Flinn WR, Batson RC. Intimal hyperplasia and neointima: an ultrastructural analysis of thrombosed grafts in humans. Surgery 1983; 93: 809- 17. IO. Gabbiani G, Elemer G, Guelpa CH, Vallotton MB, Badonnel MC, Huttner I. Morphological and functional changes of the aortic intima during experimental hypertension. Am J Path01 1979; 96: 399-405. cell replica11. Schwarz SM, Benditt EP. Aortic endothelial tion. I. Effect of age and hypertension in rats. Circ Res 1977; 41: 248-52. 12. Zamora JL, Gao ZR, Weilbaecher G, Navarro L, Ives CL, Hita C, Noon GP. Hemodynamic and morphologic feature of arteriovenous angioaccess loop grafts. Proc ASAZO, Atlanta, GA, May, 1985. 13. Ku DN, Giddens DP. Laser Doppler anemometer measurements of pulsatile flow in a model carotid bifurcation. JBiomech 1987; 20: 407-21. 14. Khodadadi JM, Valchos NS, Liepsch D? Moravec S. LDA measurements and numerical prediction of pulsatile laminar flow in a plane go-degree bifuraction. J Biomech Eng 110: 129-36.

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