High flow accesses affect all organs to different degrees, with the whole body in an ischemic state. The treatment of these conditions may be individually optimized using controlled flow reduction.
The ability to precisely control band diameter (flow) allows one to optimally balance AV and downstream flow for each patient. While monitoring AV flow and distal perfusion, one can reduce AV flow to the range 500-900 ml/min in an incremental and stable fashion. Observing the effect of flow reduction on distal perfusion and the heart, one can maximize distal perfusion for each patient.
There is no physiologic need or rationale to operate a fistula wide open. Placing a midpoint band creates high- and low-pressure segments. This configuration reduces overall AV flow and the pressure returning to the right heart. This technique was first published as a solution to a low-flow steal scenario.(12) Central banding may also reduce the ischemic stunning experienced with dialysis.(13)
The Flowband can gradually restrict a centrally placed band while monitoring upstream and downstream pressures to establish a patient-specific level of banding.
It has been known for over 100 years that opening a large fistula will damage the heart. Flow reduction has always been very effective in relieving heart failure (14).
Structural heart damage is proportional to AV flow, with the LVM increasing by 2.1g per 100 ml of access flow (8), and another study (3) seeing a graded increase in LVEDD with flow.
Median flows from 500-900 ml/min have been shown to induce reduced overall structural heart changes (8-10)
Controlled flow reductions are possible with Flowband. Reducing AV flow by only 300ml/min provides an additional 110 gallons of blood per day to the systemic circulation. While access ligation has been shown to result in regression of LV hypertrophy (15,16), controlled flow reduction may also be expected to reverse some cardiac changes.
The presence of a patent access has been shown to rob blood from transplanted kidneys. The perfusion of kidney grafts, as measured by the resistive index (RI), is increased by access closure or even temporary manual occlusion. (1,2) The increased perfusion is proportional to the access flow. An increase in RI ≥10% over the first year was found to be an independent risk factor for graft loss with a hazard ratio of 6.2. (3)
Closure of a patent access improves both kidney graft and cardiac function, with elevation of diastolic BP, reduced NT-proBNP levels, reduced LV and atrial dimensions, and stability of the eGFR slope.(4) The presence of a fistula may also be a predictor of HF in KT patients. The incident rate of de novo HF after transplantation was 58/1000 person-years in AVF patients vs. 33/1000 for non-AVF patients. (11)
The 5-year eGFR data of Weekers shows the detrimental effect of an open access on kidney graft function. (5) A 5-year graft survival study of open vs. closed accesses confirmed this: 60% with patent access, and 75% with closed accesses.(6) Also, the 5-year impact of ligation on cardiac structure shows a persistent regression of the LVM and LVM index. (17)
There is no medical reason to ligate an access when it may be saved. The work of Gkotsis and Jennings (7) demonstrated the benefit of reducing AV flow for KT patients. Twelve fistulas were banded to a flow of about 600 ml/min. All were patent at 19mo., and 2 of 12 were successfully reused after graft failure.
To conveniently reduce flow to the narrow range of 500-800 ml/min, one needs to control the band diameter to less than 0.5mm.
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