Arterial percutaneous angioplasty in upper limbs with vascular access devices for haemodialysis

Alexandra Guerra1,3,, Alain Raynaud1,2, Bernard Beyssen1,2, Jean-Yves Pagny1,2, Marc Sapoval2 and Claude Angel1

1 Department of Cardiovascular Radiology, Clinique Alleray Labrouste, 64 Rue Labrouste, F-75015 Paris, 2 Department of Radiology, Hôpital Broussais, Paris, France, and 3 Department of Nephrology, Hospital de S Bernardo, Setúbal and Clínica de Doenças Renais, Lisbon, Portugal



   Abstract
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 Conclusions
 References
 
Background. The purpose of this study was to evaluate retrospectively the clinical context and effectiveness of arterial percutaneous transluminal angioplasty (PTA) of arterio-venous fistulae in chronic haemodialysis patients.

Methods. Between May 1992 and June 1997, arterial PTA was performed in 33 patients with a total of 35 angioaccess devices of the upper limbs (18 arterio-venous fistulae and 17 PTFE grafts). Clinical indications for arterial PTA were unexplained acute thrombosis in 12 patients (34.3%), insufficient blood flow in 13 patients (37.1%), and severe limb ischaemia in 10 patients (28.6%), two of whom had skin ulcerations and one had severe neurological damage. Follow-up periods varied between 1 and 55 months (mean 15.5 months).

Results. PTA was attempted in 22 radial, 10 brachial and seven ulnar arteries. Angioplasty was successful (i.e. residual stenosis of <=30%) in all but one patient. There were no complications. Early re-thrombosis (<1 month) occurred in two of the 12 patients with acute occlusions. All the angioaccesses of patients with insufficient blood flow were improved. Eight of the patients with limb ischaemia became symptom free, and two were failures (one had partial healing of skin ulcerations and one did not improve). Re-stenosis occurred in six cases (27.3% of the 22 angiograms performed) but re-dilatation was performed in only two instances. Primary and secondary patencies were 63.5 and 90.6% at 6 months and 40.8 and 75.6% at 24 months, respectively.

Conclusion. Chronic arterial lesions in upper limbs bearing vascular access devices for haemodialysis may lead to thrombosis, ischaemia and insufficient flow for dialysis treatment. PTA is a safe and effective technique with a low rate of re-intervention.

Keywords: arterial stenosis; haemodialysis; ischaemia; PTA; thrombosis; vascular access



   Introduction
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 Conclusions
 References
 
Morbidity and mortality in chronic haemodialysis patients is strongly correlated with dialysis efficiency [1]. This in turn depends on vascular access function, which is currently one of the most important issues in improving longevity and quality of life in this group of patients.

Several complications may occur with vascular accesses, which may lead to failure due to thrombosis, impaired function due to low flow, or symptoms such as ischaemia of the limb involved. These problems are usually associated with stenosis, which is known to occur frequently in the venous outflow or inside grafts [2].

Stenosis on the arterial side is not as frequently discussed, but it is also likely to compromise angioaccess function and cause limb ischaemia. Arterial stenosis is probably common in the aged haemodialysis population, many of whom have generalized arterial disease.

Arterial disease in limbs with arterio-venous anastomoses can be associated with ischaemic symptoms or access dysfunction (low inflow), compromising dialysis and ultimately leading to thrombosis.

The approach to an access with poor inflow (insufficient blood flow for dialysis) is often to abandon the access or to change the localization of the anastomosis to a healthy segment of the same artery, thus consuming patients' vascular capital.

Ischaemia in limbs with haemodialysis access is associated with symptoms such as pain or limb dysfunction, often exacerbated during haemodialysis treatments. Most of the techniques proposed to overcome limb ischaemia are surgical. Many of these techniques are ineffective and lead to access malfunction or abandonment.

This retrospective study was undertaken in order to evaluate the effectiveness of arterial percutaneous transluminal angioplasty of arterio-venous fistulae in haemodialysis patients performed in the context of thrombosis, low-flow or limb ischaemia.



   Subjects and methods
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 Conclusions
 References
 
Patients and angioaccess data
We included all patients referred to the interventional radiology department who underwent arterial PTA in the angioaccess limb from May 1991 to the end of June 1997.

In this period, arterial PTA was performed for 35 haemodialysis accesses in 33 patients (three in 1992, six in 1993, six in 1994, three in 1995, 10 in 1996 and seven in the first half of 1997). Nephrologists requested fistulography for thrombosis in 12 accesses (34.3%), insufficient blood flow for haemodialysis treatment in 13 accesses (37.1%) and severe limb ischaemia in 10 accesses (28.6%), two of which were associated with ulcers on the fingers and one with neurological damage with motor dysfunction. Six patients had both ischaemia and poor arterial inflow, and therefore we decided to count them twice, classifying them as belonging to both groups.

Clinical and personal data, obtained through a questionnaire sent to the dialysis units, included age, gender, diabetes status, previous transplants, clinical signs of atherosclerotic disease, aetiology of end-stage renal disease and total time on dialysis. To assess the presence and localization of atherosclerotic disease, the questionnaire asked about clinical signs and technical documentation of coronary or carotid disease, arterial insufficiency in the lower limbs and history of arterial vascular surgery.

Poor arterial inflow in the access was defined as an inability to maintain a 250 ml/min flow rate during a 4 h dialysis session. Medium arterial inflow was defined as allowing blood flow rates >250, but <350 ml/min. Flow was classified as poor in all the 19 patients referred for arterial PTA due to insufficient flow.

Ischaemia was classified into three levels of severity: I, cold hand or pain during dialysis sessions; II, rest pain and numbness; and III, skin ulcerations or neurological damage with motor or sensory dysfunction. Three of the 10 patients had grade III ischaemia, six had grade II and one had grade I.

Patients' demographics and baseline clinical data are summarized in Table 1Go. Clinical success was defined as a thrombosed access which allowed the next haemodialysis treatment, a low-flow access in which it was possible to obtain a blood flow of at least 300 ml/min during the next haemodialysis session, and when symptoms normalized in cases of ischaemia. Access types (endogenous fistula or PTFE graft), localization, age and the number and type of percutaneous and surgical procedures are summarized in Table 2Go.


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Table 1.  Patient demographics and baseline clinical data

 

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Table 2.  Access data

 

Procedures
All accesses were systematically screened from the feeding artery to the superior vena cava with digital subtractive angiography.

For imaging with angiography on an outpatient basis, direct retrograde access puncture was performed with an 18G needle and arterial puncture was performed with a 20G needle. Arterial puncture had the advantage of allowing exploration and angioplasty of other distal arteries in the same limb.

For thrombosed accesses, thrombolysis was performed through two 18G needles placed at each end of the clotted segment. An initial bolus of 100 000 U urokinase was administered, then 25 000–30 000 U/h were infused through each needle for 1–4 h (total <340 000 U) and 20 mg of heparin were administered. Two 8F dilators were positioned after fibrinolysis and used to perform arterial and venous angiograms and thromboaspiration through an aspiration catheter using a regular Luer-Lok 50 cc syringe. When the access vessels appeared entirely free of thrombi, PTA was performed in identified venous or arterial stenoses. In some cases, thromboaspiration was performed directly without fibrinolysis.

For exploration of a poor inflow access or limb ischaemia, arterial puncture was usually preferred.

Arterial stenoses were crossed using soft wires with diameters of 0.035G for brachial artery lesions and 0.014G for radial or ulnar lesions. The size of the first balloon was equal to the diameter of the normal vessel adjacent to the stenosis; in the case of remaining residual stenosis >30% despite at least 3 min inflation, a 1 mm larger balloon was employed. Balloon diameters varied between 2.5 and 6 mm. For two lesions, 8F catheters were used according to the Dotter technique and a rotablator was employed in a case with stenosis involving a long segment of the radial artery.

Thirty-nine arterial PTAs were attempted in 22 radial (56.4%), 10 brachial (25.6%) and seven ulnar (18%) arteries. Dilatation was performed in two different arteries in four patients, three in cases of upper extremity ischaemia, and one in a case of poor inflow access.

In 13 cases (37.1%), venous PTA was performed in the same procedure to treat associated lesions in the venous outflow. The indications were thrombosis in eight cases, insufficient flow in five and ischaemia in two (with associated low inflow). Arterial PTA was the only intervention attempted in 33.3% (four) of the thrombosed accesses, apart from declotting, in 73.7% (14) of poor inflow accesses and in 80% (8) of the limb ischaemia cases.

Angiography
Two independent observers blindly reviewed the angiograms.

Stenosis evaluation and classification
Degree of stenosis was measured before and after the procedure and in the subsequent angiographies, and determined by the equation:


(001)
with the reference diameter measured in an uninvolved segment of the same artery. After scoring by each independent observer, the results were unblinded and the average degree of stenosis was calculated and used for the study.

The procedure was considered to have failed when residual stenosis >30% was still detectable.

Stenoses were classified in five types according to position (Figure 1Go). There were seven type I, three type II, 18 type III and one type IV stenoses, and six cases with types III and IV simultaneously. We did not find any type V or brachial access associated with forearm arterial stenosis, a possibility that was not included in our classification. The seven type I stenoses were found in four thrombosed accesses and three cases of low flow; all three type II stenoses were found in cases of ischaemia; and the 18 type III stenoses were found in eight accesses with thrombosis, eight with low flow and two with a combination of ischaemia and low-flow. Type IV was found in one case of ischaemia, and the six combined types III and IV were found in four cases of low-flow access associated with symptoms of limb ischaemia, and in two cases of poor inflow access. Stenosis types are shown in Figure 2Go according to clinical indication for PTA.



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Fig. 1.  Stenosis classification. Type I: brachial access, stenosis upstream or forearm access, brachial stenosis; type II: brachial access, stenosis downstream; type III: access in the forearm, stenosis upstream in an antibrachial arterial axis; type IV: access in the forearm; stenosis in the other antibrachial arterial axis; type V: access in the forearm; stenosis downstream.

 


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Fig. 2.  Relationship between stenoses classification and clinical manifestation (totals are not coincident with access number, but with complications).

 
Access type and anatomical location, arteries submitted to PTA, site of puncture, stenosis classification and clinical indication for PTA are detailed in Table 3Go.


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Table 3.  Types of access and stenoses, puncture places and arteries submitted to PTA

 



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Fig. 3.  Primary and secondary patency rates, after arterial PTA.

 


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Fig. 4.  Case of poor arterial inflow in a radiocephalic arteriovenous native fistula. After brachial artery puncture, PTA was attempted with a 3-mm balloon and the radial, 80% type III stenosis seen in the first picture despaired, as shown in the control after dilation where there is almost no residual stenosis.

 
Follow-up
Follow-up varied between 1 and 55 months, with mean and median periods of 17.4±15.4 and 11 months, respectively.

Patients were followed until the end of the study period, access abandonment, death or suspension of dialysis. We studied the findings concerning symptoms of limb ischaemia, blood flow achieved during haemodialysis, number of access interventions before and after arterial PTA, and number of acute thromboses before and after the procedure studied, and we analysed the occurrence of early re-thrombosis (<1 month after the procedure) and iterative thrombosis (more than three episodes in a 6 month period).

Re-stenosis was defined as the recurrence of stenosis >30%.

We reviewed degree, time and percentage of re-stenoses and the eventual need for arterial re-dilatation.

Primary access patency refers to the period of access function from arterial PTA to the next percutaneous or surgical procedure. Secondary patency begins with arterial PTA, includes all percutaneous interventions and ends with surgical revision, access abandonment or loss to appropriate follow-up. Patency graphics were designed according to the Kaplan–Meier method.

Statistical analysis
Data are described by frequency tables, by means or medians for quantitative variables and by dispersion measurements such as standard deviations and interval ranges.

The associations of each complication with patients' clinical and personal data and access types (vein or graft) as possible risk factors were evaluated by determining odds ratios (OR) and 95% confidence intervals (95% CI). The statistical significance of each risk factor obtained for categorical variables was analysed by Fisher's exact test. Comparisons of quantitative variables between those with and without complications were performed by the Mann–Whitney test. In order to categorize these variables and to obtain each odds ratio, the cut-off point defined was the median, and Fisher's exact test was then applied.

Two-tailed paired Wilcoxon test was performed to determine the differences in stenosis diameter before and after arterial PTA. Significance was based on a 5% significance level.



   Results
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 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 Conclusions
 References
 
Angiography results
Mean stenosis before PTA was 81.14±12.55% (median 80%) and 10.57±13.92% (median 0%) after PTA (P<=0.001).

There was only one angiography failure: 60% residual stenosis after using a 4 mm balloon to dilate a 90%, type I stenosis, in a patient with poor flow access. Nevertheless, the patient improved clinically.

There were no technical complications.

In total, 34 interventions were performed before arterial PTA and 28 afterwards.

During the follow-up period, arteriography of the angioaccesses limb was performed in 22 patients at a mean interval of 13.25±14.90 months (from 0.5 to 47 months). Re-stenosis rates were 0% at 1 month, 4.5% (one) at 6 months, 9.1% (two) at 12 months, 18.2% (four) at 24 months and 27.3% (six) at 36 months.

Only two of the patients with recurrence needed to be re-dilated, one patient with iterative thrombosis and one patient with low-flow access.

Cumulative primary access patency rates (Table 4Go) at 1, 6, 12, 24 and 36 months were 91.43, 63.54, 49.92, 40.84 and 24.51%, respectively; secondary patency (Table 5Go) rates were 100, 90.63, 82.19, 75.62 and 43.21% at 1, 6, 12, 24 and 48 months, respectively.


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Table 4.  Data on primary patency and failures for accesses submitted to PTA

 

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Table 5.  Data on secondary patency and failures for accesses submitted to PTA

 

Clinical results
Only two patients were lost to follow-up. Twelve patients (34.3%) died during the study period, five of whom were in the limb ischaemia group (50%).

Eleven (91.7%) thrombosed accesses were recovered and remained functional through to the next haemodialysis treatment, and in one patient the access became clotted in the 24 h following arterial angioplasty. (A 9-month-old brachial-basilic prosthesis thrombosed four times in a 4-month period. There was a 70% type I stenosis and also multiple stenoses in the subclavian vein and throughout the entire graft length; no significant residual stenosis was noted at the end of the procedure, but there were still several small clots. No other interventions were needed after the second thromboaspiration, and the patient died 49 months later with a well functioning access.)

In the group of patients with access thrombosis, there were 12 cases of thrombosis before arterial PTA and nine after. Eight of the 12 patients had had episodes of access thrombosis before arterial PTA (one had three, two had two, and five had one). The average time between the last episode and arterial PTA was 2.5 months. Five patients had thromboses after the procedure (one had five and the others one each); the mean interval to the next thrombosis was 1.8 months.

There were two patients with early re-thrombosis. The first was a patient who had had five thromboses in other accesses on the same limb. This was the first thrombotic event in the 8-month-old radiobrachial forearm PTFE prosthesis, and angiographic evaluation showed 70% type III stenosis in the radial artery and venous stenoses in brachial and subclavian veins. Arterial PTA was attempted with <30% residual stenosis, but the brachial and subclavian veins remained irregular. Another thrombosis occurred 1 month later, after which the access was abandoned.

The other early thrombosis occurred in a 5-month-old brachiobasilic PTFE access, which had had two previous episodes of clotting (8 and 5 weeks before) related to venous stenoses. The arterial stenosis was an 80% brachial type II stenosis treated by PTA after fibrinolysis, with no residual stenosis. Three weeks, 7 months and 12 months later, other thromboses occurred that were related to venous re-stenoses. The patient died with the same access 13 months after the procedure.

One of the treated patients with a 10-month-old radiocephalic forearm prosthesis had iterative thrombosis. There had been banding of the radial artery to reduce high blood flow 5.5 months before, and two thrombotic events had occurred 5 months and 2 weeks before. When the third thrombosis occurred, a 60% type III radial stenosis in the previous banded location was dilated, leaving 20% residual stenosis. The access clotted five times during the following 6 months at 2, 4, 5.5, 6 and 7 months. At months 2 and 5.5, 50% re-stenoses were re-dilated, leaving residual stenosis of <15%, and at month 7 the access was abandoned.

Statistical analysis failed to demonstrate any association with time on haemodialysis, previous renal transplantation, diabetic status, atherosclerotic symptoms or access age and the occurrence of thromboses. Females and patients older than 60 years had a three-fold greater risk of thrombotic events, although this was not statistically significant (OR=2.83 and 3.27, and 95% CI=0.68-11.85 and 0.74-14.10, respectively), and PTFE grafts had a 5.6-fold greater risk than veins (OR=5.63, CI=11.24-54.95; P=0.035).

All 20 patients with low-flow access improved after PTA. Figure 4Go shows an angiogram of a low-flow access headed successfully.

For low-flow accesses, women had a four times lower risk than men (not statistically significant: OR=0.27, CI=0.06-1.12; P=0.09). Diabetics had around nine times greater risk (OR=8.75, CI=0.94-81.26; P=0.047), and PTFE grafts nearly five times lower risk than native fistulae (OR=0.21, CI=0.05-0.85; P=0.044).

Of the patients with limb ischaemia (10), eight became symptom free and two were considered failures.

Failure occurred in a 12-month-old brachiobasilic PTFE fistula, associated with grade III ischaemia and normal blood flow for haemodialysis treatment. Angiographic evaluation showed complete type II stenosis, and stenoses in all three antebracheal arteries. PTA was performed in brachial and ulnar arteries with good angiographic results. Rest pain and numbness disappeared after the procedure, and there was healing of the finger ulcers. However, cold hand and pain persisted during dialysis sessions. Angiography 2 months later revealed 50% brachial re-stenosis. No further stenosis was noted during the 16-month follow-up period, after which the patient died.

The other failure was in a native brachiobasilic arterio-venous fistula with grade III ischaemia and normal flow for haemodialysis sessions. Upon angiography, an 80% brachial type II stenosis and occlusions of the ulnar and radial arteries were diagnosed. PTA was undertaken in the brachial artery with no residual stenosis. There was no clinical benefit immediately after the intervention, and 48 h later the patient underwent distal revascularization through a brachio-brachial prosthesis bypassing the arterio-venous anastomosis. There was reasonable clinical improvement during the first few weeks after the intervention, but the symptoms of ischaemia reappeared in the second month, and the access was abandoned in the 6th month.

Out of all the possible risk factors studied, the only associations we could find for limb ischaemia were: diabetes (seven times greater risk, OR=7.33, CI=1.40-38.46; P=0.027) and the presence of generalized atherosclerosis (impossible to determine the risk, but 38.5% of the patients with documented atherosclerosis and 0% without had limb ischaemia associated with arterial stenosis; P=0.036).



   Discussion
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 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 Conclusions
 References
 
Reduction in haemodialysis access blood flow rates can compromise the delivery of adequate dialysis and may cause acute thrombosis [3].

In some series of access declotting, up to 90% of the cases of acute thrombosis were associated with stenoses inside grafts or in the runoff vein [2]. Moreover, they have been reported to be due to factors that reduce fistula flow such as banding [4]. As found in our patients, thromboses can also occur in the context of arterial stenosis, a mechanism that has not to our knowledge been previously described, probably because it is not routinely investigated.

Our approach to clotted accesses had an immediate success of 91.7%, which, despite the small patient population, is comparable to the best series (ranging from 80 to 94% [58]). The only failure was probably due to a technical problem, i.e. residual clots left within an irregular prosthesis, as suggested by the fact that there was no further episode in 4 years. We presume that both cases of early re-thromboses could have been related to the venous stenoses with poor results to PTA. One explanation for iterative thrombosis in the patient we described is the elevated re-stenosis rate, possibly caused by previous banding surgery.

It is difficult to evaluate the exact significance of arterial stenoses in the development of access thromboses. Logically, as intra-access blood flow decreases, the risk of thrombosis increases proportionally, as would be the case in the presence of stenoses in feeding arteries, as shown in several studies describing the relationship between access flow and clotting [3,9]. Unfortunately, the nephrologists did not systematically ask for Doppler or other flow studies in these patients, and therefore there was no quantification of access blood flow.

Our findings suggest that thrombosis is basically a multifactorial problem, since in eight of the 12 cases (67%) there were associated venous stenoses. However, we presume that arterial stenosis can be a major contributor to access clotting, as shown by the fact that the total number of thrombotic events before arterial PTA was higher than after the procedure. This was rather unexpected, since access ageing and previous episodes of acute thrombosis would be expected to increase the risk of new thrombosis.

As pointed out, the only reference we had to access flow was the ability to achieve enough blood flow for haemodialysis treatment. In our group of patients with poor-inflow access, the finding that arterial stenosis was the only abnormality in 73.7% of cases and the 100% clinical success achieved with arterial PTA prove that these lesions were the only cause of access malfunction.

Chronic ischaemia related to the presence of a dialysis access is a relatively infrequent but potentially catastrophic complication. It can be due to three main mechanisms. The first, venous hypertension, is a consequence of venous stenosis, and diagnosis is easily made by clinical observation: significant limb swelling and sometimes visible collateral venous circulation. Venous PTA is always an effective treatment for this problem. Steal syndrome (flow reversal in the portion of the artery distal to the fistula due to a lower pressure system on the outflow side of the anastomosis) and arterial lesions, which often occur together, are the other two pathophysiological mechanisms underlying angioaccess limb ischaemia.

In our series, arterial disease was the main cause of ischaemia, as shown by the fact that in 80% of the cases there were no venous stenoses associated with the arterial stenoses.

In the past, fistula ligation was the preferred method of treatment for patients with hand ischaemia after access surgery. However, this approach required the abandonment of potentially valuable angioaccess sites. Several other surgical approaches have been proposed to treat steal syndrome and preserve the access, most of them reducing fistula flow [4,10,11], thus increasing the risk of thrombosis. In contrast, the treatment of ischaemia by arterial PTA increases flow to the access, but to our knowledge this has only been reported once [12].

Our stenosis classification helped us to understand the possible mechanisms underlying ischaemia. Steal syndrome could not have been involved in the three cases of type II stenosis, because it would have been increased when dilating stenoses distal to the arterio-venous anastomosis. Although two failures occurred with this kind of stenosis, in one there was clear symptomatic improvement, and in the other revascularization surgery was also ineffective. In the other seven cases (two type III, four types III and IV together, and one type IV), steal syndrome may have been a factor. However, arterial lesions are relatively independent factors and should always be corrected, as shown by the clinical success of PTA. Using a less invasive technique than any surgical approach, we were able to diagnose the arterial disease, which could have passed unnoticed on surgery, thus solving the problem in 80% of our cases and preserving the access.

The series presented is not large enough to show any trend for one type of lesion towards a particular complication. Nevertheless, it is important to note that the most frequent type (type III) was essentially related to poor inflow accesses and thrombosis, that ischaemia occurred with all types, but predominantly with types IV and types III and IV together, and that poor inflow accesses as an isolated indication were mainly associated with type III. Although our results are not conclusive, we believe this classification can help in the decision to perform PTA for arterial stenoses according to their location (for example the decision to dilate types II and V stenoses should be taken cautiously in the face of the risk of enhancing steal syndrome) and could be employed in further extended studies.

Three of the clinical factors we analysed were noteworthy: atherosclerosis, diabetes, and type of access.

Arterial disease is one of the major underlying factors leading to morbidity and mortality in end-stage renal disease patients [13]. It was not surprising to find that 75.8% of the patients treated had the confirmation of arteriopathy in at least one location, nor that this was found to be a significant risk factor for the occurrence of limb ischaemia (100% of patients).

Diabetes, an important contributor to arteriopathy, can place patients at risk of access thromboses [14] and hand ischaemia [11] following vascular access construction. Diabetes was shown to place patients at risk of symptomatic ischaemia (five times higher) or low-flow accesses (nine times higher), but surprisingly no association was found with thrombosis. This is probably because, as already mentioned, thrombotic processes are more dependent on multiple factors than the other complications studied.

Arterio-venous grafts are more prone to thrombosis [15], and more often related to limb ischaemia [16] than native fistulae. Our results agreed with the literature concerning thrombosis: of the 12 cases of thrombosis, nine were in grafts, which we found to have a 5.6 times greater risk of clotting, although they had fewer flow problems (risk five times lower). This is easy to understand, since PTFE fistulae usually have high blood flow rates, enough to permit haemodialysis treatment but not to remove the risk of thrombosis. Flow studies would have been necessary to evaluate the risk of thrombosis in these accesses. We could not find any association between ischaemia and prosthetic grafts; in fact grade III symptoms occurred in two native fistulae and one PTFE graft. As already pointed out, this shows that steal syndrome was probably not the dominant pathophysiological mechanism.

The low rate of arterial re-stenosis found in our patients (27.3% at 36 months) is noticeable, along with the fact that only two re-interventions were needed (one case had already had a disappointing result after the first arterial PTA (60% residual stenosis) and the other recurred in a location previously subjected to banding). In comparison with venous PTA, arterial stenoses usually have a lower rate of recurrence, as shown in other territories such as lower limbs [17] and coronary arteries [18]. Our recurrence rate of 18.2% at 24 months was much lower than that generally found in other arteries. This was achieved in spite of the low calibre of the arteries dilated, which were often severely diseased and highly calcified. One of the possible explanations for this is the high blood flow in the dilated locations caused by the presence of the arterio-venous anastomosis, lowering the risk of early thrombosis and favouring healing of the artery after angioplasty.

Our access patency rates were calculated without separating native from prosthetic fistulae, or thrombosis from the other indications. Nevertheless the rates we obtained (cumulative primary patency of 49.92 and 40.84% at 12 and 24 months, respectively, and cumulative secondary patency of 82.19 and 75.62% at 12 and 24 months, respectively) are equivalent to or better than the rates described in the literature. For thrombosed access, primary patency rates at 12 months varied from 26% (PTFE) [5] and 49% (native AVF) [8] and secondary patency rates from 50% (PTFE) [5] to 81% (native AVF) [8], and for percutaneous procedures due to haemodynamic problems, secondary patency rates at 12 months were found to be 82% [19]. When analysing our rates it is important to remember that patency rates might have been even better had mortality not been as high (34.3% of patients died during the study period).

In contrast to some of the studies published for venous PTA, we still report a small number of cases. However, these findings show that in addition to being a safe and effective technique for the management of problems such as poor-inflow access, thrombosis and limb ischaemia, arterial PTA has very good patency.



   Conclusions
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 Conclusions
 References
 
We intervened in 35 accesses in 6 years, each year more so than in the previous year. It will not be surprising if the progression continues as we become more aware of the importance of these lesions that we think are treatable and that are currently underestimated. We believe that it is essential to search for arterial lesions in cases of unexplained access thromboses, insufficient blood flow for dialysis treatment, or symptoms of ischaemia in limbs with accesses for haemodialysis. In such cases, a simple endovascular procedure should be enough to solve the problem while saving the access.

To our knowledge, this is the first study reporting percutaneous correction of arterial stenosis responsible for fistula dysfunction. We hope that further prospective studies will be designed to confirm that PTA is a safe, easy and effective technique to correct such lesions.



   Notes
 
Correspondence and offprint requests to: Alexandra Guerra, Clínica de Doenças Renais, Av. Forças Armadas, 49 R/C, 1600-076 Lisboa, Portugal. Email: alex.jluc{at}oninet.pt Back



   References
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 Conclusions
 References
 

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Received for publication: 20. 6.00
Accepted in revised form: 21.11.01





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