1 Second Department of Internal Medicine, 2 Second Department of Surgery, Nihon University School of Medicine, 3 Goodman Co., Ltd, Tokyo, Japan
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Abstract |
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Methods. Intravascular ultrasound studies were performed in 40 haemodialysis patients with 63 stenoses in arteriovenous fistulae who had percutaneous transluminal angioplasty. The patients were qualitatively and quantitatively evaluated for echogenic patterns and morphological changes before and after angioplasty.
Results. Morphological plaque features in stenotic lesions were classified as 37 soft (58%), five hard (8%), 20 mixed (32%), and one calcified sites. Plaque fractures after angioplasty were detected in 45/63 (71%) instances. The lumen cross-sectional area was found to be dilated approximately threefold (from 3.8±2.4 to 11.1±4.5 mm2) and the external elastic membrane cross-sectional area was dilated approximately twofold (from 11.1±5.3 to 19.8±8.1 mm2) after angioplasty.
Conclusion. These results indicate that intravascular ultrasound allows both qualitative and quantitative assessments of arteriovenous fistulae in haemodialysis patients. The results further suggest that the mechanism of expansion of arteriovenous fistulae stenoses by percutaneous transluminal angioplasty involves stretching of the vessel wall as well as plaque fractures.
Keywords: arteriovenous fistulae; haemodialysis patients; intravascular ultrasound imaging; percutaneous transluminal angioplasty
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Introduction |
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However, few data exist regarding the utility of IVUS imaging of AVF in haemodialysis patients [13]. The purpose of this study was to examine the structure and characteristics of the stenotic lesions of AVF, and conduct a quantitative evaluation of the stenotic lesions of AVF before and after angioplasty in vivo.
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Subjects and methods |
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Intravascular ultrasound
IVUS catheter comprised a 30-MHz transducer mounted on the tip of a 2.9 Fr catheter (Ultra Cross®; Scimed/Boston Scientific, MA, USA). The ultrasound beam was reflected onto a rotating transducer revolving at 1800 r.p.m., creating a 360° real-time image perpendicular to the catheter. Lateral and axial resolutions of this system were approximately 150 µm and 90 µm respectively. The IVUS console was the Clearview Ultra® (Scimed/Boston Scientific) intravascular imaging system. Images were recorded on Super-VHS videotapes. Measurements of lumen diameter and wall thickness were made on-line using the software package built into the instrument. Echogenic patterns and morphological changes of the IVUS images were qualitatively and quantitatively evaluated by two observers blinded to the results of angiography.
Qualitative analysis was performed for echogenic patterns and morphological changes following PTA. Morphological plaque features were classified as soft, hard, mixed, and calcified according to the reports of Hodgson et al. [14]. Briefly, soft plaque 80% of the plaque area through the lesion was composed of intimal echoes with less homogenous echodensity than seen in the adventitia. Hard plaque
80% of the plaque area through the lesion was composed of dense echoes with a homogenous echodensity greater than or equal to that seen in the adventitia. No calcium was present. Mixed plaque=a plaque having bright echoes with acoustic shadowing encompassing <90° of vessel-wall circumference or a mixture of soft and hard plaque, with each component occupying <80% of the plaque area through the lesion. A plaque fracture was defined as an irregular thin echolucent separation extending from the lumen for a variable length into the plaque, including plaque dissection and intimal flaps.
Quantitative analysis was performed with computer planimetry and the target lesion was assessed. The vessel lumen area was measured by tracing the lumenintimal border. The external elastic membrane (EEM) of the vessel was defined as the outer border of the sonolucent zone, which has been reported to represent media [7,10], and the area within the EEM was measured as the EEM cross-sectional area (CSA). The following measurements were investigated: (i) lumen diameter (mm), (ii) EEM diameter (mm), (iii) lumen CSA (mm2), (iv) EEM CSA (mm2), (v) cross-sectional narrowing=((EEM CSA-lumen CSA)/(EEM CSA))x100. The major and minor diameters of the lumen and EEM were measured according to the reports of Nakamura et al. [15].
PTA procedure
Angiography was performed by puncturing the distal or proximal part of the stenotic lesion of arteriovenous fistulae, or the artery. After delineation of the stenotic lesion, PTA was performed as follows: from the distal or proximal part of the lesion, a 22-gauge thin-wall needle was inserted and the first guide wire was passed through this needle into the vessel. A 5 Fr or 6 Fr sheath with a length of 5 cm was placed, and the patient immediately received 50 units/kg of heparin. Next a 0.014- or 0.018-inch guide wire was passed to the target lesion and angioplasty applied with a high-pressure balloon catheter with a diameter of 46 mm and a length of 2 or 4 cm.
Statistical analysis
Statistical analysis was performed by paired Student's t-test. Data were expressed as the mean±standard deviation (SD). Differences were considered significant at the level of P<0.05.
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Results |
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Quantitative analysis
As shown in Table 1, the major lumen diameter at the lesion site increased from 2.3±0.8 to 4.1±0.8 mm after angioplasty and the minor lumen diameter also increased from 1.9±0.7 to 3.3±0.8 mm after angioplasty (P<0.0001). The major EEM diameter at the lesion site increased from 3.9±1.0 to 5.3±1.1 mm after angioplasty and the minor EEM diameter also increased from 3.5±0.9 to 4.7±1.0 mm after angioplasty (P<0.0001). The lumen CSA at the lesion site increased from 3.8±2.4 to 11.1±4.5 mm2 after angioplasty (P<0.0001). The EEM CSA at the lesion site increased from 11.1±5.3 to 19.8±8.1 mm2 after angioplasty (P<0.0001). The percentage cross-sectional narrowing decreased from 64.8±14.7 to 41.9±12.2% after angioplasty (P<0.0001).
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Discussion |
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Veins have thinner walls than their arterial counterparts. Histologically, veins contain an abundance of connective tissue, whereas elastin fibres and smooth-muscle cells occur in smaller numbers. The walls of veins consist of three poorly defined layers: the intima, media, and adventitia. Gussenhoven et al. [8] reported that the walls of veins did not allow ultrasonic distinction between the intima, media, and adventitia.
In our study, the echo pattern of native AVF revealed a triple layer appearance of the hyperechoic intima, the hypoechoic media, and hyperechoic adventitia. This is regarded as a result of arterialization of veins. The phenomenon of arterial blood circulating into veins in vivo exists in saphenous vein grafts for coronary artery bypass surgery and for AVF of haemodialysis patients. Willard et al. [16] reported that a chronically implanted saphenous vein graft demonstrated a variety of pathological changes, including intimal proliferation and atherosclerosis. IVUS can distinguish between the normal appearance of freshly harvested veins and intimal hyperplasia, atherosclerosis, and vein graft wall fibrosis, and reveals a triple-layer appearance. Correlation between the ultrasound examination of plaque morphology and the histological characteristics of the corresponding vessel wall was established. According to these reports, soft echoes are reflective of fibromuscular tissue (intimal proliferation as well as lesions that consist of fibromuscular tissue and diffusely dispersed lipid), and bright and homogeneous (hard) echoes are representative of collagen-rich fibrous tissues [8,11].
When examining plaque composition (hard or soft) of AVF by ultrasound imaging, Davidson et al. [13] reported that 34 (89%) lesions had soft plaque aspect and 4 (11%) lesions had hard plaque aspect. These data are in accordance with our findings in which hard plaque was found in only five (8%) lesions. Moreover, their report demonstrated dissections in 16/38 cases (42%). In our study, plaque fractures were detected with a high frequency. Because of this difference, although our results showed plaque fractures including plaque dissection and intimal flaps as described above, they reported a higher frequency of dissections. This may be due to differences in the choice of balloon catheter used and in the IVUS catheter used. The size of our balloon catheter was surely smaller than that of their report. In our study, however, the mean major EEM diameter of lesions was 3.9 mm and that of the reference sites was below 6.0 mm, and the mean major lumen diameter was also below 5.0 mm. We chose a suitable balloon catheter and could not use a larger balloon catheter because of the risk of complications.
The investigation of morphological changes of angioplasty by ultrasound revealed that the lumen diameter and cross-sectional diameter of the EEM showed significant increases after angioplasty compared with the respective values before angioplasty. Consequently, lumen CSA was dilated by about threefold after angioplasty (from 3.8±2.4 to 11.1±4.5 mm2). It was surprising that the EEM CSA also was dilated approximately twofold after angioplasty (from 11.1±5.3 to 19.8±8.1 mm2). In previous ultrasound examinations of arteries submitted to angioplasty, the vessel CSA of artery was either unchanged or slightly increased after angioplasty [1719]. These findings strongly suggest that this is a characteristic phenomenon of arterialized venous lesions, and the mechanism of dilatation of AVF stenoses by angioplasty is due mainly to vessel stretch.
We report qualitative and quantitative assessments of the AVF in haemodialysis patients by ultrasound imaging. IVUS imaging provided valuable information on the vessels. Our interest is in the increase of long-term AVF patency in patients undergoing PTA, stent placement and atherectomy or surgical repair. We recommend the clinical use of IVUS combined with angiography.
In conclusion, both qualitative and quantitative assessments of AVF in haemodialysis patients by IVUS are possible, and the viable mechanism of expansion of the stenoses by angioplasty is via stretching of the vessel wall and plaque fractures. This technique may be an important key with regard to the causes of AVF stenosis and restenosis following angioplasty.
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Notes |
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References |
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