Morphological Lesion Types Are Associated with Primary and Secondary Patency Rates after High-Pressure Balloon Angioplasty for Dysfunctional Arteriovenous Fistulas

Abstract

Background: Neointimal hyperplasia (NIH) is believed to be the main reason for arteriovenous fistula (AVF) dysfunction, but other mechanisms are also recognized to be involved in the pathophysiological process. This study investigated whether different morphological types of AVF lesions are associated with the patency rate after percutaneous transluminal angioplasty (PTA).

Methods: This retrospective study included 120 patients who underwent PTA for autogenous AVF dysfunction. All the cases were evaluated under Doppler ultrasound (DU) before intervention and divided into 3 types: Type I (NIH type), Type II (non-NIH type), and Type III (mixed type). Prognostic and clinical data were analyzed by Kaplan-Meier analysis and the Cox proportional hazards model.

Results: There was no statistical difference in baseline variables among groups, except for lumen diameter. The primary patency rates in Type I, Type II, and Type III groups were 78.4, 93.2, and 83.2% at 6 months and 59.5, 84.7, and 75.5% at 1 year, respectively. The secondary patency rates in Type I, Type II, and Type III groups were 94.4, 97.1, and 100% at 6 months and 90.5, 97.1, and 94.7% at 1 year, respectively. The Kaplan-Meier curve showed that the primary and secondary patency rates of Type I group were lower than those of Type II group. Multivariable Cox regression analysis demonstrated that postoperative primary patency was correlated with end-to-end anastomosis (hazard ratio [HR] = 2.997, p = 0.008, 95% confidence interval [CI]: 1.328-6.764) and Type I lesion (HR = 5.395, p = 0.004, 95% CI: 1.730-16.824).

Conclusions: NIH-dominant lesions of AVF evaluated by DU preoperatively were a risk factor for poor primary and secondary patency rate after PTA in hemodialysis patients.

Keywords: Arteriovenous fistula dysfunction; Hemodialysis; Morphological type; Neointimal hyperplasia; Patency rate.

Fig. 1

Ultrasonograms of typical AVF lesions. a Type I, intimal hyperplasia at the proximal vein: distance 1 shows the thickness of intima (1.5 mm); the residual lumen is 0.8 mm. b Type II, conduit constriction at the vein: distance 1 and 2, respectively, represent the normal (4.4 mm) and constricted lumen (1.7 mm); the intima (*) is <0.3 mm. c Type III, plaque at the artery: distance 1 and 2 represent the bypass (2.0 mm) and the thickness of plaque (2.0 mm), respectively. The borders between intima and lumen are shown on the figure as dotted lines. + measure; * intima; A, artery; V, vein; AVF, arteriovenous fistula.

Fig. 2

Ultrasonic and histopathological images of AVF lesions. Ultrasonic images show an AVF with significant Type I lesion (a) and an AVF with significant Type II lesion (b). HE stain (c, d) and Masson's trichrome stain (e, f) of these samples show their respective histopathology. L, lumen; I, intima; M, media; A, adventitia; AVF, arteriovenous fistula; HE, hematoxylin and eosin.

Fig. 3

Kaplan-Meier curve of primary (a) and secondary patency (b) of patients with Type I, Type II, and Type III lesions.