The aim of this study was to identify the predictive factors for the development of type II endoleaks (EL-II) after endovascular aneurysm repair (EVAR).
Methods
We assessed the preoperative and postoperative computed tomography data of 308 patients who underwent EVAR between 2000 and 2012 and in 84 of whom primary or secondary EL-II occurred. The data analyzed were: demographics, number and diameter of lumbar arteries (LAs), inferior mesenteric artery (IMA), median sacral artery (MSA), accessory renal arteries (ARas), maximum diameter of infrarenal abdominal aortic aneurysm, diameter and length of proximal aortic neck. Statistical analysis was performed using Stata software (version 12). Categorical parameters were compared between groups using chi-squared or Fisher's exact tests as appropriate. Continuous variables were analyzed using Student's t-test or Mann–Whitney test as appropriate (normality studied by the Shapiro–Wilk and homoscedasticity verified using the Fisher–Snedecor test).
Results
Of the 308 patients included (mean age, 73.8 ± 8.74 years), 284 (92%) were men, 61 (20%) were smokers, 113 (37%) had chronic obstructive pulmonary disease, 215 (70%) were taking antiplatelet. Respectively, 13, 51, 60, 103, 28, 40, 2, and 7 patients had 1, 2, 3, 4, 5, 6, 7, and 8 patent LAs. Before surgery, 221 IMAs and 136 MSA were patent. The sources of EL-II were: LA (n = 51), IMA (n = 22), MSA (n = 1), IMA and LA (n = 8), IMA and ARa (n = 1), and unknown (n = 1). Logistic regression models adjusting for clinically relevant covariables (age, American Society of Anesthesiologists, smoking status, dyslipidemia, and diuretics) were proposed to study morphologic EL-II predictive factors, first in the entire population, and then in the more specific population for whom IMA was patent. Risk factors of occurrence EL-II were: permeability of the IMA (70 patients [83%] vs. 155 [69%], P = 0.01), IMA diameter (3.49 mm vs. 2.71 mm, P < 0.001), number of LAs patent higher than or equal to 4 (P < 0.001), the mean LA diameter greater than 2.4 mm (P < 0.001), and MSA diameter (2.28 mm vs. 1.94 mm; P < 0.01).
Conclusions
Our results show the major role of the number and diameter of the patent aortic branches in the development of EL-II. As they can result in complications increasing the morbidity and mortality after EVAR, it is relevant to identify the risk factors of their occurrence.
