ORIGINAL ARTICLE  AORTIC DISEASE Free access

International Angiology 2022 August;41(4):277-84

DOI: 10.23736/S0392-9590.22.04847-7

Copyright © 2022 EDIZIONI MINERVA MEDICA

language: English

Positive association between calcium channel blocker treatment and persistent type II endoleak

Mária RAŠIOVÁ ¹ ✉, Martin KOŠČO ¹, Matej MOŠČOVIČ ¹, Viera HABALOVÁ ², Jozef ŽIDZIK ², Zuzana TORMOVÁ ¹, Marta BAVOĽÁROVÁ ³, Slavomír PEREČINSKÝ ⁴, Marek HUDÁK ¹, Ladislav KOČAN ⁵, Ivan TKÁČ ⁶

¹ Department of Angiology, East Slovak Institute of Cardiovascular Diseases, Faculty of Medicine, Šafárik University, Košice, Slovakia; ² Department of Biology, Faculty of Medicine, Šafárik University, Košice, Slovakia; ³ Department of Cardiology, Štefan Kukura Hospital, Michalovce, Slovakia; ⁴ Department of Occupational Medicine and Clinical Toxicology, Faculty of Medicine, Šafárik University, Košice, Slovakia; ⁵ Department of Anesthesiology and Intensive Medicine, Faculty of Medicine, East Slovak Institute of Cardiovascular Diseases, Šafárik University, Košice, Slovakia; ⁶ Department of Internal Medicine4, Faculty of Medicine, Šafárik University, Košice, Slovakia

BACKGROUND: Type II endoleaks are the most common complication occurring after endovascular abdominal aortic aneurysm repair (EVAR). The aims of our study were to evaluate the impact of persistent type II endoleak on sac dynamics post-EVAR, and to study the association between non-anatomical factors including polymorphisms associated with abdominal aortic aneurysm (AAA) and persistent type II endoleak.
METHODS: The cohort comprises 210 patients undergoing EVAR between January 2010 and December 2018. A persistent type II endoleak was defined as any type II endoleak lasting longer than six months and included also a type II endoleak diagnosed after six months or more post-EVAR during the 36-month follow-up period confirmed with CT-angiography. Anteroposterior AAA maximum diameter and AAA volume were measured pre-EVAR and 36 months post-EVAR using CT-angiographic pictures. Sac progression was defined as at least 5 mm increase, sac regression as at least 5 mm decrease in the sac diameter in relation to the preprocedural diameter. Sociodemographic information, comorbidities, treatment, laboratory parameters, selected anatomical and genetic factors were all analyzed to determine their impact on persistent type II endoleak. The adjustments included age, hypertension, diabetes mellitus, dyslipidemia, sex, smoking in multivariate analyses. When postprocedural diameter and volume were evaluated, adjustments included also preprocedural diameter/volume.
RESULTS: After exclusion, 178 patients with mean age 72.4±7.60 years remained for analysis. Persistent type II endoleak was found in 27.5% of patients (N.=49) and 2.94-times increased risk of sac progression in multivariate analysis (P=0.033). In multivariate analysis, AAA diameter in patients with persistent type II endoleak was 4.31 mm greater than in patients without (B=4.31; P=0.014); and its presence was also associated with 22.0 cm³ greater sac volume (B=22.0; P=0.034) compared to patients without persistent type II endoleak. Treatment with calcium channel blockers increased risk of persistent type II endoleak 2.11-times in multivariate analysis (OR=2.11; 95% CI: 1.05-4.25; P=0.037). No association between persistent type II endoleak and selected polymorphisms associated with AAA and other observed factors were found.
CONCLUSIONS: Risk of persistent type II endoleak was more than doubled in patients taking calcium channel blockers. Patients with persistent type II endoleak had greater anteroposterior sac diameter and sac volume compared to patients without persistent type II endoleak.

KEY WORDS: Endoleak; Calcium channel blockers; Aortic aneurysm, abdominal