Low Common Carotid Artery Systolic Occlusion Pressure and Symptomatic Carotid Artery Stenosis Are Associated with Development of Neurologic Intolerance during Proximal Protected Carotid Artery Stenting
- Author:
Hee Jin KWON
1
;
Jae Hyeong PARK
;
Jae Hwan LEE
;
Hye Seon JEONG
;
Hee Jung SONG
;
Jei KIM
;
Mijoo KIM
;
In Sun KWON
;
In Whan SEONG
Author Information
- Publication Type:Original Article
- From:Korean Circulation Journal 2018;48(3):217-226
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND AND OBJECTIVES:Neurologic intolerance (NI) is defined as the occurrence of neurological symptoms during carotid artery stenting (CAS). Because NI is inevitable problem, it may be helpful to anticipate its occurrence. So, we studied factors associated with NI during proximal protected CAS.
METHODS:We retrospectively analyzed all consecutive patients underwent proximal protected CAS from August 2012 to January 2017.
RESULTS:We included total 123 patients (109 males, 72±8 years old). The total procedure time was 43±12 minutes, and mean occlusion time was 4.8±1.2 minutes. We divided CAS patients into 2 groups according to presence of NI; neurologic tolerance (NT; n=74, 60%) and NI (n=49, 40%) groups. After the univariate analysis, symptomatic carotid artery stenosis (p = 0.003), absence of anterior communicating artery (p = 0.015) and low common carotid artery occlusion pressure (CCAOP, p < 0.001) were associated with NI. After the multivariate analysis, NI was significantly associated with symptomatic carotid artery stenosis (odds ratio [OR], 5.549; p = 0.014) and systolic CCAOP≤42 mmHg (OR, 6.461; p < 0.001). In NI group, 43 patients (88%) recovered right after the balloon deflation and 2 patients were normalized within 2 hours. However, 1 had major stroke and 3 had minor strokes in 4 patients with persistent NI ≥24 hours.
CONCLUSIONS:About 40% showed NI during the CAS. Most of them (88%, 43 of 49 patients) recovered after the balloon deflation, but stroke incidence was significantly higher in NI group. Symptomatic carotid artery stenosis and systolic CCAOP ≤42 mmHg were significantly associated with the development of NI during proximal protected CAS.
