Involvement of Matrix Metalloproteinase 9 in Vertebral Arterial Dissection With Posterior Circulation Ischemic Stroke

Background Spontaneous vertebral arterial dissection (VAD) is an important cause of posterior circulation ischemic stroke (PCS), but its pathogenesis remains elusive. Matrix metalloproteinase 9 (MMP‐9) is a gelatinase involved in inflammation process and several vascular diseases, such as aorta diss...

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Main Authors: Chun‐Yu Chen, Feng‐Chi Chang, I‐Hui Lee, Chih‐Ping Chung
Format: Article
Language:English
Published: Wiley 2020-10-01
Series:Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Subjects:
Online Access:https://www.ahajournals.org/doi/10.1161/JAHA.120.016743
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author Chun‐Yu Chen
Feng‐Chi Chang
I‐Hui Lee
Chih‐Ping Chung
author_facet Chun‐Yu Chen
Feng‐Chi Chang
I‐Hui Lee
Chih‐Ping Chung
author_sort Chun‐Yu Chen
collection DOAJ
description Background Spontaneous vertebral arterial dissection (VAD) is an important cause of posterior circulation ischemic stroke (PCS), but its pathogenesis remains elusive. Matrix metalloproteinase 9 (MMP‐9) is a gelatinase involved in inflammation process and several vascular diseases, such as aorta dissection, but its role in VBD is unclear yet. The present study aimed to determine the association between serum MMP‐9 level and VAD‐related PCS. Methods and Results We recruited 149 patients with PCS, of which 30 were VAD and 119 had other determined etiologies (non‐VAD), and 219 non‐stroke individuals. Serum MMP‐9 was measured within 14 days from stroke onset. The age of VAD group was 59.6±15.0 years, which is similar to non‐stroke group (P=0.510) but significantly younger than non‐VAD group (69.9±14.0 years, P<0.001). Males and vascular risk factors were significantly more prevalent in VAD and non‐VAD groups than non‐stroke group (P<0.001). Multivariate logistic regression analysis adjusting potential confounders revealed that every 100 ng/mL of serum MMP‐9 level increment significantly predicted VAD (versus non‐stroke group: odds ratio (OR), 4.572; 95% CI, 2.240–9.333, P<0.001; versus non‐VAD group: OR, 1.819; 95% CI, 1.034–3.200, P=0.038). Conclusions Patients with VAD‐related PCS had higher levels of serum MMP‐9 at the acute stage of stroke compared with non‐stroke individuals and PCS of other causes, supporting the potential involvement of extracellular matrix‐degrading protease in the mechanism of VAD, which leads to ischemic events.
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spelling doaj.art-0682da5ef0e74bddb97a5dbd3df90e172022-12-22T02:38:38ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802020-10-0191910.1161/JAHA.120.016743Involvement of Matrix Metalloproteinase 9 in Vertebral Arterial Dissection With Posterior Circulation Ischemic StrokeChun‐Yu Chen0Feng‐Chi Chang1I‐Hui Lee2Chih‐Ping Chung3Department of Neurology Neurological Institute Taipei Veterans General Hospital Taipei TaiwanDepartment of Radiology Taipei Veterans General Hospital Taipei TaiwanDepartment of Neurology Neurological Institute Taipei Veterans General Hospital Taipei TaiwanDepartment of Neurology Neurological Institute Taipei Veterans General Hospital Taipei TaiwanBackground Spontaneous vertebral arterial dissection (VAD) is an important cause of posterior circulation ischemic stroke (PCS), but its pathogenesis remains elusive. Matrix metalloproteinase 9 (MMP‐9) is a gelatinase involved in inflammation process and several vascular diseases, such as aorta dissection, but its role in VBD is unclear yet. The present study aimed to determine the association between serum MMP‐9 level and VAD‐related PCS. Methods and Results We recruited 149 patients with PCS, of which 30 were VAD and 119 had other determined etiologies (non‐VAD), and 219 non‐stroke individuals. Serum MMP‐9 was measured within 14 days from stroke onset. The age of VAD group was 59.6±15.0 years, which is similar to non‐stroke group (P=0.510) but significantly younger than non‐VAD group (69.9±14.0 years, P<0.001). Males and vascular risk factors were significantly more prevalent in VAD and non‐VAD groups than non‐stroke group (P<0.001). Multivariate logistic regression analysis adjusting potential confounders revealed that every 100 ng/mL of serum MMP‐9 level increment significantly predicted VAD (versus non‐stroke group: odds ratio (OR), 4.572; 95% CI, 2.240–9.333, P<0.001; versus non‐VAD group: OR, 1.819; 95% CI, 1.034–3.200, P=0.038). Conclusions Patients with VAD‐related PCS had higher levels of serum MMP‐9 at the acute stage of stroke compared with non‐stroke individuals and PCS of other causes, supporting the potential involvement of extracellular matrix‐degrading protease in the mechanism of VAD, which leads to ischemic events.https://www.ahajournals.org/doi/10.1161/JAHA.120.016743dissectionmatrix metalloproteinasesposterior circulationstrokevertebrobasilar
spellingShingle Chun‐Yu Chen
Feng‐Chi Chang
I‐Hui Lee
Chih‐Ping Chung
Involvement of Matrix Metalloproteinase 9 in Vertebral Arterial Dissection With Posterior Circulation Ischemic Stroke
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
dissection
matrix metalloproteinases
posterior circulation
stroke
vertebrobasilar
title Involvement of Matrix Metalloproteinase 9 in Vertebral Arterial Dissection With Posterior Circulation Ischemic Stroke
title_full Involvement of Matrix Metalloproteinase 9 in Vertebral Arterial Dissection With Posterior Circulation Ischemic Stroke
title_fullStr Involvement of Matrix Metalloproteinase 9 in Vertebral Arterial Dissection With Posterior Circulation Ischemic Stroke
title_full_unstemmed Involvement of Matrix Metalloproteinase 9 in Vertebral Arterial Dissection With Posterior Circulation Ischemic Stroke
title_short Involvement of Matrix Metalloproteinase 9 in Vertebral Arterial Dissection With Posterior Circulation Ischemic Stroke
title_sort involvement of matrix metalloproteinase 9 in vertebral arterial dissection with posterior circulation ischemic stroke
topic dissection
matrix metalloproteinases
posterior circulation
stroke
vertebrobasilar
url https://www.ahajournals.org/doi/10.1161/JAHA.120.016743
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