Involvement of Matrix Metalloproteinase 9 in Vertebral Arterial Dissection With Posterior Circulation Ischemic Stroke
Author(s) -
ChunYu Chen,
FengChi Chang,
IHui Lee,
ChihPing Chung
Publication year - 2020
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.120.016743
Subject(s) - medicine , stroke (engine) , odds ratio , confounding , dissection (medical) , etiology , matrix metalloproteinase , cardiology , vertebral artery dissection , gastroenterology , surgery , engineering , mechanical engineering
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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