Relationship of lysophosphatidic acid and matrix metalloproteinase-9 with carotid atheromatous plaque stability in patients with cerebral infarction
10.3760/cma.j.issn.0254-9026.2010.02.008
- VernacularTitle:脑梗死患者血浆溶血磷脂酸及基质金属蛋白酶-9与颈动脉斑块稳定性研究
- Author:
Chunlian PAN
;
Lifang ZHENG
- Publication Type:Journal Article
- Keywords:
Lysophospholipids;
Matrix metalloproteinase 9;
Carotid Stenosis;
Brain infarction
- From:
Chinese Journal of Geriatrics
2010;29(2):115-118
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the correlation of plasma lysophosphatidic acid (LPA) and matrix metalloproteinase-9 (MMP-9) with carotid atheromatous plaque stability in patients with cerebral infarction. Methods The duplex uhrasonography and transcranial Doppler-detected microemboli were performed in the carotid arteries of all the 87 patients with cerebral infarction located in arteriae carotis interna system. The patients were divided into the intima thickening group (n=16),unstable plaque group (n=41), stable plaque group (n=21) and non-plaque group (n=9). And there were 27 patients with positive microembolic signal and 60 patients with negative microembolic signal.The plasma levels of LPA and MMP-9 were determined by quantitative determination of inorganic phosphorus and enzyme-linked immunosorbent assay. Results The levels of LPA and MMP-9 were significantly higher in unstable plaque group than in the other three groups (F=49.98 and 106.49,both P<0.01), MMP-9 in intima thickening group and stable plaque group were both higher than in non-plaque group (q=7.04 and 7.51, both P=0. 00). LPA was higher in intima thickening group than in stable plaque group (q=7.37, P=0. 00), and higher in the above two groups than in non-plaque group (both P<0.05). The levels of LPA and MMP-9 were higher in microembolic signal-positive patients than in signal-negative patients (t=42.57 and 16.61, both P=0.00). LPA level was positively correlated with MMP-9 (r=0.22, P<0.05). Conclusions LPA and MMP-9 may serve as a potential risk signal to hint the formation and rupture of unstable carotid atheromatous plaque which may cause ischemic cerebrovascular disease.
