AI Article Synopsis
- Matrix metalloproteinase-9 (MMP-9) is linked to blood-brain barrier disruption and may contribute to hemorrhagic transformation (HT) in stroke patients treated with tPA, particularly in those carrying a specific genetic mutation (C-1562T).
- A study analyzed 61 stroke patients receiving tPA, comparing genetic and MMP-9 levels with healthy controls, and checking for HT occurrence.
- Results showed no significant difference in HT rates between mutation carriers and non-carriers, indicating that while MMP-9 levels can predict hemorrhagic events, the C-1562T mutation does not significantly influence MMP-9 levels in response to stroke.
Article Abstract
Background And Purpose: Matrix metalloproteinase-9 (MMP-9) expression, related to blood-brain barrier disruption, has been implicated in the appearance of hemorrhagic transformation (HT) after tissue plasminogen activator (tPA) treatment in stroke patients. Because an in vitro functional polymorphism of the promoter region of MMP-9 gene (C-1562T) has been described, we hypothesize that patients carrying this mutation might have higher MMP-9 levels and greater susceptibility to developing HT when receiving tPA.
Methods: We studied strokes involving the middle cerebral artery territory of 61 patients who received tPA <3 hours after stroke onset. Blood samples were obtained before tPA administration. Plasmatic MMP-9 determinations were performed (enzyme-linked immunosorbent assay, ng/mL), and C-1562T genotype was determined by polymerase chain reaction. Healthy age-matched control subjects were used to study allele distribution (n=59). Hemorrhagic events were classified according to CT criteria (petechial hemorrhagic infarctions [HI,1 to 2] and large parenchymal hemorrhages [PH,1 to 2]).
Results: Allele distribution was similar in patients and control subjects (CC/CT/TT: 72.3/27.7/0% versus 79.7/20.3/0%, respectively; P=0.37). Among patients, mutation carriers (CT/TT alleles) had similar rates of HT and PH than noncarriers (HT: 23.1% versus 38.2%, P=0.49; PH: 15.4% versus 17.6%, P=1.0). Although the highest MMP-9 level corresponded to patients who later developed a PH (PH, 191.4 ng/mL; non-PH, 68.05 ng/mL; P=0.022), no relation between MMP-9 mutation presence and plasmatic levels was found (CC, 127.12 ng/mL; CT/TT, 46.31 ng/mL; P=0.11).
Conclusions: Although MMP-9 level predicts PH appearance after tPA treatment, no relationship exists with the C-1562T polymorphism, probably because this mutation is not functional in response to cerebral ischemia in vivo.
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| http://dx.doi.org/10.1161/01.STR.0000098648.54429.1C | DOI Listing |
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