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Tissue plasminogen activator -7351C/T enhancer polymorphism is a risk factor for lacunar stroke
Jim Jannes1, Monica A Hamilton-Bruce, Louis Pilotto
1Department of Medicine, University of Adelaide, The Queen Elizabeth Hospital, Woodville South, South Australia.
Stroke
|March 20, 2004
Summary
The TPA -7351C/T polymorphism, specifically the TT genotype, is linked to an increased risk of lacunar stroke. This suggests impaired fibrinolysis may contribute to lacunar stroke development.
Area of Science:
- Genetics and Molecular Biology
- Neurology
- Cardiovascular Research
Background:
- Occlusive thrombosis is a key factor in ischemic stroke.
- Endogenous tissue plasminogen activator (TPA) mediates fibrinolysis and is linked to the TPA -7351C/T polymorphism.
- This polymorphism may influence TPA release and lacunar stroke pathogenesis.
Purpose of the Study:
- To investigate the association between the TPA -7351C/T polymorphism and the risk of lacunar and nonlacunar ischemic stroke.
- To determine if the TPA -7351C/T polymorphism is an independent risk factor for stroke subtypes.
Main Methods:
- A case-control study involving 182 ischemic stroke cases and 301 controls.
- Genotyping for the TPA -7351C/T polymorphism using polymerase chain reaction (PCR).
- Logistic regression analysis adjusted for known cerebrovascular risk factors.
Main Results:
- The TT genotype prevalence was 9% in controls and 13% in stroke patients.
- The TT genotype was significantly associated with an increased risk of ischemic stroke (OR: 1.9).
- A significant association was found between the TT genotype and lacunar stroke (OR: 2.7), but not nonlacunar stroke.
Conclusions:
- The TPA -7351C/T polymorphism, particularly the TT genotype, is an independent risk factor for lacunar stroke.
- Impaired fibrinolysis is suggested to play a role in the pathogenesis of lacunar stroke.
- Further research into genetic factors influencing fibrinolysis in stroke is warranted.