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Fibrinolytic gene polymorphism and ischemic stroke.
Stroke. 2005 Oct; 36(10):2077-81.S

Abstract

BACKGROUND AND PURPOSE

The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke.

METHODS

In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria.

RESULTS

There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P<0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke.

CONCLUSIONS

Neither the tPA -7351C>T nor the PAI-1 to 675 4G>5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart.

Authors+Show Affiliations

Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16179568

Citation

Jood, Katarina, et al. "Fibrinolytic Gene Polymorphism and Ischemic Stroke." Stroke, vol. 36, no. 10, 2005, pp. 2077-81.
Jood K, Ladenvall P, Tjärnlund-Wolf A, et al. Fibrinolytic gene polymorphism and ischemic stroke. Stroke. 2005;36(10):2077-81.
Jood, K., Ladenvall, P., Tjärnlund-Wolf, A., Ladenvall, C., Andersson, M., Nilsson, S., Blomstrand, C., & Jern, C. (2005). Fibrinolytic gene polymorphism and ischemic stroke. Stroke, 36(10), 2077-81.
Jood K, et al. Fibrinolytic Gene Polymorphism and Ischemic Stroke. Stroke. 2005;36(10):2077-81. PubMed PMID: 16179568.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fibrinolytic gene polymorphism and ischemic stroke. AU - Jood,Katarina, AU - Ladenvall,Per, AU - Tjärnlund-Wolf,Anna, AU - Ladenvall,Claes, AU - Andersson,Maria, AU - Nilsson,Staffan, AU - Blomstrand,Christian, AU - Jern,Christina, Y1 - 2005/09/22/ PY - 2005/9/24/pubmed PY - 2006/1/13/medline PY - 2005/9/24/entrez SP - 2077 EP - 81 JF - Stroke JO - Stroke VL - 36 IS - 10 N2 - BACKGROUND AND PURPOSE: The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke. METHODS: In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria. RESULTS: There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P<0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke. CONCLUSIONS: Neither the tPA -7351C>T nor the PAI-1 to 675 4G>5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart. SN - 1524-4628 UR - https://www.unboundmedicine.com/medline/citation/16179568/Fibrinolytic_gene_polymorphism_and_ischemic_stroke_ L2 - https://www.ahajournals.org/doi/10.1161/01.STR.0000183617.54752.69?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -