Plasminogen activator inhibitor-1 promoter 4G/5G genotype is not a risk factor for myocardial infarction in a Japanese population

Sugano, Tomoko; Tsuji, Hisako; Masuda, Hiroya; Nakagawa, Keiko; Nishimura, Hideo; Kasahara, Tomoko; Yoshizumi, Masami; Nakahara, Yoshifumi; Kitamura, Hidetsugu; Yamada, Koichi; Yoneda, Mitsuru; Maki, Kei; Tatsumi, Tadashi; Azuma, Arata; Nakagawa, Masayuki

doi:10.1097/00001721-199803000-00013

Cited by 17 publications

(9 citation statements)

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“…Of immediate note in this study was the markedly lower frequency of the PAI 1 4G allele (12–15%) in this African population compared with 30% in the Japanese (22) and approximately 50% reported in Caucasians by Hooper et al (23) and ourselves in the present study (Table I). Given this low frequency, coupled with the 2% incidence of homozygosity, it would seem unlikely that the hypofibrinolytic effect of the PAI 1 4G allele has any major impact on Black African women, at least in the patho‐etiolgy of PE, a condition that affects approximately 18% of pregnancies (21).…”

Section: Discussionsupporting

confidence: 47%

Plasminogen activator inhibitor type 1 (PAI1) and platelet glycoprotein IIIa (PGIIIa) polymorphisms in Black South Africans with pre‐eclampsia

Pegoraro¹,

Hira

Rom³

et al. 2003

Acta Obstet Gynecol Scand

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Neither the 4G allele of the plasminogen activator inhibitor Type 1 nor the PlA2 allele of the platelet glycoprotein IIIa have any significant role as risk factors in the patho-etiology of pre-eclampsia in Black South Africans, although these genes cannot yet be excluded as contributory to this disorder. It is possible that the underlying causes of pre-eclampsia may vary between different ethnic populations.

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Section: Discussionsupporting

confidence: 47%

Plasminogen activator inhibitor type 1 (PAI1) and platelet glycoprotein IIIa (PGIIIa) polymorphisms in Black South Africans with pre‐eclampsia

Pegoraro¹,

Hira

Rom³

et al. 2003

Acta Obstet Gynecol Scand

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“…13,15,[35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50] From those, 11 studies were excluded because they did not use solid diagnostic criteria for myocardial infarction [43][44][45][46][47][48][49] or because of inadequate delineation of cases 15,50 or an inadequate spectrum of cases, 13,42 leaving 7 studies in the analysis. The qualifying 7 studies described a total of 2813 patients and 3358 controls from 8 distinct populations.…”

Section: Pai-1 4g/5g Polymorphismmentioning

confidence: 99%

Genetic Variation in Coagulation and Fibrinolytic Proteins and Their Relation With Acute Myocardial Infarction

et al. 2001

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Background-It is pathophysiologically conceivable that genetic variations in coagulation and fibrinolytic proteins are associated with the risk of myocardial infarction. Methods and Results-We performed a literature search to identify published case-control studies correlating the factor V Leiden or prothrombin G20210A mutations or fibrinogen GϪ455A or plasminogen activator inhibitor-1 (PAI-1) 4G/5G polymorphisms with the risk of myocardial infarction. Studies were included only if they used solid diagnostic criteria and complied with published methodological criteria. A common OR with corresponding 95% CI was calculated for the risk of myocardial infarction in a fixed-effect model according to Mantel-Haenszel. The factor V Leiden and prothrombin G20201A mutations did not significantly correlate with myocardial infarction (OR 1.26, 95% CI 0.94 to 1.67, Pϭ0.12 and OR 0.89, 95% CI 0.59 to 1.35, Pϭ0.6, respectively). Inclusion of the studies that investigated young patients (Ͻ55 years) made the association significant for factor V Leiden (OR 1.29, 95% CI 1.03 to 1.61, Pϭ0.02). Homozygosity for the fibrinogen Ϫ455A allele was significantly associated with a decreased risk of myocardial infarction (OR 0.66, 95% CI 0.44 to 0.99, Pϭ0.04), whereas the PAI-1 4G4G genotype was significantly associated with increased risk (OR 1.20, 95% CI 1.04 to 1.39, Pϭ0.04). Conclusions-Associations between these genetic variations and myocardial infarction were weak or absent. In the absence of clinical implications, our results indicate that screening of patients with myocardial infarction for these genetic variations is not warranted. Key Words: myocardial infarction Ⅲ genetics Ⅲ coagulation T hrombosis, triggered by atherosclerotic plaque rupture, is generally accepted as the most common pathogenetic pathway of acute myocardial infarction. 1 In recent years, several genetic variations in coagulation and fibrinolytic proteins have been described, and numerous case-control studies have sought to correlate these genetic variations with the risk of myocardial infarction. However, clear relationships have not been established, possibly owing to lack of statistical power of the individual studies or their heterogeneity in terms of methodological design, outcome definition, or selection of cases and controls. We hypothesized that a meta-analysis could provide stronger evidence in favor of the hypothesis that genetic variations in coagulation or fibrinolytic proteins are associated with the risk of myocardial infarction. We limited our analysis to 4 genetic variations that are common and on which sufficient published data were available, ie, the factor V Leiden and prothrombin G20210A mutations and the fibrinogen ␤-chain GϪ455A and plasminogen activator inhibitor-1 (PAI-1) 4G/5G polymorphisms. Methods Literature SearchWe identified all case-control studies correlating the factor V Leiden mutation, the prothrombin G20210A mutation, the fibrinogen ␤-chain GϪ455A polymorphism, or the PAI-1 4G/5G polymorphism with myocardial infarction. The lit...

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“…Previous studies had demonstrated the association between 4G allele, high PAI-1 concentrations and CAD [12][13][14][15][16] . Although this may be a promising correlation, it may not be demonstrated in all populations [17][18][19] . This is the first study to demonstrate this correlation in the Brazilian population.…”

Section: Discussionmentioning

confidence: 93%

Associação de níveis plasmáticos de PAI-1 e polimorfismo 4G/5G em pacientes com doença arterial coronariana

Lima

Carvalho

Neto

et al. 2011

Arq. Bras. Cardiol.

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Plasminogen activator inhibitor-1 promoter 4G/5G genotype is not a risk factor for myocardial infarction in a Japanese population

Cited by 17 publications

References 0 publications

Plasminogen activator inhibitor type 1 (PAI1) and platelet glycoprotein IIIa (PGIIIa) polymorphisms in Black South Africans with pre‐eclampsia

Plasminogen activator inhibitor type 1 (PAI1) and platelet glycoprotein IIIa (PGIIIa) polymorphisms in Black South Africans with pre‐eclampsia

Genetic Variation in Coagulation and Fibrinolytic Proteins and Their Relation With Acute Myocardial Infarction

Associação de níveis plasmáticos de PAI-1 e polimorfismo 4G/5G em pacientes com doença arterial coronariana

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