Prevalence of factor v leiden and prothrombin variant g20210a in patients age &lt;50 years with no significant stenoses at angiography three to four weeks after myocardial infarction

Water, Neil S. Van De; French, John K.; Lund, Mayanna; Hyde, T. A.; White, Harvey D.; Browett, Peter

doi:10.1016/s0735-1097(00)00772-5

“…However, other studies have demonstrated increased myocardial infarction risk associated with FVL carriers. 5,7,8,20 Because the prevalence of the homozygous state is so rare, 17 subjects (0.2%) in the Copenhagen City Heart Study and 0 subjects from the Physicians Health Study analysis, the associated risk for arterial thrombotic complications is difficult to determine. Mice homozygous for FVL have been previously generated and develop normally on a C57BL/6J genetic background.…”

Section: Discussionmentioning

confidence: 99%

Homozygosity for Factor V Leiden Leads to Enhanced Thrombosis and Atherosclerosis in Mice

Eitzman

¹

,

Westrick

²

,

Shen

³

et al. 2005

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Background— Activated protein C resistance due to factor V Leiden (FVL) is a common genetic risk factor for venous thrombosis in humans. Although the impact of FVL on the development of venous thrombosis is well established, its effect on arterial thrombosis and atherosclerosis is controversial. Methods and Results— To determine the effect of the FVL mutation on arterial thrombosis in the mouse, wild-type ( Fv +/+ ), heterozygous FVL ( Fv Q /+ ), and homozygous FVL ( Fv Q/Q ) mice underwent photochemical carotid arterial injury to induce occlusive thrombosis. Fv Q/Q mice formed occlusive thromboses 27±3 minutes (n=7) after the onset of injury, which was significantly shorter than that observed for Fv +/+ mice (56±7 minutes, n=9, P <0.01), whereas Fv Q /+ mice (41±7 minutes, n=5) were intermediate ( P =0.5, compared with Fv +/+ ). To determine the source of FVL relevant to the enhanced vascular thrombosis, bone marrow transplantation experiments were performed between Fv +/+ and Fv Q/Q mice. Fv Q/Q mice transplanted with Fv +/+ bone marrow formed occlusive thromboses at 35±5 minutes (n=7, P <0.05 compared with Fv +/+ mice), whereas Fv +/+ mice transplanted with Fv Q/Q bone marrow occluded at 59±7 minutes (n=6, P <0.001 compared with Fv Q/Q mice). To assess the effect of the FVL mutation on the development of atherosclerosis, Fv Q/Q mice were crossed with the atherosclerosis-prone apolipoprotein E (ApoE)–deficient strain ( ApoE −/− ) to generate Fv Q/Q ,ApoE −/− mice. By 52 weeks of age, Fv Q/Q ,ApoE −/− mice (n=8) had developed more aortic atherosclerosis (40±6% lesion area) compared with Fv +/+ ,ApoE −/− mice (15±3% lesion area; n=12, P <0.02). Conclusions— In conclusion, homozygosity for the FVL mutation in mice leads to enhanced arterial thrombosis and atherosclerosis. The source of the FVL leading to accelerated thrombosis appears to be circulating, non–platelet-derived plasma FVL.

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“…16,17,20) Van de Water, et al investigated the prevalence of prothrombin 20210GA and factor V Leiden mutations in 271 patients with myocardial infarction. Sixty of these patients (41 patients aged < 50 years and 19 patients aged > 50 years) had normal or near normal coronary arteries.…”

Section: Discussionmentioning

confidence: 99%

“…[13][14][15] Several recently published studies claim that there is a relation between both mutations and the risk for myocardial infarction. 16,17) However, there is no consensus yet on this subject. This study was planned to determine the prevalence of prothrombin 20210GA and factor V Leiden mutations, and their impacts on the development of myocardial infarction in patients younger than 55 years of age in Southern Turkey.…”

mentioning

confidence: 99%

Prothrombin 20210GA and Factor V Leiden Mutations in Patients Less Than 55 Years Old With Myocardial Infarction

Dönmez

¹

,

Kanadaşı

²

,

Tanrıverdi

³

et al. 2004

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SUMMARYSeveral studies claim that prothrombin 20210GA and factor V Leiden mutations are related to arterial thrombosis. We investigated the frequencies of these mutations and their significance in the development of early atherosclerosis in acute myocardial infarction (AMI) patients younger than 55 years of age. We investigated 96 patients with AMI and 77 control subjects. The diagnosis of AMI was established by typical chest pain and ST elevations on the presentation electrocardiogram and characteristic cardiac enzyme elevations. None of the control subjects had evidence of cardiovascular disease. DNA samples were isolated from all subjects and prothrombin 20210GA and factor V Leiden mutations were determined by the RealTime PCR technique with the aid of a Light Cycler device. The prevalence of factor V Leiden mutation was 6.3% and 5.2% in the patient and control groups, respectively (OR 0.6 [95% CI 0.1-3.9], P = 0.6), whereas the prevalence of prothrombin G20210A mutation was 4.2% and 2.6% in the patient and control groups, respectively (OR 2.8 [95% CI 0.2 -32.2], P = 0.4). None of the patients had both mutations. Prothrombin 20210GA and factor V Leiden mutations are not significant risk factors for the development of myocardial infarction in patients less than 55 years old in Southern Turkey. (Jpn Heart J 2004; 45: 505-512)

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“…Two meta-analyses showed that MI risk is increased 1.3 fold in patients carrying the 1691A allele [27]. The elevation of the risk did not reach statistical significance in another meta-analysis [22].…”

Section: Discussionmentioning

confidence: 94%

Polymorphisms of some increased cardiovascular risk related genes in acute coronary syndromes and their relation to coronary artery disease severity

Gül¹,

Küçükdurmaz²,

Kalay³

et al. 2012

pwki

0

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A b s t r a c tBackground: β-Fibrinogen 455G/A, factor V 1691G/A, 1299H/A and glycoprotein IIb/IIIa PL A1/A2 polymorphisms are tought to be related to arterial thrombotic disorders, especially coronary artery disease (CAD) and myocardial infarction (MI).Aim: The aims of this study were to investigate the frequencies of these polymorphisms in subgroups of acute coronary syndromes (ACS) and the effects of these polymorphisms on the angiographic findings of patients with ACS.Material and methods: The study included 35 patients (mean age 61 years) diagnosed with ACS who underwent coronary angiography. The patients with ST elevation MI comprised group I and patients without ST elevation comprised group II.Results: The groups were not different regarding clinical properties of patients and CAD risk factors. The numbers of patients with β-fibrinogen 455A, factor V 1691A and 1299A, and glycoprotein IIb/IIIa PL A2 alleles were 7 (46.7%) and 8 (40%), 3 (20%) and 4 (20%), 3 (20%) and 3 (15%), and 3 (20%) and 5 (25%), in groups I and II respectively (p = 0.69, p = 1.0, p = 0.69, p = 0.72, respectively). Angiographic findings were not related to these polymorphisms.Conclusions: We did not find any relation among ACS subtype and angiographic severity of coronary atherosclerosis with β-fibri nogen 455G/A, factor V 1691G/A, 1299H/A and glycoprotein IIb/IIIa PL A1/A2 polymorphisms. These findings suggest that these polymorphisms have no effects on the relative magnitude of thrombus responsible for ACS or the severity of the occlusion of the coronary artery related ACS. Future studies with larger groups may reveal whether these genetic alterations have a significant impact on ACS.Key words: acute coronary syndrome, coagulation protein, genes, polymorphism S t r e s z c z e n i e Wstęp: Polimorfizmy 455G/A β-fibrynogenu, 1691G/A i 1299H/A czynnika V oraz PL A1/A2 glikoproteiny IIb/IIIa wiążą się z powikła-niami zakrzepowymi w układzie tętniczym, zwłaszcza z chorobą wieńcową i zawałem serca.Cel: Celem badania była ocena częstości występowania badanych polimorfizmów u pacjentów z różnymi typami ostrych zespołów wieńcowych (OZW) oraz ocena wpływu tych polimorfizmów na zmiany stwierdzane w koronarografii u pacjentów z OZW.Materiał i metody: Badaniem objęto 35 pacjentów (średni wiek 61 lat) z rozpoznaniem OZW, u których wykonano koronarografię. Pacjenci z zawałem serca z uniesieniem odcinka ST stanowili grupę I, a pacjenci bez uniesienia odcinka ST -grupę II.Wyniki: Nie wykazano różnic dotyczących charakterystyki klinicznej i obecności czynników ryzyka wystąpienia choroby wień-cowej pomiędzy grupami. Liczba pacjentów z allelem 455A β-fibrynogenu, 1691A i 1299A czynnika V oraz PL A2 glikoproteiny IIb/IIIa wynosiła odpowiednio w grupie I i II: 7 (46,7%) i 8 (40%), 3 (20%) i 4 (20%), 3 (20%) i 3 (15%) oraz 3 (20%) i 5 (25%) (odpowiednio: p = 0,69, p = 1,0, p = 0,69, p = 0,72). Zmiany stwierdzane w koronarografii nie wykazywały związku z obecnością tych polimorfizmów.Wnioski: Nie stwierdzono żadnego związku pomiędzy typem OZW, ciężkością n...

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Prevalence of factor v leiden and prothrombin variant g20210a in patients age <50 years with no significant stenoses at angiography three to four weeks after myocardial infarction

Abstract: The frequencies of factor V Leiden and/or prothrombin variant G20210A are increased in patients age <50 years with normal or near normal coronary arteries after MI.

Cited by 72 publications

References 36 publications

Homozygosity for Factor V Leiden Leads to Enhanced Thrombosis and Atherosclerosis in Mice

Homozygosity for Factor V Leiden Leads to Enhanced Thrombosis and Atherosclerosis in Mice

Prothrombin 20210GA and Factor V Leiden Mutations in Patients Less Than 55 Years Old With Myocardial Infarction

Polymorphisms of some increased cardiovascular risk related genes in acute coronary syndromes and their relation to coronary artery disease severity

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