Factor V Leiden (Resistance to Activated Protein C) Increases the Risk of Myocardial Infarction in Young Women

Rosendaal, Frits R.; Siscovick, David S.; Schwartz, Stephen M.; Beverly, Robert K.; Psaty, Bruce M.; Longstreth, W. T.; Raghunathan, Trivellore E.; Koepsell, Thomas D.; Reitsma, Pieter H.

doi:10.1182/blood.v89.8.2817

Cited by 362 publications

(142 citation statements)

References 30 publications

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“…The prevalence of FV Leiden mutation was similar in patients with and without AT (5/79, 5.9% and 9/211, 4% respectively, p ‫ס‬ 0.337). This is not surprising, as no clear association of FV Leiden mutation and arterial thrombosis has been found in general population and in selected cases [25][26][27][28]. Our results suggest that the presence of FV Leiden in patients with PV and ET and arterial thrombosis may indeed be casual.…”

Section: Discussionmentioning

confidence: 45%

Factor V Leiden mutation carriership and venous thromboembolism in polycythemia vera and essential thrombocythemia

et al. 2002

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Polycythemia Vera (PV) and Essential Thrombocythemia (ET) are chronic myeloproliferative disorders complicated by a high incidence of thrombotic complications. Extensive coagulation studies failed to demonstrate a consistent pattern of abnormalities associated with thrombosis. Recently, a poor anticoagulant response to activated protein C (APC), due to a mutation of factor V (FV Leiden), has been identified as the most frequent hereditary disorder associated with venous thrombophilia. We investigated in 304 patients with PV and ET whether the presence of FV Leiden could be a risk factor for thrombosis. FV Leiden was found in 14/304 patients (4.6%) and was associated with venous thromboembolism (VTE) occurred before and at diagnosis (5/27,16%, with a significant difference of prevalence in comparison of that observed in asymptomatic patients, 9/263, 3%, p = 0.003). Carriership of FV Leiden was associated with VTE relapse, with a prevalence of 3.6% in asymptomatic patients, 6.9% in patients with a single episode of VTE and 18.1% in patients with recurrent VTE. The prevalence of FV Leiden in patients with and without arterial thrombosis was similar (5/79, 6% and 9/211, 4%, respectively, p = 0.337). This study indicates that the prevalence of the FV Leiden mutation in patients with PV and ET is comparable with that observed in the general population. FV Leiden mutation is a risk factor for VTE before and at time of diagnosis and for VTE recurrences. Screening for FV Leiden may be considered to identify PV and ET patients at higher risk of recurrences. Am. J. Hematol. 71:1-6, 2002.

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Section: Discussionmentioning

confidence: 45%

Factor V Leiden mutation carriership and venous thromboembolism in polycythemia vera and essential thrombocythemia

et al. 2002

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“…Combined genetic defects appear to act synergistically, increasing the risk of VTE several fold: 73% of family members with combined protein C deficiency and factor V Leiden and 80% of patients with factor V Leiden and protein S deficiency will exhibit a VTE before age 40 [5,6]. Furthermore, co-existing clinical risk factors and the factor V Leiden mutation also increase the risk of thromboembolic events, e.g., oral contraceptives increase the risk 35-fold [7] while tobacco increases the risk of developing myocardial infarction 32-fold [8]. In addition, management of venous thrombosis is influenced by the laboratory findings [9].…”

Section: Discussionmentioning

confidence: 99%

Spontaneous venous thrombosis in a young patient with combined factor V Leiden and lupus anticoagulant

et al. 1999

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We describe a case of a 28-year-old man who developed an extensive spontaneous deep venous thrombosis. Testing revealed heterozygotic factor V Leiden mutation, and the presence of both lupus anticoagulant (LA) and elevated IgM anticardiolipin antibody (ACA). Several family members were found to be heterozygous for factor V Leiden. A paternal aunt had the factor V Leiden mutation, an elevated plasma homocysteine and a borderline increased IgG ACA level. No other family member had a history of a venous thrombotic event. This case illustrates that evaluation of young patients who present with venous thrombosis should be performed for both hereditary and acquired thrombophilic defects. The family studies suggest that the presence of a lupus anticoagulant may be more clinically significant then elevated ACA in risk assessment. Although screening family members when the proband carries factor V Leiden is controversial, psychological reassurance of those who test negative and simple advice on occupations or social habits (e.g., smoking) for those who test positive may be important benefits. Am. J. Hematol. 62:58-60, 1999.

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“…157,166 Carriers of this mutation appear to be at increased risk of deep vein thrombosis, 152,167,168 and young women carriers are at increased risk of myocardial infarction, particularly if they smoke. 169 implicated in poor pregnancy outcomes related to thrombotic events in the mother, the placenta and the fetus 152±156,170,171 although it does not appear to relate to miscarriage. 172 The maternal genotype affects thrombotic risk in the mother, whereas the fetal genotype may affect thrombosis in the fetus and placenta.…”

Section: Social and Personal Antecedents In The Maternal Vascular Dismentioning

confidence: 99%

Pregnancy outcomes and community health: the POUCH study of preterm birth

Holzman¹,

Bullen²,

Fisher

et al. 2001

Paediatric Perinatal Epid

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In light of the social/ethnic disparity in preterm delivery (PTD) rates, the Pregnancy Outcomes and Community Health (POUCH) Study takes a broad view of the determinants of PTD by attempting to link underlying biological and psychosocial factors. The relationships between placental pathology, maternal biomarkers, and antecedent psychosocial factors are evaluated in three hypothesised pathways of PTD – one characterised primarily by infection, one by maternal vascular disease, and one by premature elevations in corticotropin releasing hormone in the absence of histological evidence of placental pathology. Within each pathway, an emphasis is placed on understanding the roles of stress and of maternal serum alpha‐fetoprotein, an early biomarker associated with PTD. The POUCH Study enrols pregnant women from five Michigan communities. Information about these women and their environments is gathered through detailed interviews and collection of biological samples including hair, urine, saliva, blood, vaginal fluid, and vaginal smear at 15–26 weeks of gestation. We have chosen to focus on the second trimester – a time when pathological processes may have evolved to a detectable stage, but generally before the onset of biological changes that accompany labour. This focus is consistent with the long‐range goal of early detection/intervention and prevention of PTD.

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Factor V Leiden (Resistance to Activated Protein C) Increases the Risk of Myocardial Infarction in Young Women

Cited by 362 publications

References 30 publications

Factor V Leiden mutation carriership and venous thromboembolism in polycythemia vera and essential thrombocythemia

Factor V Leiden mutation carriership and venous thromboembolism in polycythemia vera and essential thrombocythemia

Spontaneous venous thrombosis in a young patient with combined factor V Leiden and lupus anticoagulant

Pregnancy outcomes and community health: the POUCH study of preterm birth

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