Ischaemic stroke patients with heterozygous factor V Leiden present with multiple brain infarctions and widespread atherothrombotic disease

2009 ◽  
Vol 101 (01) ◽  
pp. 145-150 ◽  
Author(s):  
Johanna Helenius ◽  
Dimitrije Jakovljeviâ ◽  
Lauri Soinne ◽  
Martti Syrjälä ◽  
Markku Kaste ◽  
...  
Keyword(s):  
Family History ◽  
Ischaemic Stroke ◽  
Arterial Thrombosis ◽  
Clinical Laboratory ◽  
Positive Family History ◽  
Factor V Leiden ◽  
Stroke Severity ◽  
Cerebrovascular Event ◽  
Factor V ◽  
History Of

SummaryFactor V Leiden (FVL) mutation is a risk factor for venous and, to a degree, arterial thrombosis. It is unknown whether and how FVL affects the manifestations of ischaemic stroke (IS). We assessed the clinical, laboratory, radiological, and prognostic characteristics in an observational study with adult IS patients having FVL. We tested 860 patients with first-ever IS for FVL and found 48 FVL positive patients. Detailed clinical, laboratory, and radiological evaluation were compared with that of 144 (1:3) gender and age matched IS patients without FVL. All patients underwent a prognostic evaluation at an average of five years follow-up. Despite the relatively young age (mean 48.5 years, range 44–54 years) of the FVL positive IS patients, peripheral arterial occlusive disease (PAOD), coronary artery disease (CAD), and previous transient cerebrovascular event occurred more frequently compared with controls. Family history of cardiovascular disease (CVD) and multiple silent brain infarctions were revealed in half of the FVL positive patients, whereas these were seldom encountered among controls. Stroke severity, long-term recovery, and recurrence rates seemed similar irrespective of FVL status. Our findings indicate that the clinical profile of IS patients with FVL associated with wider manifestation of atherothrombosis, positive family history of arterial thrombosis, and presence of multiple silent infarctions on brain images.

Application of Thrombomodulin-Thrombin Generation to Diverse Abnormalities of the Protein C System

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 31-32
Author(s):  
Marilyn J Manco-Johnson ◽  
Linda Jacobson ◽  
Dianne Thornhill ◽  
Christine Baird ◽  
Beth Boulden Warren
Keyword(s):  
Family History ◽  
Lupus Anticoagulant ◽  
Protein C ◽  
Thrombin Generation ◽  
Conflicts Of Interest ◽  
Positive Family History ◽  
Factor V Leiden ◽  
Healthy Controls ◽  
Blood Draw ◽  
History Of

Background: Increased thrombin generation is an interesting candidate as a potential indicator of hypercoagulability and thrombosis risk. Increased thrombin generation using the calibrated automated thrombogram (CAT) has been reported in antithrombin deficiency but the CAT does not reflect protein C deficiency without the addition of thrombomodulin (TM). TM activates protein C (PC) in the CAT and reduces thrombin generation. Objective: The objective of this study was to determine the capacity of the TM-augmented CAT to detect defects in various protein C system components; the lupus anticoagulant was also investigated as a cause of decreased protein C activation. Methods: The CAT-TM was performed with reagents and methods per the manufacturer's instructions using 5 pM tissue factor and TM (Stago). Other assays included: PC (chromogenic), free protein S (PS, LIA), activated protein C resistance (aPTT-based clotting assay), factor V Leiden (FVL PCR) and lupus anticoagulant (LA, dRVVT and Staclot LA, Stago). Platelet poor plasma samples were obtained from the biobank of a consented prospective inceptional cohort study of thrombosis and thrombophilia or a positive family history of either (ThromboPICS #05-0339); samples from healthy controls with no personal or family history of thrombosis or thrombophilia were collected on a consented protocol (#09-0816). Samples from participants on therapeutic inhibitors of factor Xa or thrombin were treated with appropriate neutralizers; no sample was tested on warfarin. Clinical data included gender, age (< 18 versus ≥ 18 years), history of thrombosis, timing of sample from most recent thrombosis (acute < 14 days; subacute 14-90 days; or chronic > 90 days) and use of anticoagulants at the time of the blood draw. Tests for violations of normality were negative. Therefore, results of cohorts versus controls were compared with independent sample t-test and subgroup analyses relative to control used One-Way ANOVA. Post-hoc comparisons of each subgroup to the controls were collected for multiple comparisons using the Bonferroni correction. Results: Ninety-nine cases and 45 normal controls were studied. Overall half of the cases had a history of thrombosis and 66% of those with thrombosis were on no anticoagulation at the time of testing. Table 1 displays results of the CAT-TM in the 2 control and 6 study groups. Control adults and children showed a mean 50% thrombin reduction in thrombin generation with CAT-TM; overall, persons with protein C system defects showed approximately 25% reduction, with the least reduction of thrombin generation in the cohort of PC deficiency at 19%. Sensitivity of the CAT-TM was 100% for PC deficiency, 81% for LA positivity, 80% for PS deficiency and 72% for FVL positivity with no difference in degree of thrombin reduction between hetero- and homozygous FVL. In addition, we identified 14 individuals with CAT-TM results similar to protein C system defects but with confirmed normal PC, PS, FVL and LA tests. Although 9 of these unknowns had a personal (7) or family (2) history of thrombosis, five came from the healthy controls. The false positive results in 3 adult and 2 pediatric controls conferred a CAT-TM test specificity of 89%. Furthermore, analyses showed no differences in CAT-TM results related to gender, age group, history of thrombosis, age of clot at blood draw (acute, subacute or chronic) or use of anticoagulation at the time of blood draw. Conclusions: The CAT-TM is a useful screening test for defects in the protein C system, including LA, although this test could not discriminate between heterozygous and homozygous FVL. The etiology of positive CAT-TM in normal individuals or individuals with a personal or family history of thrombosis without identified PC system defects is currently unknown and under ongoing investigation. Disclosures No relevant conflicts of interest to declare.

Risk Factors for Clinical Manifestations in Patients with Factor V Leiden and Prothrombin Gene Mutations.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4090-4090
Author(s):  
Maria Teresa De Sancho ◽  
Nickisha Berlus ◽  
Jacob H. Rand
Keyword(s):  
Risk Factors ◽  
Family History ◽  
Clinical Characteristics ◽  
Clinical Manifestations ◽  
Gene Mutations ◽  
Factor V Leiden ◽  
Factor V ◽  
Female Hormones ◽  
Significant Difference ◽  
History Of

Abstract Factor V Leiden (FVL) and prothrombin G20210A gene mutations are the most prevalent hereditary thrombophilias (HT). Carriers of these HT are at greater risk for developing thromboembolic events (TEE) and/or pregnancy complications (PC) compared to non-carriers, but not all carriers develop clinical manifestations. We retrospectively analyzed the risk factors (RF) for clinical manifestations of all subjects who tested positive for FVL and/or PG20210A gene mutations in our hematology clinic between January 2000 and July 2006. Symptomatic carriers (cases) and asymptomatic carriers (controls) were compared. Cases were defined as having had a TEE (venous and/or arterial) or a PC (pregnancy loss (PL), preeclampsia, abruption placenta and intrauterine growth restriction). Data analyzed included secondary RF for thrombosis, use of female hormones (FH), family history of thrombosis (FHT), and the presence of other thrombophilias. During the study period, 197 subjects were fully evaluable; 9 were excluded due to insufficient data. The clinical characteristics are shown in Table 1. Of the 85 venous thromboses (VT), 59 (69%) had DVT and/or PE, 10 (12%) had superficial thrombophlebitis, 9 (11%) intra-abdominal thrombosis, 2 (2%) cerebral VT, 2 (2%) had retinal VT and 3 (4%) had > 1 site of VT. Of the 25 arterial thromboses (AT), 11 (44%) were CVA, 7 (28%) had TIA, 6 (24%) had other AT, and 1 (4%) had an MI. Of the 52 cases with PL, 27 (52%) were early recurrent 1st trimester PL, 8 (15%) were 2nd or 3rd trimester PL, 4 (8%) had infertility and 13 (25%) had both PL and infertility. Of the 5 PC, 3 were abruption placenta, 1 preeclampsia and 1 had > 1 PC. The most common RF was the presence of > 1 secondary RF (Table 2). There was no significant difference between cases and controls regarding the use of FH, FHT, and presence of other thrombophilias. Fertility medications were used by 12 (10%) of cases vs. 1 (2%) of controls. Antiphospholipid (aPL) antibody-positivity was the most prevalent concurrent thrombophilic factor and occurred in 18 of cases (12%) vs. 2 (4%) of controls. Cases and controls were similar regarding gender, age, family history of thrombosis, and presence of other thrombophilias. In summary, fertility medications and aPL antibodies appear to be significant risk factors for clinical manifestations in cases. Larger multicenter studies are warranted to identify additional RF in carriers of these HT. Clinical Characteristics Cases (n=145) Controls (n=52) *85 heterozygous, 6 homozygous, **29 heterozygous, 2 homozygous, ***37 heterozygous, 2 homozygous, ****100% heterozygous Mean Age, yr [+/−SD] 44+/−13 42+/−13 Gender, female 115 (79%) 42 (81%) FVL 91 (63%)* 31 (60%)** PG20210A 39 (27%)*** 18 (35%)**** FVL + PG20210A 15 (10%) 3 (6%) VT 85 (59%) --- AT 25 (17%) --- PC and infertility (female carriers, n=115) 57 (50%) --- Risk Factors Cases (n=145) Controls (n=52) p value Includes obesity, postoperative period, pregnancy, puerperium, long airplane flight, smoking, hypertension, hypercholesterolemia, and immobilization; **oral contraceptives, hormone replacement therapy, selective estrogen receptor modulators, progesterone OC, fertility medications Secondary RF* 74 (51%) 15 (29%) 0.265 NS Use of female hormones**, n=115 59 (51%) 21 (50%) 0.478 NS Family history of thrombosis 73 (50%) 34 (65%) 0.252 NS Other thrombophilias 60 (41%) 21 (40%) 0.232 NS

Evidence of Increased Plasma Coagulative Capacity by CloFAL Assay among Pediatric Factor V Leiden and Prothrombin G20210A Heterozygotes with, Versus without, a First-or Second-Degree Family History of Venous Thromboembolism

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5345-5345
Author(s):  
Chris Bombardier ◽  
Linda J. Jacobson ◽  
Marilyn J. Manco-Johnson ◽  
Neil A Goldenberg
Keyword(s):  
Venous Thromboembolism ◽  
Family History ◽  
Positive Family History ◽  
Personal History ◽  
Clot Formation ◽  
Factor V ◽  
History Of ◽  
Study Population ◽  
Fv Leiden ◽  
Thrombophilia Testing

Abstract BACKGROUND: The factor V (FV) Leiden and prothrombin (PT) G20210A polymorphisms in heterozygous state are present in 5% and 1–2% of Caucasians, respectively, and confer approximately 5-fold and 2-fold increases in the risk of incident venous thromboembolism (VTE). While some families who carry these genetic thrombophilia traits exhibit a prothrombotic phenotype, others have no (or only a limited) history of VTE. The ability to discern which individuals with personal and familial carriage of these genetic thrombophilias possess a clinically meaningful increase in VTE risk remains elusive, and (particularly among children) is perhaps best informed presently by family history of VTE. OBJECTIVE AND HYPOTHESES: We sought to evaluate overall plasma coagulative capacity in FV Leiden and PT G20210A heterozygotes using the Clot Formation and Lysis (CloFAL) assay, a global turbidimetric plasma assay of tissue-factor induced fibrin clot formation and tissue-type plasminogen activator enhanced fibrinolysis. We hypothesized that children heterozygous for either thrombophilia would not uniformly demonstrate hypercoagulability, but that coagulative capacity would be increased among heterozygotes who have a family history of VTE. PATIENTS AND METHODS: Children aged birth to 18 years (inclusive) enrolled in prospective inceptional cohort study of thrombosis/thrombophilia/stroke were included in the analysis if they were found to be heterozygous for FV Leiden or PT G20210A upon comprehensive thrombophilia testing and had undergone CloFAL assay testing on a research basis. Data on personal and family history of thrombotic events, thrombophilia testing, and CloFAL assay findings were analyzed. Intergroup comparisons of continuous data were performed by Mann-Whitney U test and proportions were compared between groups using chi-square or Fisher’s exact test, as appropriate. RESULTS: Characteristics of the study population are shown in Table 1. Approximately 70% of patients were evaluated for a family history of VTE (with/without known thrombophilia) and nearly 50% had personal histories of VTE or arterial ischemic stroke (AIS)/recurrent transient ischemic attack (TIA); those evaluated for events were significantly older than those without events, and this difference was statistically significant among those with a positive family history fo VTE. Hypercoagulability was shown in 50% of patients and hypofibrinolysis in 13% using the CloFAL assay. Plasma coagulative capacity and maximal amplitude (MA) of the CloFAL waveform were significantly increased in patients with, versus without, family history of VTE (coagulation index, CI: 102% vs. 72% of the adult normal pooled plasma standard, respectively, p=0.04; MA: 0.415 vs. 0.322, p=0.02), and were not explained by age differences between groups. However, in this relatively small study population, the proportion of CloFAL CI results that exceeded the upper limit of normal values did not significantly differ between those with, versus without, family history of VTE. Pediatric FV Leiden or PT G20210A heterozygotes with positive family history of VTE were more likely to have multi-trait (>1) thrombophilia, in which case a trend toward increased plasma coagulability was demonstrated (CI: 139% [multi-trait] vs. 86% [isolated trait]; p=0.07); superimposed thrombophilias in this group most often consisted of elevated factor VIII activity and Lp(a) concentration. CONCLUSIONS: The present findings using the CloFAL global assay indicate that, while pediatric FV Leiden or PT G20210A heterozygotes do not uniformly exhibit hypercoagulability, plasma coagulative capacity is nevertheless significantly increased among heterozgyotes who have a family history of VTE, which may relate to the presence of superimposed thrombophilias. Table 1. Summary characteristics of the study population. *VTE, AIS, or recurrent TIA **Two patients were dual heterozygotes. N 32 Median age at evaluation (range) 9.5 y (1–18 y) Personal history of events* 14 y (1–18 y) No personal history of events* 8 y (2–18 y) FV Leiden heterozygote (n) 26** PT G20210A heterozygote (n) 8** Personal history of VTE (n) 11 Personal history of AIS/recurrent TIA 4 Family history (1st/2nd degree) of VTE 71% Multi-trait (>1) thrombophilia 45% Acquired thrombophilia 24% Hypercoagulability by CloFAL assay 50% Hypofibrinolysis by CloFAL assay 13%

scholarly journals Neonatal Arterial Ischemic Stroke: Risk Related to Family History, Maternal Diseases, and Genetic Thrombophilia

2017 ◽  
Vol 24 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Juan Arnaez ◽  
Gemma Arca ◽  
Ana Martín-Ancel ◽  
Thais Agut ◽  
Alfredo Garcia-Alix
Keyword(s):  
Ischemic Stroke ◽  
Family History ◽  
Thromboembolic Event ◽  
Positive Family History ◽  
Cerebrovascular Event ◽  
Arterial Ischemic Stroke ◽  
Familial Predisposition ◽  
Vein Thrombosis ◽  
History Of ◽  
Deep Vein

The objective of this study was to evaluate the heritability of neonatal arterial ischemic stroke (NAIS) in relation to family history of thromboembolic event, maternal diseases, and thrombophilia in both parents ( F5G1691A, F2G20210A, and MTHFRC677 T mutations). Forty-two consecutive infants ≥36 weeks of gestation <28 days of life with acute symptomatic NAIS and their parents, as well as 129 controls, were prospectively recruited. Information on maternal data (age, body mass index, oral contraception, migraine, epilepsy, hypertension, and immune disease) and a 3-generation pedigree regarding myocardial infarction, pulmonary embolism, cerebrovascular event, and deep vein thrombosis were obtained. Thrombophilia and maternal diseases did not differ between cases and controls, except for the use of oral contraceptives (more frequent in mothers of controls). No differences were found regarding each studied antecedent of thromboembolic event in the families. The NAIS group showed a higher presence of positive family history among second-degree maternal relatives than did the control infants (odds ratio 4.10; 95% confidence interval 1.29-12.99). Our study does not support the hypothesis that common genetic thrombophilia or familial predisposition to thromboembolic events is associated with the occurrence of idiopathic NAIS.

Selective Screening for the Factor V Leiden Mutation: Is it Advisable prior to the Prescription of Oral Contraceptives?

1997 ◽  
Vol 78 (06) ◽  
pp. 1480-1483 ◽  
Author(s):  
Christian M Schambeck ◽  
Stefan Schwender ◽  
Imme Haubitz ◽  
Ulrich E Geisen ◽  
Ralf E Grossmann ◽  
...  
Keyword(s):  
Family History ◽  
Oral Contraceptives ◽  
Odds Ratio ◽  
Factor V Leiden ◽  
Oral Contraception ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Thrombotic Risk ◽  
History Of ◽  
Fv Leiden

SummaryThe cumulative thrombotic risk of Factor V (FV) Leiden and oral contraceptives (OC) recommends screening for the mutation. Assuming that a family history of thrombosis increases the patient’s likelihood of bearing FV Leiden, a selective rather than universal screening would be performed. We studied the utility of a family history of thrombosis for screening of FV Leiden before prescription of OC and, furthermore, the utility of screening even if oral contraception is favoured. 101 patients who had their first and single thromboembolic event while using OC were interviewed. 609 women without any history of thromboembolism recruited by gynecologists completed a standard questionnaire. 101 of these women, age-matched and currently using OC, were selected for a case-control study. Regarding patients with previous thromboembolism, a family history in a first-degree relative had a positive predictive value (PPV) of only 14% for FV Leiden. A PPV of 12% was calculated by investigating the 609 thrombosis-free women. Inherited FV Leiden (odds ratio = 4.9) and acquired risk factors (odds ratio = 10.1) were both found to be the most prominent, but independent additional risks. Nevertheless, FV Leiden carriers, both heterozygotes and homozygotes, did not suffer earlier from thromboembolism than patients without the mutation. In conclusion, family history is an unreliable criterion to detect FV Leiden carriers. Screening for factor V Leiden can be worthwhile even if the advantages of oral contraception are higher assessed than the thrombotic risk. Affected women knowing about their additional risk could contribute to the prevention of thrombosis in risk situations.

scholarly journals Clinical profile, common thrombophilia markers and risk factors in 85 young Indian patients with arterial thrombosis

2013 ◽  
Vol 131 (6) ◽  
pp. 384-388 ◽  
Author(s):  
Mahendra Narain Mishra ◽  
Ravi Kalra ◽  
Shalesh Rohatgi
Keyword(s):  
Myocardial Infarction ◽  
Family History ◽  
Arterial Thrombosis ◽  
Protein C ◽  
Positive Family History ◽  
Protein S ◽  
Factor V ◽  
C Protein ◽  
Indian Patients ◽  
Low Levels

CONTEXT AND OBJECTIVE: Arterial thrombosis may occur consequent to hereditary thrombophilia and increased lipoprotein(a) [Lp(a)] and fibrinogen. Our aim was to study the prevalence of common thrombophilia markers in 85 consecutive cases of arterial thrombosis. DESIGN AND SETTING: A retrospective study was conducted from 85 consecutive young patients treated as outpatients or admitted due to stroke or myocardial infarction at a tertiary care hospital. METHODS: Eighty-five Indian patients (age < 45 years) presenting ischemic stroke (n = 48) or myocardial infarction (n = 37) and 50 controls were studied for seven thrombophilia markers including antithrombin (AT), factor V, protein C, protein S, activated protein C resistance (APC-R), fibrinogen and Lp(a). Functional assays for protein C, protein S, factor V and APC-R were performed using clotting-based methods. Semi-quantitative estimation of fibrinogen was done using Clauss's method and Lp(a) using immunoturbidimetry. Statistical analysis was done using the Epi Info 6 software. RESULTS: Thirty-three samples (38.8%) tested positive for one or more thrombophilia markers. The three commonest abnormalities were elevated Lp(a) (20%), fibrinogen (17.6%) and low APC-R (14.2%). Low levels of protein C, protein S and AT were present in 4.7, 9.4 and 7% of the patients, respectively. Overall, the risk factor profile was: smoking (33%), positive family history (15.3%), hyperlipidemia (7%), hypertension, diabetes mellitus and obesity (2.3% each). CONCLUSIONS: An association was found between low levels of protein C, protein S and AT and arterial thrombosis, but only elevated fibrinogen levels, smoking, positive family history and hyperlipidemia showed statistical significance.

Selective testing for thrombophilia in patients with first venous thrombosis: results from a retrospective family cohort study on absolute thrombotic risk for currently known thrombophilic defects in 2479 relatives

Blood ◽  
2009 ◽  
Vol 113 (21) ◽  
pp. 5314-5322 ◽  
Author(s):  
Willem M. Lijfering ◽  
Jan-Leendert P. Brouwer ◽  
Nic J. G. M. Veeger ◽  
Ivan Bank ◽  
Michiel Coppens ◽  
...  
Keyword(s):  
Family History ◽  
Venous Thrombosis ◽  
Protein C ◽  
Positive Family History ◽  
Protein S ◽  
Factor V ◽  
Recurrence Rates ◽  
Thrombotic Risk ◽  
History Of ◽  
Fv Leiden

Abstract Thrombophilia screening is controversial. In a retrospective family cohort, where probands had thrombosis and a thrombophilic defect, 2479 relatives were tested for thrombophilia. In antithrombin-, protein C–, and protein S–deficient relatives, annual incidences of venous thrombosis were 1.77% (95% CI, 1.14-2.60), 1.52% (95% CI, 1.06-2.11), and 1.90% (95% CI, 1.32-2.64), respectively, at a median age of 29 years and a positive family history of more than 20% symptomatic relatives. In relatives with factor V (FV) Leiden, prothrombin 20210G>A, or high FVIII levels, these were 0.49% (95% CI, 0.39-0.60), 0.34% (95% CI, 0.22-0.49), and 0.49% (95% CI, 0.41-0.51), respectively. High FIX, FXI, and TAFI, and hyperhomocysteinemia were not independent risk factors. Annual incidence of major bleeding in antithrombin-, protein C–, or protein S–deficient relatives on anticoagulants was 0.29% (95% CI, 0.03-1.04). Cumulative recurrence rates in relatives with antithrombin, protein C, or protein S deficiency were 19% at 2 years, 40% at 5 years, and 55% at 10 years. In relatives with FV Leiden, prothrombin 20210G>A, or high levels FVIII, these were 7%, 11%, and 25%, respectively. Considering its clinical implications, thrombophilia testing should address hereditary deficiencies of antithrombin, protein C, and protein S in patients with first venous thrombosis at young age and/or a strong family history of venous thrombosis.

scholarly journals Family History of Venous Thromboembolism and Identifying Factor V Leiden Carriers During Pregnancy

2010 ◽  
Vol 115 (3) ◽  
pp. 521-525 ◽  
Author(s):  
Amanda L. Horton ◽  
Valerija Momirova ◽  
Donna Dizon-Townson ◽  
Katharine Wenstrom ◽  
George Wendel ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Family History ◽  
Factor V Leiden ◽  
Factor V ◽  
History Of

Pregnancy-Related Venous Thromboembolism

2014 ◽  
Vol 27 (3) ◽  
pp. 243-252 ◽  
Author(s):  
Emily M. Armstrong ◽  
Jessica M. Bellone ◽  
Lori B. Hornsby ◽  
Sarah Treadway ◽  
Haley M. Phillippe
Keyword(s):  
Venous Thromboembolism ◽  
Family History ◽  
Factor V Leiden ◽  
Ease Of Use ◽  
Factor V ◽  
Thromboembolic Risk ◽  
Increased Risk ◽  
History Of ◽  
Prothrombin Gene Mutation ◽  
Prothrombin Gene

Pregnancy is associated with an increased risk of venous thromboembolism (VTE), with a reported incidence ranging from 0.49 to 2 events per 1000 deliveries. Risk factors include advanced maternal age, obesity, smoking, and cesarian section. Women with a history of previous VTE are at a 4-fold higher risk of recurrent thromboembolic events during subsequent pregnancies. Additionally, the presence of concomitant thrombophilia, particularly factor V Leiden (homozygosity), prothrombin gene mutation (homozygosity), or antiphospholipid syndrome (APS), increases the risk of pregnancy-related VTE. Low-molecular-weight heparin (LMWH) and unfractionated heparin (UFH) are the drugs of choice for anticoagulation during pregnancy. LMWH is preferred due to ease of use and lower rates of adverse events. Women with high thromboembolic risk particularly those with a family history of VTE should receive antepartum thromboprophylaxis. Women with low thromboembolic risk or previous VTE caused by a transient risk factor (ie, provoked), who have no family history of VTE, may undergo antepartum surveillance. Postpartum anticoagulation can be considered in women with both high and low thromboembolic risk.

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