scholarly journals Risk of future arterial cardiovascular events in patients with idiopathic venous thromboembolism

Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 259-266 ◽  
Author(s):  
David Green
Keyword(s):  
Myocardial Infarction ◽  
Risk Factor ◽  
Venous Thromboembolism ◽  
Venous Thrombosis ◽  
Arterial Thrombosis ◽  
Coronary Calcification ◽  
Arterial Disease ◽  
Venous Disease ◽  
Clotting Factors ◽  
History Of

Abstract Venous and arterial thromboses have traditionally been considered distinct pathophysiologic entities. However, the two disorders have many features in common, and there is evidence that persons with venous thrombosis may be at greater risk for arterial events. The pathogenesis of both disorders includes endothelial injury, platelet activation, elevated levels of intrinsic clotting factors and inflammatory markers, increased fibrinogen, and impaired fibrinolysis. In addition, older age, obesity, dyslipidemia, and smoking predispose to both venous and arterial thrombosis. While the evidence that arterial disease is a risk factor for venous thrombosis is inconclusive, arterial disease does appear to occur with a modestly increased frequency in patients with a history of venous thromboembolism. Reported odds ratios in such patients were 1.2 for myocardial infarction, 1.3 for stroke, 2.3 for carotid plaque, and 4.3 for coronary calcification. Of note, in persons under age 40 with unprovoked venous thrombosis, the odds ratio for acute myocardial infarction was as high as 3.9. In general, however, venous disease is considered to be a weak risk factor for arterial thrombosis, and the use of agents specifically targeted to the prevention of heart attack or stroke in the majority of persons with VTE cannot be recommended at present.

Family history of myocardial infarction is an independent risk factor for venous thromboembolism: the Tromsø study

2008 ◽  
Vol 6 (11) ◽  
pp. 1851-1857 ◽  
Author(s):  
S. K. BRAEKKAN ◽  
E. B. MATHIESEN ◽  
I. NJØLSTAD ◽  
T. WILSGAARD ◽  
J. STØRMER ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Risk Factor ◽  
Venous Thromboembolism ◽  
Family History ◽  
Independent Risk Factor ◽  
History Of

Evidence-based indications for thrombophilia screening

VASA ◽  
2008 ◽  
Vol 37 (1) ◽  
pp. 19-30 ◽  
Author(s):  
Lindhoff-Last ◽  
Luxembourg
Keyword(s):  
Venous Thromboembolism ◽  
Family History ◽  
Venous Thrombosis ◽  
Arterial Thrombosis ◽  
Pregnancy Loss ◽  
Late Pregnancy ◽  
Evidence Based ◽  
Increased Risk ◽  
Thrombophilia Screening ◽  
History Of

Thrombophilic defects have been shown to be associated with an increased risk of venous thrombosis, fetal loss, and gestational complications. The knowledge about the clinical relevance of thrombophilic defects is increasing, and evidence-based indications for thrombophilia screening are therefore discussed in this review. Selective thrombophilia screening based on previous personal and/or family history of venous thromboembolism is more cost-effective than universal screening in all patient groups evaluated. In the majority of patients with acute venous thrombosis, the results of thrombophilia screening do not influence the duration of oral anticoagulation. The only patient population who clearly profits from thrombophilia screening in this situation are patients with a newly diagnosed antiphospholipid syndrome, because prolonged anticoagulation can avoid the high incidence of recurrence in this patient population. Because of the increased risk of venous thrombosis during pregnancy and the puerperium, thrombophilia screening is indicated in selected patients with a previous history of venous thrombosis or a positive family history. Significant associations with early and late pregnancy loss are observed for carriers of the heterozygous factor V Leiden mutation, the heterozygous prothrombin-mutation G20210A and anticardiolipin antibodies, while protein S deficiency is significantly associated with late pregnancy loss. Antithrombotic drugs like UFH, LMWH or low-dose aspirin may have a potential therapeutic benefit in patients with recurrent pregnancy loss and thrombophilia, but placebo-controlled, multicenter trials are urgently needed to clarify this issue. Although a supra-additive effect for the risk of venous thrombosis is observed between oral contraceptives and some thrombophilias, the absolute incidence of venous thromboembolism is low in premenopausal women and mass screening strategies are therefore unlikely to be effective. While antiphospholipid antibodies are known to be associated with arterial thrombosis, screening for heritable thrombophilias is not useful in arterial thrombosis, although subgroup analysis indicates that they may play a role particularly in young patients and children.

Family history of venous thrombosis or sudden death as a risk factor for venous thromboembolism

2012 ◽  
Vol 107 (06) ◽  
pp. 1191-1192 ◽  
Author(s):  
Paolo Prandoni ◽  
Martin Prins ◽  
Angelo Ghirarduzzi ◽  
Vittorio Pengo ◽  
Maria Sartori ◽  
...  
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Family History ◽  
Sudden Death ◽  
Venous Thrombosis ◽  
History Of

Lupus Anticoagulant is the Strongest Risk Factor for both Venous and Arterial Thrombosis in Patients with Systemic Lupus Erythematosus

1996 ◽  
Vol 76 (06) ◽  
pp. 0916-0924 ◽  
Author(s):  
Daniëlle A Horbach ◽  
Erica V Oort ◽  
Richard C J M Donders ◽  
Ronald H W M Derksen ◽  
Philip G de Groot
Keyword(s):  
At Risk ◽  
Risk Factor ◽  
Venous Thrombosis ◽  
Arterial Thrombosis ◽  
Lupus Anticoagulant ◽  
Plasma Proteins ◽  
Patients At Risk ◽  
History Of ◽  
Thrombotic Complications ◽  
Risk For Thrombosis

SummaryAntiphospholipid antibodies (aPL) characterize patients at risk for both arterial and venous thrombotic complications. Recently it has been recognized that the presence of plasma proteins such as β2-glycoprotein I (β2GPI) and prothrombin are essential for the binding of aPL to phospholipids and that these proteins are probably the real target of aPL. The discovery of these new antigens for aPL introduces the possibility of new assays to detect the presence of aPL. However, it is not known whether these assays improve the identification of patients at risk for thrombosis.In this retrospective study we compared the value of the classic assays LAC (lupus anticoagulant) and ACA (anticardiolipin antibodies) to detect aPL associated with thrombotic complications, with new assays which are based on the binding of aPL to the plasma proteins prothrombin and P2GPI. To do so, we have used these assays in a group of 175 SLE patients and correlated the positivity of the different assays with the presence of a history of venous and arterial thrombosis. Control groups were patients without SLE but with LAC and/or ACA and thrombosis (n = 23), patients with thrombosis without LAC and ACA (n = 40) and 42 healthy controls.In the univariate analysis, in which no distinction has been made between high and low antibody levels, we confirmed LAC and ACA to be related to both arterial and venous thrombosis. Anti-β2GPI- and anti-prothrombin-antibodies, both IgG and IgM correlate with venous thrombosis and anti-β2GPI-IgM with arterial thrombosis. Multivariate analysis showed that LAC is the strongest risk factor (OR 9.77; 95% CI 1.74-31.15) for arterial thrombosis. None of the other factors is a significant additional risk factor. For venous thrombosis LAC is the strongest risk factor (OR 6.55; 95% Cl 2.36-18.17), but ACA-IgM above 20 MPL units also appeared to be a significant (p = 0.0159) risk factor (OR 3.90; 95% Cl 1.29-11.80). Furthermore, the presence of anti-β2GPI- and/or anti-prothrombin-antibodies in LAC positive patients (n = 60) does not increase the risk for thrombosis.The results showed that (i) the LAC assay correlates best with a history of both arterial and venous thrombosis and (ii) neither the anti-P2GPI ELISA nor the anti-prothrombin ELISA gives additional information for a thrombotic risk in SLE patients.

Higher Baseline Hemoglobin and Splenectomy Are Risk Factors for Venous Thromboembolism in Adults with Sickle Cell Variant Genotypes

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3243-3243
Author(s):  
Rakhi P. Naik ◽  
Michael B. Streiff ◽  
Julie Nelson ◽  
Sophie Lanzkron
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Venous Thromboembolism ◽  
Venous Thrombosis ◽  
Sickle Cell ◽  
Research Funding ◽  
Hemoglobin Level ◽  
History Of ◽  
Cell Variant ◽  
Baseline Hemoglobin

Abstract Abstract 3243 Background: Sickle cell disease (SCD) is a hypercoagulable state, leading to increased rates of thrombotic complications such as stroke and venous thromboembolism (VTE). We have previously demonstrated an increased risk of non-catheter-related VTE among patients with sickle cell variant syndromes compared to those with sickle cell anemia (SS/Sβ0) genotypes. Variations in baseline laboratory values, including hemoglobin and hemolytic rate, have been shown to modify the risk of developing complications such as acute chest syndrome and retinopathy in SCD patients. In addition, splenectomy has been identified as a risk factor for VTE in patients with other hemoglobinopathies such as β-thalassemia intermedia. Therefore, we sought to determine the hematologic and clinical risk factors associated with VTE among our cohort of patients with SC and Sβ+thalassemia genotypes. Methods: We conducted a retrospective cohort study of all patients with hemoglobin SC or Sβ+thalassemia genotypes cared for at the Sickle Cell Center for Adults at Johns Hopkins between August 2008 and July 2012. Baseline hematologic parameters were recorded for all patients and were defined as steady-state outpatient laboratory values that were taken at least 1 month after a hospitalization and at least 3 months after a transfusion. Clinical data such as SCD-specific comorbidities and history of surgical splenectomy were also collected for all patients. A history of VTE was confirmed by radiography in the majority of cases. In cases where radiology was not available, only patients with a verified history of anticoagulation were included. Patients with a history of catheter-related VTE only were excluded (n=2). Results: Ninety-five patients with sickle variant genotypes had complete data and were included for analysis. The median age at follow-up was 42 years (range 21–72 years), and 55.8% of patients were female. Twenty-six (27.4%) patients had a history of VTE, 28.6% (8/28) with Sβ+thalassemia genotype and 26.9% (18/67) with SC genotype. Patients with a history of VTE had higher baseline hemoglobin levels compared to those without history of clot (11.6 g/dL vs. 10.8 g/dL, p<0.001). Additional laboratory parameters, including baseline WBC, platelet levels, and reticulocyte counts, did not significantly correlate to a history of VTE. A history of splenectomy was noted in 26.9% (7/26) of patients with VTE, 4 of whom developed a pulmonary embolism (PE) only, 2 of whom had a history of both deep venous thrombosis (DVT) and PE, and 1 of whom experienced an abdominal vein thrombosis. Splenectomy was significantly correlated to VTE on bivariate analysis (p=0.001), whereas other prevalent comorbidities such as avascular necrosis and retinopathy did not appear to be associated with VTE. On multivariate analysis controlling for demographics and genotype, older age (odds ratio (OR) 1.05, 95% confidence interval (CI) 1.01–1.10, p=0.015), hemoglobin level (OR 3.82, CI 1.83–7.98, p<0.001) and history of splenectomy (OR 4.93, CI 1.10–22.14, p=0.038) were found to be independent risk factors for VTE in our cohort. On subgroup analysis by VTE type, increased hemoglobin level persisted as a risk factor for both DVT (OR 5.69, CI 2.04–15.83, p=0.001) and PE (OR 3.55, CI 1.65–7.68, p=0.001), but splenectomy was statistically correlated to PE only (OR 4.79, CI 1.05–21.78, p=0.043). Conclusions: In patients with SC and Sβ+ thalassemia genotypes, VTE is common complication and is associated with higher baseline hemoglobin levels. In addition, splenectomy appears to be a risk factor for VTE, and specifically PE, in this population. These findings suggest that increased whole blood viscosity and surgical splenectomy may play a role in the development of venous thrombosis in SCD. Further studies will be needed to determine if functional asplenia is also associated with VTE in patients with sickle cell variant genotypes, and whether laboratory parameters can be used to predict VTE risk in SCD. Disclosures: Naik: NHLBI (K12): Research Funding. Streiff:sanofi-aventis: Consultancy, Honoraria; BristolMyersSquibb: Research Funding; Eisai: Consultancy; Janssen Healthcare: Consultancy; Daiichi-Sankyo: Consultancy. Lanzkron:Hemaquest: Membership on an entity's Board of Directors or advisory committees; NHLBI: Research Funding.

The influence of thrombophilia on the long-term survival of patients with a history of venous thromboembolism

2013 ◽  
Vol 109 (01) ◽  
pp. 79-84 ◽  
Author(s):  
Sylvia Reitter-Pfoertner ◽  
Thomas Waldhoer ◽  
Michaela Mayerhofer ◽  
Ernst Eigenbauer ◽  
Cihan Ay ◽  
...  
Keyword(s):  
Risk Factors ◽  
Venous Thromboembolism ◽  
Multivariable Analysis ◽  
Factor V Leiden ◽  
Arterial Disease ◽  
Factor V ◽  
Term Survival ◽  
Long Term Survival ◽  
History Of

SummaryData on the long-term survival following venous thromboembolism (VTE) are rare,and the influence of thrombophilia has not been evaluated thus far. Our aim was to assess thrombophilia-parameters as predictors for long-term survival of patients with VTE. Overall, 1,905 outpatients (99 with antithrombin-, protein C or protein S deficiency, 517 with factor V Leiden, 381 with elevated factor VIII and 160 with elevated homocysteine levels, of these 202 had a combination and 961 had none of these risk factors) were included in the study between September 1, 1994 and December 31, 2007. Retrospective survival analysis showed that a total of 78 patients (4.1%) had died during the analysis period, among those four of definite or possible pulmonary embolism and four of bleeding. In multivariable analysis including age and sex an association with increased mortality was found for hyperhomocysteinemia (hazard ratio 2.0 [1.1.-3.5]) whereas this was not the case for all other investigated parameters. We conclude that the classical hereditary thrombophilia risk factors did not have an impact on the long-term survival of patients with a history of VTE. Thus our study supports the current concept that thrombophilia should not be a determinant for decision on long term anticoagulation. However, hyperhomocysteinaemia, known as a risk factor for recurrent VTE and arterial disease, might impact survival.

Decreased anticoagulant response to tissue factor pathway inhibitor in patients with venous thromboembolism and otherwise no evidence of hereditary or acquired thrombophilia

2004 ◽  
Vol 91 (01) ◽  
pp. 80-86 ◽  
Author(s):  
Brigitte Piccapietra ◽  
Johanna Boersma ◽  
Joerg Fehr ◽  
Thomas Bombeli
Keyword(s):  
Venous Thromboembolism ◽  
Venous Thrombosis ◽  
Mean Value ◽  
Healthy Controls ◽  
Crude Odds Ratio ◽  
Sensitivity Ratio ◽  
Increased Risk ◽  
History Of ◽  
Anticoagulant Response ◽  
Acquired Thrombophilia

SummaryNo relevant deficiency of TFPI or genetic polymorphisms could thus far consistently be associated with venous thromboembolism. We hypothesized that the substrates of the TFPI protein, including FVII or FX (rather than the protein itself) could induce a hypercoagulable state. We created a novel TF-based clotting assay that evaluated the anticoagulant response to exogenously added recombinant TFPI. The response to TFPI was expressed as the ratio of the clotting time with and without TFPI. By using 118 healthy controls, we established a reference range between 1.31 and 1.93 (mean value ± 2 standard deviations (SD), 1.62 ± 0.31). We then evaluated samples from 120 patients with a history of venous thromboembolism but no evidence of hereditary and acquired thrombophilia. The range of the patients’ ratios was significantly (P < 0.001) lower, falling between 1.2 and 1.78 (mean value ± 2 SD, 1.49 ± 0.29). Of the 120 patients, 39 (32.5%) had a TFPI sensitivity ratio below the 10th percentile of the controls, compared with 11 (9.3%) of the healthy controls. The crude odds ratio for venous thrombosis for subjects with a TFPI sensitivity ratio below the 10th percentile was 13 (95% CI; range, 3.1 to 54.9) compared with those with a ratio above 1.8 (90th percentile). Patients with idiopathic thromboembolism did not have a decreased TFPI sensitivity ratio more often than patients with thrombosis with a circumstantial risk factor. Based on these results, a reduced response to TFPI may lead to an increased risk of venous thrombosis.

Long-term Clinical Follow-up in 265 Patients with Deep Venous Thrombosis Initially Treated with either Unfractionated Heparin or Dalteparin: A Retrospective Analysis

1999 ◽  
Vol 82 (10) ◽  
pp. 1222-1226 ◽  
Author(s):  
W. Åberg ◽  
D. Lockner ◽  
C. Paul ◽  
M. Holmström
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Unfractionated Heparin ◽  
Malignant Disease ◽  
Duration Of Treatment ◽  
Post Thrombotic Syndrome ◽  
Recurrent Vte

SummaryThe primary objective of this retrospective study was to describe the frequency of a post-thrombotic syndrome in 265 patients previously treated for deep venous thrombosis (DVT). The secondary objectives were to document the frequency of recurrent venous thromboembolism (VTE) and mortality, especially from malignant disease. The patients were evaluated 5-14 years after inclusion in three randomized trials comparing continuous intravenous (i. v.) infusion of unfractionated heparin (UFH) (n = 85) with a low molecular weight heparin (LMWH), dalteparin (n = 180). The median post-thrombotic score at follow-up was 2 (range 0-8). In a multiple step-wise regression analysis the post-thrombotic score was significantly higher among patients with initial proximal DVT (p = 0,0001) as compared with those who had distal DVT. A recurrent venous thromboembolic event was diagnosed in 29,4% of the patients treated with dalteparin and in 23,5% of the patients treated with UFH (ns). A secondary risk factor for venous thromboembolism and a longer duration of treatment with oral anticoagulants (OAC) were significantly associated with a lower risk for recurrent VTE, whereas malignant disease diagnosed during follow-up was associated with a higher risk. During follow-up a total of 40,7% of patients had died. No difference in total mortality or mortality from malignant disease was demonstrated between the two drugs. In conclusion, a severe post-thrombotic syndrome occured relatively infrequent. considering the long observation period. Proximal DVT was significantly associated with a more severe post-thrombotic syndrome. After 14 years follow-up, no significant differences were observed in overall mortality, mortality from malignant disease or recurrent VTE between UFH- and dalteparin-treated patients. Malignant disease was a risk factor for recurrent VTE, the presence of a secondary risk factor and a longer duration of treatment with OAC decreased the risk for recurrent VTE.

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