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PubMed1994

Cerebral sinus and venous thrombosis in rats induces long-term deficits in brain function and morphology--evidence for a cytotoxic genesis.

The pathophysiology of cerebral venous infarctions is poorly understood, due partially to the lack of a suitable experimental model. Therefore, we developed a model in rats to study acute and long-term changes of brain function and morphology following thrombosis of the superior sagittal sinus. The superior sagittal sinus of rats was exposed, ligated, and injected with thrombogenic material. Thrombosis of the longitudinal sinus and ascending cortical veins was monitored by intravital fluorescence angiography. Histology was studied at 24 h and 4 weeks after thrombosis and changes in intracranial pressure, electroencephalogram (EEG), and tissue impedance were noted. Spontaneous locomotor activity was followed for 4 weeks after thrombosis. The effect of heparin treatment on tissue impedance was evaluated. Thrombosis of the superior sagittal sinus could be regularly induced, although pathological sequelae developed only if ascending veins were affected. Sinus and venous thrombosis was histologically characterized by bilateral, parasagittal infarctions. Thrombosis induction was followed by an increase in intracranial pressure from 4.7 +/- 1.6 to 12.8 +/- 2.4 mm Hg (n = 4) at 1 h after thrombosis, associated with an exponential rise in tissue impedance to 165 +/- 14% (n = 8) of the control. EEG changes were similar to those following global cerebral ischemia and remained pathological for up to 6 months after thrombosis (n = 6). As a permanent behavioral deficit spontaneous locomotor activity was reduced to 60 +/- 10% (n = 6) of the control. Finally, the administration of heparin (1 IU/g body weight) after thrombosis induction was found to reverse the pathological tissue impedance response of the brain. In conclusion, involvement of ascending cortical veins following sinus thrombosis appears to be critical for the development of irreversible tissue damage, such as infarction. Changes in intracranial pressure and tissue impedance suggest that the venous thrombosis was followed by brain edema of a predominantly cytotoxic nature. Venous thrombosis led to long-term changes of brain function, as demonstrated by persistent disturbances of the EEG or of the spontaneous locomoter drive. These deficits may be amenable to treatment with heparin.

Animals↗
PubMed2004

Incidence and risk factors of early venous thrombosis associated with permanent pacemaker leads.

INTRODUCTION: Pacemaker lead implantation can cause thrombosis, which can be associated with serious local morbidity and complicated by pulmonary embolism. Few reliable estimates of the incidence of thrombosis have been reported. The contribution of established risk factors to venous thrombosis in patients with implanted pacemaker leads is unknown. METHODS AND RESULTS: One hundred forty-five consecutive patients n = 145) underwent routine clinical and Doppler ultrasound evaluation for thrombosis before and 3, 6, and 12 months after lead implantation. Established risk factors for venous thrombosis were assessed in detail for all patients. Clinical outcome, including clinically manifest thrombosis, pulmonary embolism, associated pacemaker lead infection, complicated reinterventions, and death, was evaluated. Thrombosis was observed in 34 (23%) of 145 patients. Thrombosis did not cause any signs or symptoms in 31 patients but resulted in overt clinical symptoms in 3 patients. The absence of anticoagulant therapy, use of hormone therapy, and a personal history of venous thrombosis were associated with an increased risk of thrombosis. The risk of thrombosis increased in the presence of multiple pacemaker leads compared to a single lead. CONCLUSION: Established risk factors for venous thrombosis and the presence of multiple pacemaker leads contribute substantially to the occurrence of thrombosis associated with permanent pacemaker leads. Risk factor assessment prior to implantation may be useful for identifying patients at risk for thrombotic complications. Preventive management in these patients is warranted.

Adult↗
PubMed2002

Association between blood pressure, ultrafiltration, and hemodialysis graft thrombosis: a multivariable logistic regression analysis.

Although a low blood flow (Q(a)) is the most important cause of graft thrombosis, several studies have shown that Q(a) measurements do not accurately predict thrombosis. This suggests that additional variables may influence thrombosis. Identification of such variables may be essential to designing surveillance protocols that accurately predict thrombosis. In this nested case-control study, we prospectively followed 105 patients for up to 2.5 years in order to test the association of a number of variables with thrombosis. These included Q(a) (monthly by ultrasound dilution), percentage stenosis (quarterly by duplex ultrasound), mean arterial pressure (MAP), percentage ultrafiltration (%UF) during dialysis (%UF = 100[liters]/[kilogram of weight]), and other variables that defined patient and graft characteristics. Patients were divided into patent (n = 53) and thrombosed groups (n = 52), and MAP and %UF from seven consecutive dialysis sessions were analyzed. In the thrombosed group, the last session was the final session before thrombosis. A multivariable logistic regression model showed that Q(a), MAP (the predialysis average of seven sessions), and %UF (from the last session) were independently associated with thrombosis, whereas all other variables were not. The model yielded the following odds ratios for thrombosis: for a single Q(a) value (reduction of 1,000 mL/min), 12.0 (P < 0.01); for %UF (increase of 4%), 5.3 (P < 0.01); for MAP (reduction of 30 mm Hg), 4.1 (P = 0.02); and for percentage decrease in Q(a) (> or =20% versus <20%), 2.4 (P = 0.12). We conclude that in addition to Q(a), both %UF at the last session before thrombosis and average predialysis MAP from seven sessions are independently associated with thrombosis. These results help explain why Q(a) alone does not accurately predict thrombosis. A prospective study is needed to determine whether %UF at each session and a moving average MAP from seven sessions improve the prediction of thrombosis. However, it should be recognized that a large %UF is a preterminal event that likely provides too short a warning for intervention before thrombosis.

Blood Pressure↗
PubMed1997

Risk factors for vascular thrombosis in pediatric renal transplantation: a special report of the North American Pediatric Renal Transplant Cooperative Study.

Vascular thrombosis remains a major cause of graft failure, accounting for 12.2% of failed index transplants and 19.2% of repeat transplants. We conducted a special study to identify the risk factors for vascular thrombosis. A total of 4394 transplants (2060 living donor [LD] transplants and 2334 cadaver donor [CAD] source transplants) were evaluated. The respective vascular thrombosis rates for LD and CAD transplants were 38/2060 (1.8%) and 100/2334 (4.2%) (P<0.001). Univariate analysis showed that the rate of graft loss due to thrombosis was significantly higher in younger children (less than 2 years of age) as compared with older age groups (2-5 years, 6-12 years, and more than 12 years of age) (9.0% vs. 5.5%, 4.4%, and 3.5% for CAD transplant recipients and 3.5% vs. 3.4%, 0.7%, and 1.9% for LD graft recipients). Recipients of kidneys from cadaver donors less than 5 years of age had a significantly higher thrombosis rate (8.3%) than did recipients from older donor groups (5-10 years, 4.5%; greater than 10 years, 3.2%). Recipients of kidneys with cold ischemia time greater than 24 hr also had a higher thrombosis rate (5.6%), as compared with recipients of kidneys with a shorter cold ischemia time (3.2%). Recipients of antilymphocyte therapy on day 0 or day 1 were at dimished risk of graft loss due to thrombosis (2.2% vs. 4.1%, P=0.001). Comparable trends were seen for both LD and CAD organ recipients. LD organ recipients with a history of prior transplantation had a significantly higher rate of thrombosis as compared with those who received a primary transplant (4.6% vs. 1.6%, P=0.005). For both LD and CAD organ recipients, the occurrence of acute tubular necrosis was a significnat risk factor for the development of thrombosis. Regression analysis showed that for LD organ recipients, a history of prior transplantation increased the risk for thrombosis, whereas increasing recipient age had a linear decreasing risk effect. The use of antilymphocyte antibody or cyclosporine on day 0/1 decreased the risk for thrombosis. For CAD kidney recipients, organ cold ischemia time greater than 24 hr increased the risk for thrombosis. The use of antibody induction therapy, donors greater than 5 years of age, and increasing recipient age were factors that decreased the risk for thrombosis.

Age Factors↗
PubMed2006

Hormonal factors and risk of recurrent venous thrombosis: the prevention of recurrent venous thromboembolism trial.

BACKGROUND: In some but not all studies, men with venous thrombosis had a higher risk of recurrence than women. Information on women with initial hormone-related thrombosis is scant. OBJECTIVE: We assessed the incidence of recurrent thrombosis by gender, and among women using exogenous hormones or pregnant/postpartum at the time of index thrombosis. PATIENTS/METHODS: A total of 508 men and women with one or more previous venous thrombosis episodes were observed while participating in a randomized trial of low-intensity warfarin or placebo for 2.1 years. Index thrombosis events during treatment with postmenopausal hormones, oral contraceptives, or during pregnancy, or the puerperium were considered to be hormone-related events. RESULTS: Among 268 men the 3-year probability of recurrent thrombosis was 18.4% (95% confidence intervals; CI 12.3-24.4). Among 109 women without hormone-related thrombosis, the rate was 15.0% (95% CI 6.3-23.8). Among 129 women with hormone-related thrombosis, the rate was 5.0% (95% CI 1.1-8.9). Adjusting for other risk factors and treatment assignment, women had a 39% lower thrombosis recurrence risk than men: hazard ratio (HR) 0.61 (95% CI 0.34-1.08). Women with hormone-related thrombosis had a 58% lower risk than men: HR 0.42 (95% CI 0.19-0.97); and a 46% lower recurrence risk than other women; HR 0.54 (95% CI 0.19-1.54). Women without hormone-related index events had a recurrence rate similar to men; HR 0.83 (95% CI 0.42-1.66). CONCLUSIONS: In this trial population, women had a lower risk of recurrent venous thrombosis than men. This difference was explained by a low risk of recurrence among women with hormone-related index thrombosis.

Aged↗
PubMed2000

Lupus anticoagulants and thrombosis: clinical association of different coagulation and immunologic tests.

The dilute Russell's viper venom time (dRVVT) and the kaolin clotting time (KCT) are two among the most commonly used coagulation tests for the detection of lupus anticoagulants. The dRVVT seems superior to the KCT in identifying LA-positive patients at risk of thrombosis. However, this relationship is greatly influenced by both the source of reagents and the instrumentation employed to carry out the assays. Therefore, 4 dRVVTs ("home-made" dRVVT, DVV test, Bioclot LA, LA Screen), and one KCT (Kaoclot) were performed in two centers and compared for their retrospective correlation with the thrombotic complications of 72 patients with a previously established diagnosis of lupus anticoagulants. Two other assays ("home-made" KCT, and Colloidal Silica Clotting Time, CSCT) were performed in one of the two centers, and compared with Kaoclot for their clinical correlations in the same population of patients, 44 of whom (61%) had suffered from arterial and/or venous thrombosis. A rather good degree of inter-laboratory and inter-assay correlations of the different tests was found. However, a statistically significant association with thrombosis was found only with the coagulation profile generated using the "home-made" dRVVT. When the commercially available dRVVTs were used, none of the coagulation profiles remained associated with thrombosis. When the assays were analyzed separately, the association with thrombosis was statistically significant for LA screen (p = 0.0019), DVV test (p = 0.0043), and Bioclot (p = 0.0255), and of borderline significance for the "home-made" dRVVT (p = 0.0503) in one center. This last assay was also significantly associated with thrombosis in the other center (p = 0.0139). When venous and arterial thrombosis were considered separately, DVV test was statistically associated with venous thrombosis in both centers (p = 0.0076 and p = 0.0187, respectively), and LA screen in one center (p = 0.0303). No dRVVT was found to correlate with arterial thrombosis. Kaoclot, Colloidal Silica Clotting Time, and the "home-made" KCT did not correlate with thrombosis. The prevalence of IgG and/or IgM antibodies to cardiolipin, beta2-glycoprotein I and prothrombin were 74%, 86% and 85%, respectively. Increased titers of IgG anticardiolipin antibodies were associated with arterial thrombosis (p = 0.0375), whereas IgM anti-beta2-glycoprotein I antibodies were associated with venous thrombosis (p = 0.0433). In conclusion, these retrospective data support the notion that the dRVVT, rather than other coagulation or ELISA tests, are able to identify lupus anticoagulant-positive patients at risk of thrombosis. This property appears common to several commercially available dRVVT kits, making this type of assay the ideal target of future efforts of laboratory standardization.

Adult↗
PubMed1994

The clinical course of distal deep venous thrombosis after total hip and total knee arthroplasty, as determined with duplex ultrasonography.

Duplex ultrasonography was used to screen 273 consecutive patients, on the fourth day after a total hip or total knee arthroplasty, for the presence of a distal deep venous thrombosis. Patients who had a history of thromboembolic disease or who had an active neoplasm were excluded from the study. Of the 273 patients, twenty-four (9 per cent) were found to have a proximal deep venous thrombosis (a thrombosis involving the femoral or popliteal veins) and forty-one (15 per cent), a distal deep venous thrombosis (a thrombosis involving the veins of the calf). All of the thromboses were asymptomatic. The forty-one patients in whom a distal deep venous thrombosis had been detected with duplex screening subsequently had serial duplex examinations, on the seventh and fourteenth postoperative days. If a proximal deep venous thrombosis was detected, anticoagulation was begun immediately. If no proximal thrombosis was observed, the distal thrombosis was considered stable, the serial duplex examinations were terminated, and clinical observation was continued. Of the forty-one patients who had serial examinations, seven (17 per cent) had a proximal deep venous thrombosis in the ipsilateral limb by the fourteenth postoperative day; all seven were asymptomatic, and all were managed with anticoagulation. Thirty-four patients (83 per cent) were determined to have a stable distal deep venous thrombosis on the fourteenth postoperative day, and no additional duplex examinations were performed. Thirty-three (97 per cent) of these thirty-four patients remained asymptomatic for deep venous thrombosis thereafter; the remaining patient (3 per cent) had a proximal deep venous thrombosis in the ipsilateral limb eleven months postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Female gender and resistance to activated protein C (FV:Q506) as potential risk factors for thrombosis after elective hip arthroplasty.

Resistance to activated protein C (APC) caused by the R506Q mutation in factor V is the most common inherited risk factor for venous thrombosis. To elucidate whether APC-resistance is a risk factor for venous thrombosis after elective total hip replacement, the association between APC-resistance (presence of FV:Q506 allele) and postoperative thrombosis was investigated in patients (n = 198) randomised to received short (during hospitalisation, n = 100) or prolonged prophylaxis (three weeks after hospitalisation, n = 98) with low molecular weight heparin (LMWH). Among APC-resistant individuals receiving short prophylaxis, 7/10 developed thrombosis as compared to 2/12 receiving long prophylaxis (p <0.0179). Odds ratio for association between APC-resistance and thrombosis in the short prophylaxis group was 4.2 (CI 95% 1.02-17.5) (p <0.0465). Among those receiving prolonged prophylaxis, there was no increased incidence of thrombosis associated with APC-resistance. Two unexpected observations were made. One was that APC-resistance was much more common in women (19/109) than in men (3/89) (p <0.001). The other was that even women without APC-resistance were much more thrombosis-prone than men. Thus, 24/48 of women with normal FV genotype and short prophylaxis developed thrombosis vs 8/42 among men, p = 0.002. The increased risk of thrombosis associated with female gender and APC-resistance was neutralised by the prolonged treatment. In conclusion, among patients receiving short prophylaxis, female gender was found to be a strong risk factor for venous thrombosis. Even though APC-resistance appeared to be a risk factor for postoperative thrombosis, the uneven distribution of APC-resistance between men and women, taken together with the increased risk of thrombosis among women, precluded valid conclusions to be drawn about the association between APC-resistance and an increased risk of thrombosis. Our results suggest that prolonged prophylaxis with LMWH after hip surgery is more important for women than for men.

Adult↗
PubMedDate not supplied

Venous thrombosis after long-haul flights.

BACKGROUND: The risk for venous thromboembolism after long-haul flights represents a controversial issue. The aim of our study was to assess the incidence of venous thrombosis associated with long-haul flights in a prospective, controlled cohort study. METHODS: We included 964 passengers returning from long-haul flights (flight duration, > or =8 hours) and 1213 nontraveling control subjects. We excluded participants who were being treated with anticoagulant drugs or who used compression stockings. Main outcome measures were the incidence of ultrasonographically diagnosed thrombosis in the calf muscle and deep veins, symptomatic pulmonary embolism, and death. RESULTS: We diagnosed venous thrombotic events in 27 passengers (2.8%) and 12 controls (1.0%) (risk ratio [RR], 2.83; 95% confidence interval [CI], 1.46-5.49). Of these, 20 passengers (2.1%) and 10 controls (0.8%) presented with isolated calf muscle venous thrombosis (RR, 2.52; 95% CI, 1.20-5.26), whereas 7 passengers (0.7%) and 2 controls (0.2%) presented with deep venous thrombosis (RR, 4.40; 95% CI, 1.04-18.62). Symptomatic pulmonary embolism was diagnosed in 1 passenger with deep venous thrombosis (P =.44). All of these individuals had normal findings at baseline ultrasonography. Passengers with isolated calf muscle venous thrombosis or deep venous thrombosis had at least 1 risk factor for venous thrombosis (>45 years of age or elevated body mass index in 21 of 27 passengers). The follow-up after 4 weeks revealed no further venous thromboembolic event. CONCLUSIONS: Long-haul flights of 8 hours and longer double the risk for isolated calf muscle venous thrombosis. This translates into an increased risk for deep venous thrombosis as well. In our study, flight-associated thrombosis occurred exclusively in passengers with well-established risk factors for venous thrombosis.

Adolescent↗
PubMed2004

Estrogen plus progestin and risk of venous thrombosis.

CONTEXT: Postmenopausal hormone therapy increases the risk of venous thrombosis. It is not known whether other factors influencing thrombosis add to this risk. OBJECTIVE: To report final data on incidence of venous thrombosis in the Women's Health Initiative Estrogen Plus Progestin clinical trial and the association of hormone therapy with venous thrombosis in the setting of other thrombosis risk factors. DESIGN, SETTING, AND PARTICIPANTS: Double-blind randomized controlled trial of 16,608 postmenopausal women between the ages of 50 and 79 years, who were enrolled in 1993 through 1998 at 40 US clinical centers with 5.6 years of follow up; and a nested case-control study. Baseline gene variants related to thrombosis risk were measured in the first 147 women who developed thrombosis and in 513 controls. INTERVENTION: Random assignment to 0.625 mg/d of conjugated equine estrogen plus 2.5 mg/d of medroxyprogesterone acetate, or placebo. MAIN OUTCOME MEASURES: Centrally validated deep vein thrombosis and pulmonary embolus. RESULTS: Venous thrombosis occurred in 167 women taking estrogen plus progestin (3.5 per 1000 person-years) and in 76 taking placebo (1.7 per 1000 person-years); hazard ratio (HR), 2.06 (95% confidence interval [CI], 1.57-2.70). Compared with women between the ages of 50 and 59 years who were taking placebo, the risk associated with hormone therapy was higher with age: HR of 4.28 (95% CI, 2.38-7.72) for women aged 60 to 69 years and 7.46 (95% CI, 4.32-14.38) for women aged 70 to 79 years. Compared with women who were of normal weight and taking placebo, the risk associated with taking estrogen plus progestin was increased among overweight and obese women: HR of 3.80 (95% CI, 2.08-6.94) and 5.61 (95% CI, 3.12-10.11), respectively. Factor V Leiden enhanced the hormone-associated risk of thrombosis with a 6.69-fold increased risk compared with women in the placebo group without the mutation (95% CI, 3.09-14.49). Other genetic variants (prothrombin 20210A, methylenetetrahydrofolate reductase C677T, factor XIII Val34Leu, PAI-1 4G/5G, and factor V HR2) did not modify the association of hormone therapy with venous thrombosis. CONCLUSIONS: Estrogen plus progestin was associated with doubling the risk of venous thrombosis. Estrogen plus progestin therapy increased the risks associated with age, overweight or obesity, and factor V Leiden.

Age Factors↗
PubMed2002

Prevalence of hereditary thrombophilia in patients with thrombosis in different venous systems.

The prevalence of hereditary thrombophilia is well known in patients with lower-extremity thrombosis but only poorly studied in patients with thrombosis at unusual sites. Consequently, it is still unclear whether such patients should generally be screened for hereditary thrombophilia. We retrospectively analyzed 260 patients with thrombosis at unusual sites including thrombosis in portal, cerebral, retinal, and upper-extremity veins with respect to the prevalence of FV Leiden, prothrombin G20210A, protein C, protein S, and antithrombin deficiency. In addition, all thrombotic episodes were analyzed for circumstantial risk factors. Used as controls, healthy volunteers (120) and patients with lower-extremity thrombosis (292) showed overall prevalence of hereditary thrombophilia of 9.1% and 39.0%, respectively. The corresponding numbers were 33.3%, 34.3%, and 39.0% in patients with portal vein, upper-extremity, and lower-extremity thrombosis, respectively. In patients with cerebral vein thrombosis, however, the prevalence was significantly lower (23.5%). Patients with retinal vein occlusion did not show an increased frequency of thrombophilia at all (5.9%). In all five groups FV Leiden was by far the most frequent defect (4.4-27.1%), while prothrombin G20210A occurred rarer (2.5-7.6%). Protein C, protein S, and antithrombin deficiency were much less prevalent (0-3.1%) except for patients with portal vein thrombosis (4.8-7.1%). Compared to healthy individuals, the relative risk of thrombosis was 4.3 (2.2-8.1), 3.8 (1.8-7.7), 2.5 (1.0-6.1), 3.7 (1.5-8.6), and 0.6 (0.2-2.1) for patients with lower-extremity, upper-extremity, cerebral vein, portal vein, and retinal vein thrombosis, respectively. Circumstantial risk factors were more frequent in patients without than with hereditary thrombophilia and were found most often in patients with upper-extremity thrombosis. In each group the most frequent circumstantial risk factor was different. However, oral contraceptives and cancer were found in all five groups. In conclusion, independent upon the presence of circumstantial risk factors, screening for hereditary thrombophilia is warranted in all patients with thrombosis at unusual sites except in those with retinal vein occlusion.

Adolescent↗
PubMed2002

PAI-1 gene 4G/5G genotype: A risk factor for thrombosis in vessels of internal organs.

Although the common 4G/5G polymorphism in the promoter of the PAI-1 gene was suggested to be a risk factor for some of the thrombotic disorders, its significance in the development of thrombosis is still controversial. This study presents the data on a total of 357 patients with different types of thrombosis and 281 unrelated healthy controls. It was found that the 4G/4G genotype is associated with a higher risk of thrombosis (OR, 1.7; 95% CI, 1.1-2.5). Patients were divided into five distinct groups according to the site of thrombosis. Both 4G/4G and 4G/5G genotypes were associated with a higher risk of thrombosis development in a group of 69 patients with internal organ thrombosis (OR, 6.35; 95% CI, 2.5-16.1 and OR, 4.85; 95% CI, 2.0-12.1, respectively). Interestingly, this association was even stronger in a subgroup of 33 patients with portal vein thrombosis (PVT) and 4G/4G and 4G/5G genotypes conferred more than 10- and 6-fold increases in the risk of developing PVT (95% CI: 2.3-47.1 and 1.4-28.8), respectively. No statistically significant association was found between 4G/4G genotype and the groups of deep vein thrombosis (126 patients), cerebral thrombosis (80 patients), retinal thrombosis (72 patients), and purpura fulminans (16 patients). Factor V Leiden or prothrombin G20210A mutations did not emerge as additional risk factors for thrombosis in any of the groups studied. To conclude, this study suggests that there may be an association between 4G/4G and 4G/5G genotypes and the thrombosis in vessels of internal organs especially in the portal veins.

Adolescent↗
PubMed2003

Analysis of risk factors and comorbid diseases in the development of thrombosis in patients with anticardiolipin antibodies.

Our objective was to identify the role of various disease states and additional risk factors in the development of thrombosis in patients with anticardiolipin antibodies (aCL). We undertook a retrospective chart review of patients with aCL (IgG or IgM titres > 20 GPL or 20 MPL by ELISA). Patients with a thrombotic event were compared to patients without thrombosis for potential risk factors: age, gender, ethnicity, hypertension (HTN), diabetes (DM), hyperlipidaemia, tobacco use and sequential aCL determinations. The role of systemic lupus erythematosus (SLE), human immunodeficiency virus (HIV), hepatitis C and renal disease was also analysed. Statistical analysis was performed using the t-test, the chi(2) test and multivariate analysis. Of the 107 patients who had moderately positive aCL (IgM and/or IgG), 53 had a thrombotic event. The patients with thrombosis were significantly older than patients without thrombosis (mean age 46.6 vs. 38.75 years, respectively, P=0.014). No significant differences in gender, race, HTN, DM, hyperlipidaemia, tobacco use or concomitant diseases were identified in the two groups. Thrombosis was more frequent in patients who were seropositive for both IgG and IgM ( P=0.027). Thrombosis was observed in equal frequencies in patients with aCL on both determinations and in patients with aCL on only one of the two determinations. In patients with aCL on two determinations a high-titre IgG aCL was associated with thrombosis. Patients with renal disease and aCL on only one of the two determinations had fewer thrombotic events ( P=0.0046). Mean aCL IgM titres were higher in thrombosis groups containing venous thromboses than in the thrombosis group with arterial thrombosis only. We concluded that risk factors for thrombosis with a single aCL determination include older age and both IgM and IgG aCL. With persistent aCL, high-titre IgG aCL was associated with thrombosis.

Adult↗
PubMed2005

Evaluation of D-dimer and factor VIII in cirrhotic patients with asymptomatic portal venous thrombosis.

D-dimer and factor VIII levels raise in advanced cirrhosis. We investigated the behavior and the diagnostic usefulness of D-dimer and factor VIII in cirrhotic patients with asymptomatic portal venous thrombosis. Factor VIII coagulant and D-dimer values were measured in 136 consecutive outpatients with stable cirrhosis divided according to Child-Pugh (CP) classification, who underwent color/power ultrasonography to detect portal thrombosis. Portal thrombosis was found in 33 patients (24.2%). In patients without thrombosis, factor VIII was significantly higher in CP class C compared with class A and B. Conversely, class C patients with portal thrombosis had lower factor VIII levels than those without thrombosis. In both groups, D-dimer was significantly increased in class C compared with class A and B. In class C, thrombotic patients showed higher D-dimer values than did patients without thrombosis. In class C, a D-dimer value > or = 0.55 microg/mL provided a sensitivity and a negative predictive value for portal thrombosis of 100%, and a factor VIII coagulant level < or = 80% showed a specificity and a negative predictive value of 76% and 84%, respectively. In class B, a D-dimer value > or = 0.225 microg/mL had a sensitivity of 89% and a negative predictive value of 82%. In conclusion, our study shows that factor VIII values increase in severe cirrhosis but significantly decrease in the presence of concomitant portal thrombosis, likely because of consumption during thrombosis; D-dimer is enhanced by both liver failure and portal thrombosis; in severe cirrhosis, normal D-dimer and factor VIII values may safely exclude the presence of asymptomatic portal thrombosis.

Aged↗
PubMed2003

Comparison of four clinical prediction scores for the diagnosis of lower limb deep venous thrombosis in outpatients.

PURPOSE: We compared three scores for the prediction of deep venous thrombosis with a new score designed specifically for outpatients. METHODS: Patients referred for evaluation because of suspected deep venous thrombosis were examined by ultrasonography. Sensitivity and specificity were calculated for three clinical scores (Wells [nine components], Kahn [four components], and St. André [six components]). We developed a new score by multivariate analysis, and then compared this score with the others in a new sample. RESULTS: Four hundred and forty-four outpatients were included in the first sample, of whom 126 (28%) had deep venous thrombosis. The Wells score was a better predictor of deep venous thrombosis than the Kahn and St. André scores. According to the Wells score, 73 patients had a high probability of deep venous thrombosis (of whom 51 [70%] actually had a thrombosis) and 178 had a low probability of deep venous thrombosis (of whom 19 [11%] had a thrombosis). A new score was developed as follows: male sex (+1), lower limb palsy or immobilization (+1), confinement to bed >3 days (+1), lower limb enlargement (+1), unilateral lower limb pain (+1), and other plausible diagnosis (-1). In a validation sample of 282 outpatients, this score identified 31 patients who had a high probability of deep venous thrombosis (score > or =3), of whom 18 (58%) had a thrombosis, and 70 patients who had a low probability (score < or =0), of whom 3 (4%) had a thrombosis. The Wells score and this ambulatory score had similar test operating characteristics in the validation sample. CONCLUSION: Our new six-component score had similar diagnostic utility as the nine-component Wells score among outpatients being evaluated for deep venous thrombosis.

Female↗
PubMed2003

Central venous catheter related thrombosis in haematology patients and prediction of risk by screening with Doppler-ultrasound.

Patients with a central venous catheter (CVC) who receive intensive chemotherapy or a stem cell transplantation for haematological disease are at risk for developing CVC-related thrombosis. To study the incidence of thrombosis, 105 consecutive patients underwent serial Doppler-ultrasound and we evaluated whether clinically manifest thrombosis could be predicted by screening with Doppler-ultrasound. Patients with subclavian or jugular inserted CVCs were clinically assessed each day for signs and symptoms of thrombosis. Additional Doppler-ultrasound screens were performed weekly by an independent physician in all patients until CVC removal. Doppler-ultrasound recordings were assessed by two blinded observers. In cases of clinically suspected thrombosis, the attending physicians followed routine diagnostic and therapeutic procedures. The overall cumulative incidence of CVC-related thrombosis was 28.6% (30 of 105 patients). Of the 30 patients with thrombosis, 26 had subclinical thrombosis by Doppler-ultrasound, nine of whom developed clinically manifest thrombosis later. Four patients had clinically manifest thrombosis without prior abnormal Doppler-ultrasound. In cases of subclinical thrombosis the risk of developing symptomatic disease increased sevenfold (34.6% vs. 5.1%). Doppler-ultrasound screening may be useful to identify those patients that are at high and low risk for clinically manifest CVC-related thrombosis.

Catheterization, Central Venous↗
PubMed1999

Hyperhomocysteinemia, anticardiolipin antibody status, and risk for vascular access thrombosis in hemodialysis patients.

BACKGROUND: Vascular access failure is an important cause of morbidity in end-stage renal failure patients on hemodialysis. Currently, little is known about risk factors that predispose certain hemodialysis patients to recurrent access thrombosis. Hyperhomocysteinemia (common in patients with renal failure) predisposes people with normal renal function to recurrent and early-onset venous thrombosis, although the effect on vascular access thrombosis is currently unknown. Previous studies have suggested that high titers of IgG anticardiolipin antibody (IgG-ACA) predispose hemodialysis patients to access thrombosis. This cross sectional study was designed to assess for an association between two predictive variables, hyperhomocysteinemia and elevated titers of IgG-ACA, and vascular access thrombosis in patients undergoing chronic hemodialysis. METHODS: Risk factors for vascular access thrombosis were documented, and the number of episodes of access thrombosis was recorded for the previous three years in patients undergoing hemodialysis. Midweek predialysis total homocysteine and IgG-ACA levels were measured in all subjects. RESULTS: Of the 118 patients who were enrolled, 75.4% had a native arteriovenous fistula. Episodes of vascular access thrombosis were recorded for the previous three years; 34 (28.8%, 95% CI 20.9 to 37.9%) patients had 72 episodes of access thrombosis over the period of risk. Mean homocysteine levels were not significantly different between these 34 patients (28.6 micromol/liter, 95% CI 24.5 to 32.7) and the patients who had no episodes of graft thrombosis (29.8 micromol/liter, 95% CI 26.7 to 32.9). Sixty-seven unselected patients had IgG-ACA levels drawn for analysis, and all assays were negative. The only variable that was associated with a higher risk for graft thrombosis was the type of vascular access placed (odds ratio 4.0, 95% CI 1.6 to 9.6 for patients with a synthetic graft compared with those with an arteriovenous fistula). CONCLUSIONS: No association was found between homocysteine levels or anticardiolipin antibody and vascular access thrombosis in our patient population.

Antibodies, Anticardiolipin↗
PubMed2002

Inferior vena cava thrombosis at its hepatic portion (obliterative hepatocavopathy).

The Budd-Chiari syndrome was primarily described as hepatic vein thrombosis within the liver, but it now includes inferior vena cava (IVC) thrombosis and other conditions that cause hepatic vein outflow obstruction. This author and several others maintain that primary hepatic vein thrombosis and primary IVC thrombosis represent two different clinical disorders. Primary thrombosis of the IVC most commonly occurs in its hepatic portion, which seems to be predisposed to thrombosis and has been called membranous obstruction of IVC, because the thrombus organizes into a fibrous and frequently membranous occlusion of the IVC. The hepatic vein orifices are affected to varying degrees, resulting in congestive liver damage. The cause of IVC thrombosis may be a hypercoagulable state such as coagulation factor deficiency and myeloproliferative disorders, but is more often idiopathic. In Nepal, it is endemic with a suspected association with infections. To consider IVC thrombosis and the congestive liver damage as a disease entity, this author proposes the term obliterative hepatocavopathy, separate from hepatic vein thrombosis. Clinically obliterative hepatocavopathy is less severe in its acute phase compared with hepatic vein thrombosis, but it aggravates occlusion of hepatic vein orifices with recurrent thrombosis. Primary hepatic vein thrombosis and obliterative hepatocavopathy display different hemodynamics of the hepatic veins, IVC, and portal vein; dilatation of the subcutaneous veins in the body trunk is more pronounced in obliterative hepatocavopathy because the ascending lumbar vein becomes the major collateral route. Congestive liver cirrhosis develops after a long clinical course that may be complicated by hepatocellular carcinoma.

Budd-Chiari Syndrome↗