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PubMed1998

[Do the prevention and treatment of deep venous thrombosis have specificity in the cancer patient?].

An increased incidence of deep vein thrombosis is reported in cancer patients as compared with general population. Several risk factors for deep vein thrombosis have been identified: venous stasis, direct invasion of venous wall by tumor, and hypercoagulability state by inadequate secretion of procoagulant activities. Reports have suggested that chemotherapeutic agents and hormonal treatment may contribute to this risk. Few papers are available concerning the prophylaxis and curative treatment of deep vein thrombosis in cancer patients and no consensus has been reached yet. This predisposition for deep vein thrombosis should be taken into consideration for perioperative prophylaxis. Efficacy and safety of heparin and antivitamin K in the curative treatment of deep vein thrombosis are discussed but can not be accurately evaluated because of diversity of clinical presentations and mechanism of activation of coagulation. Prospective studies are necessary.

Anticoagulants↗

PubMed2004

Thrombolysis for cerebral vein and dural sinus thrombosis.

BACKGROUND: Treatment of cerebral sinus thrombosis with thrombolytics has been reported in cases with a deteriorating clinical course despite anticoagulant therapy. The rationale of this treatment is to promote rapid recanalisation of the occluded sinus. OBJECTIVES: To review the available evidence on the efficacy and safety of thrombolysis in confirmed cerebral sinus thrombosis. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register (March 2003), the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 1, 2003), MEDLINE (1966 to March 2003), EMBASE (1980 to March 2003), and reference lists of all relevant publications. SELECTION CRITERIA: We aimed to analyse separately unconfounded randomised controlled trials comparing thrombolytic agent with placebo, or thrombolytic agent with antithrombotic therapy, or thrombolytic agent and antithrombotic with antithrombotic alone, in patients with dural sinus thrombosis (confirmed by MR venography, intra-arterial venography or CT venography). DATA COLLECTION AND ANALYSIS: Two groups of reviewers independently applied the inclusion criteria. MAIN RESULTS: No randomised controlled trials were found. REVIEWER'S CONCLUSIONS: There is currently no available evidence from randomised controlled trials regarding the efficacy or safety of thrombolytic therapy in dural sinus thrombosis. A randomised controlled trial is justified to test this therapy especially in patients predicted to have a poor prognosis.

Cerebral Veins↗

PubMed2003

Pregnancy-associated thrombosis.

Venous thromboembolism (VTE) occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium. In the general population the incidence of pregnancy associated VTE is approximately 1 in 1500 deliveries The risk of VTE is five times higher in a pregnant than in a non-pregnant woman. Postpartum the VTE-risk is even higher. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. In individuals with well defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A variation, antithrombin-deficiency or protein C-deficiency, a relative risk of pregnancy associated VTE between 3.4 and 15.2 has been found. Women with previous VTE have an approximately 3.5 fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Our ability to diagnose pregnancy-associated VTE clinically is generally poor, since dyspnea, tachypnea, swelling and discomfort in the legs are common. Objective diagnosis is essential for treatment decisions. Exposure to radiation of less than 50,000 microGy (5 rad) has not been associated with a significant risk of fetal injury Therefore, besides sonography, routine diagnostic procedures should be performed, if clinically necessary. Heparin does not cross the placenta and is therefore the anticoagulant of choice. In case of acute thrombosis during pregnancy, treatment is performed like in nonpregnant patients. There is ongoing debate, whether or not pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. In patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality or a history of a severe thrombotic event (pulmonary embolism, extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Post partum prophylaxis should be given in all women with an increased risk for VTE.

Acute Disease↗

PubMed1997

Isolated deep cerebral venous thrombosis treated by direct endovascular thrombolysis.

BACKGROUND: Isolated thrombosis of the deep cerebral venous system is very rare and is associated with a poor prognosis. Antithrombin III (AT III) deficiency is a disorder of hypercoagulability associated with deep venous thrombosis and recurrent pulmonary emboli. We report a case of an 18-year-old man who presented with spontaneous thrombosis of the deep cerebral veins and straight dural sinus as the initial presentation of a previously undiagnosed AT III deficiency. METHODS: The patient was managed using direct endovascular infusion of the fibrinolytic agent urokinase followed by intravenous heparin. RESULTS: The technique was successful in establishing patency of the deep cerebral venous system. The patient experienced a good clinical outcome. CONCLUSIONS: Direct endovascular thrombolysis is a potentially effective management strategy for isolated thrombosis of the deep cerebral venous system.

Adult↗

PubMed1997

The pill and thrombosis: epidemiological considerations.

The oral contraceptive is one of the most widely taken medications in the healthy population. The clinically important side-effects are venous and arterial thrombosis. Accurate estimates of incidence of these side-effects have proven to be difficult. Diagnostic modalities for thrombosis are sub-optimal and the problems of study methodology, primarily a reliance on non-experimental studies, have limited the ability to define the attributable risk of thrombosis from oral contraception. Pharmacological attempts to further decrease venous thrombotic side-effects by the use of third-generation oral contraceptives have failed. This places a greater emphasis on the selection of patients to help avoid giving medication to those patients with underlying thrombotic risk factors. An example of this approach has been the clear confirmation of the adverse effects of cigarette smoking and arterial thrombosis in oral contraceptive users. At the biochemical level, hypercoagulability testing may be useful. Screening for high-frequency prothrombotic abnormalities, such as the Factor V Leiden genotype, represents an important addition to the process by which patients are selected, and may be prototypic of further advances.

Adult↗

PubMed2000

Prevalence of methylenetetrahydrofolate reductase C677T and its association with arterial and venous thrombosis in the Chinese population.

Moderate hyperhomocysteinaemia (MHH) is associated with arterial and venous thrombosis. A main genetic defect related to MHH is a C to T substitution at nucleotide 677 of the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene. A prothrombin 20210A mutation was recently identified as a risk factor for arterial and venous thrombosis. However, studies on the prevalence of mutant MTHFR C677T and prothrombin G20210A and their association with thrombosis were controversial and seldom reported in the Chinese population. We investigated the prevalence of MTHFR C677T and prothrombin G20210A genotypes by polymerase chain reaction (PCR) followed by restriction enzyme digestion in 420 Chinese subjects: 53 with deep venous thrombosis (DVT); 145 with cerebrovascular disease [115 cerebral infarction, 30 cerebral haemorrhage (CH)]; 100 with coronary artery disease (CAD); and 122 control subjects. The prevalence of the mutated MTHFR 677TT genotype and the 677T allele in normal controls was 12.3% and 30.7% respectively, similar to that in Caucasians and Japanese. The mutant 677T homozygotes and alleles were more frequent in patients with DVT than in controls (18.9% vs. 12.3%, 0.01 < P < 0. 025; 48.1% vs. 30.7%, P < 0.005). The relative risk of DVT among the carriers of 677TT and 677T were significantly increased [odds ratios: 3.4, 95% confidence interval (CI) 1.3-9.5, and 3.6, 95% CI 1. 7-7.7, respectively). The mutant MTHFR heterozygous 677C/T carriers were increased in patients with cerebral infarction compared with controls (53.9% vs. 36.9%, 0.01 < P < 0.025). Relative risk of cerebral infarction was 0.96 (95% CI 0.4-2.3) for 677TT homozygotes and 1.99 (95% CI 1.2-3.4) for 677C/T heterozygotes. However, the distribution of the MTHFR TT genotype was less frequent in patients with CAD with coronary artery stenosis of > 50% than in controls (2. 8% vs. 12.3%, 0.025 < P < 0.05). Relative risk of CAD was not increased among the carriers of 677TT and 677T (odds ratios: 0.2, 95% CI 0-1.1, and 0.97, 95% CI 0.5-1.8, respectively). There were no differences in the distribution of the MTHFR genotypes among CH, CAD with coronary artery stenosis of < 50% and controls. The prothrombin 20210A mutation was not found in any patients or controls. These results demonstrated that MTHFR 677T was associated with DVT and cerebral infarction but was less associated with CAD in the Chinese population.

Adolescent↗

PubMed2001

Prenatal diagnosis of thrombosis of the dural sinuses with real-time and color Doppler ultrasound.

OBJECTIVE: To assess the sonographic findings and clinical implications of fetal thrombosis of dural sinuses. DESIGN: Retrospective study of cases with a prenatal diagnosis of thrombosis of the dural sinuses. RESULTS: The diagnosis of fetal thrombosis of the dural sinuses was established in three uncomplicated pregnancies at 21, 22 and 28 weeks' gestation by transabdominal and transvaginal sonography, demonstrating a blood clot within the dilated dural sinuses, always in the region of the torcular Herophilii. The diagnosis was further confirmed by the color Doppler demonstration of absence of blood flow within the dilated dural sinuses. Upon request of the couples two pregnancies were terminated. One infant was delivered at term by Cesarean section and died during neurosurgery. CONCLUSIONS: Thrombosis of the cerebral venous circulation can occur antenatally. Accurate diagnosis can be made using fetal real-time and color Doppler ultrasound.

Blood Flow Velocity↗

PubMed2003

Thrombosis in inherited factor VII deficiency.

Thrombosis in congenital factor (F) VII deficiency was investigated through extensive phenotypic and molecular-genetic studies. Patients with a history of thrombosis among 514 entries in the FVII Deficiency Study Group database were evaluated. Thrombotic events were arterial in one case, disseminated intravascular coagulation in another and venous in seven. Gene mutations were characterized in eight patients: three were homozygous, three compound heterozygous and two heterozygous. FXa and IIa generation assays were consistent with the genetic lesions. One patient was heterozygous for the FV Leiden and one for the FIIG20210A mutation. In seven patients, surgical interventions and/or replacement therapies had a close temporal relationship with thrombosis, while in the remaining, events were apparently spontaneous. Thromboses were not associated with any specific age, phenotype, mutation zygosity or thrombophilic abnormalities. In particular, severe FVII deficiency did not seem to offer protection from strong thrombosis risk factors such as surgery and replacement therapy.

Adolescent↗

PubMed2001

Microcirculatory alterations in a Mongolian gerbil sinus-vein thrombosis model.

BACKGROUND AND PURPOSE: The pathophysiology of sinus vein thrombosis (SVT) is still controversial in patients and experimental animals, the microcirculatory alterations in particular. This study was designed to develop a new sinus vein thrombosis model and to further elucidate pathophysiological events such as the relationship between local and regional cerebral blood flow and haemoglobin oxygen saturation (HbSO2), changes of the microvasculature, leukocyte behaviour and brain tissue damage. METHODS: In a first experimental series, animals were divided into two groups which resulted from different procedures of inducing SVT. In the SSS middle occlusion group (SMO group), SVT was induced by the ligation of the superior sagittal sinus right in the middle between the bregma and the confluence sinum. In the SSS posterior occlusion group (SPO group) the ligation was performed close to the confluence sinum. Regional cerebral blood flow (rCBF) was assessed at 36 identical locations by laser Doppler flowmetry together with regional haemoglobin oxygen saturation (HbSO2). In a second series of experiments SVT was induced by ligation of the SSS close to the confluence sinum (SVT group) to study effects on the cortical microcirculation. A sham operation was performed in six animals (sham group). In both groups, an intravital microscopic double tracing technique was utilised for evaluating microvessel structures and leukocyte behaviour. The images were recorded on videotape for evaluating alterations of microvessel (venules, arterioles and capillaries) diameters and numbers of leukocyte rollers and stickers by a digital video analyser. Animals were sacrificed for histological evaluation after 5 days. RESULTS: The posterior sinus ligation caused a significant decrease of rCBF and HbSO2 and brain tissue damage which was not seen in the SMO group. Alteration of rCBF and HbSO2 were positively correlated with infarct size in the SPO group only, where venous infarction was easily reproduced. Therefore, it is suggested that this model is suitable for studying SVT in Mongolian gerbils. Intravital microscopy of the cortical microcirculation revealed no significant changes of vessels diameter in the sham group, whereas a significant dilation of veins and capillaries was seen in the SVT group. Numbers of leukocyte rollers and stickers were positively correlated with infarct size. CONCLUSION: Microcirculatory alterations and brain tissue damage from SVT in the Mongolian gerbil depend on the SSS occlusion site. The newly established mongolian gerbil sinus-vein thrombosis model has advantages compared to previously reported sinus-vein thrombosis models such as easy handling, easy technique, highly reproducibility, and good observation of microcirculatory event. The model allows for studies of cerebral low-flow conditions such as expected to occur in an ischaemic penumbra zone.

Animals↗

PubMed2003

Isolated internal cerebral venous thrombosis in a neonate with increased lipoprotein (a) level: diagnostic and therapeutic considerations.

Background. Internal cerebral venous thrombosis is a life-threatening condition, which requires immediate therapy. Being infrequent in childhood, internal venous thrombosis is very rare in the neonate and has never been observed without concomitant occlusion of further dural sinuses. Case Description. We report a neonate born at term, who developed seizures on the third day of life after normal pregnancy and uneventful delivery. Ultrasound and CT disclosed bilateral intraventricular and intracerebral hemorrhage with an unusual distribution for germinal matrix hemorrhage. MRI disclosed thrombotic occlusion of the straight sinus and the internal cerebral veins with concomitant bleeding into the ventricles, the basal ganglia, thalamus and the periventricular hemispheres. The other sinuses were not affected. The clinical condition of the child improved after initiation of a low-dose heparin treatment with subsequent partial recanalization of the occluded vessels. The screening for risk factors disclosed an elevated lipoprotein (a) level, also present in both parents. Conclusion. Internal cerebral venous thrombosis may be encountered in neonates and must be included in the list of differential diagnosis of perinatal intraventricular and intracerebral bleeding. MRI allows the diagnosis even in the absence of widespread dural sinus occlusion. Low dose heparin may be a therapeutic option in these cases. This is the first report of neonatal internal venous thrombosis due to hereditary lipoprotein (a) level elevation, which must be included in the list of possible predisposing conditions.

Humans↗

PubMed1993

Superior activity of a thromboxane receptor antagonist as compared with aspirin in rat models of arterial and venous thrombosis.

We determined the effects of aspirin and a novel thromboxane A2/prostaglandin endoperoxide (TP)-receptor antagonist, BMS-180291, on thrombosis and bleeding times in skin and mesenteric arteries. In anesthetized rats, occlusive thrombosis was induced in the carotid artery by topical application of ferrous chloride and in the vena cava by blood flow stasis combined with either infusion of thromboplastin or hypotonic saline. Aspirin (1, 10, and 50 mg/kg) did not reduce arterial or venous thrombus weight significantly. BMS 180,291 (150 micrograms/kg/min) decreased arterial thrombus weight and hypotonic saline-induced caval thrombus weight by 58 and 57%, respectively. BMS-180291 lacked antithrombotic activity at a lower dose (50 micrograms/kg/min) and failed to inhibit thromboplastin-induced caval thrombosis. BMS-180291 (150 micrograms/kg/min) significantly reduced arterial thrombus weight by 40% when plasma epinephrine concentration was increased to 5 ng/ml. BMS-180291 and aspirin produced increases of only < or = 30% in bleeding times. These results demonstrate that BMS-180291 has antithrombotic activity in experimental aspirin-resistant arterial and venous thrombosis. Both aspirin and BMS-180291 have only modest effects on small artery hemostasis in rats.

Animals↗

PubMed2004

The accumulation of specific types of proteoglycans in eroded plaques: a role in coronary thrombosis in the absence of rupture.

PURPOSE OF REVIEW: Although fibrous cap rupture is the primary cause of coronary thrombosis, plaque erosion is responsible for 30%-40% of acute thrombotic events. The interface of the eroded surface involves a denuded endothelium allowing direct contact of the platelet/fibrin thrombus with the underlying lesion. This review discusses the putative role of extracellular matrix molecules, in particular proteoglycans/hyaluronan, in the development of acute coronary thrombosis associated with erosion. RECENT FINDINGS: The plaque/thrombus interface in erosion presents a unique surface since it consists of predominantly SMCs and proteoglycans with minimal or no inflammation. The lack of significant inflammation raises the possibility that erosion represents chronic wounding rather than true atherogenesis. The abundance of proteoglycan and hyaluronan matrix suggests their potential role in the development of thrombosis. Matrix changes may contribute to endothelial loss, the magnitude of the thrombotic event, or both. Versican facilitates platelet adhesion at low shear and cooperates with collagen to promote platelet aggregation. Further, versican may, in part, regulate water content and in turn support coagulation because water-dependent functionality of anticoagulation molecules. Finally, experimental models of plaque erosion are currently being developed guided by the premise that the loss of surface endothelium together with other procoagulant factors may underlie the development of platelet-rich thrombi. SUMMARY: The loss of endothelium and exposure of a potentially procoagulant versican-hyaluronan matrix may be largely responsible for plaque erosion. The development of relevant animal models should allow further insight into the pathophysiology of coronary thrombosis in the absence of rupture.

Adult↗

PubMed2006

ERK2 activation in arteriolar and venular murine thrombosis: platelet receptor GPIb vs. P2X.

The functional significance of extracellular signal-regulated kinase 2 (ERK2) activation was investigated during shear induced human platelet aggregation (SIPA) in vitro and during shear controlled thrombosis in vivo in intestinal arterioles and venules of wild type (WT) and transgenic (TG) mice with platelet-specific overexpression of human P2X(1) (TG). In SIPA, ERK2 was rapidly phosphorylated during GPIb stimulation, its activation contributing to SIPA for 50%, independently of P2X(1) regulation. Thrombotic occlusion of injured arterioles occurred considerably faster in TG (4.3 +/- 2.3 min) than in WT (38 +/- 8 min) arterioles, but occlusion times in TG (19 +/- 12) and WT (48 +/- 4.5 min) venules differed less. Both the alphabeta-meATP triggered desensitization of platelet P2X(1), as well as P2X(1) antagonism by NF279 or NF449 prolonged mean occlusion to about 75 min in WT and 65 min in TG arterioles, but venular occlusion times were less affected. Preventing ERK2 activation by U0126 prolonged occlusion times in TG (41 +/- 10 min) and WT (51 +/- 17) arterioles more than in TG (46 +/- 5 min) and WT (56 +/- 6 min) venules, uncovering a role for ERK2 in shear controlled thrombosis. Antagonism of GPIb by a recombinant murine von Willebrand factor (VWF)-A1 fragment prolonged occlusion times to comparable values, ranging from 55 to 58 min, both in TG and WT arterioles and venules. Further inhibition strategies, combining VWF-A1, U0126 and NF449 in WT and TG mice and resulting in occlusion in various time windows, identified that inhibition by VWF-A1 largely abrogated the ERK2 contribution to thrombosis. In conclusion, P2X(1) and ERK2 both participate in shear stress controlled thrombosis, but ERK2 activation is initiated predominantly via GPIb-VWF interactions.

Animals↗

PubMedDate not supplied

Vascular bed specific alterations in coagulation and fibrinolytic parameters in young women following myocardial infarction, lacunar cerebral infarction and deep vein thrombosis.

The possible existence of distinctive, vascular bed specific alterations of coagulation and fibrinolytic parameters associated with three different types of thrombosis was investigated in young women (n = 68, <45 years at onset of the event) following myocardial infarction (MI) (n = 22), lacunar cerebral infarction (LACI) (n = 16), idiopathic deep vein thrombosis (VT) (n = 14) and venous thrombosis due to oral contraceptive use (n = 16) in the stable period after the acute thrombotic event. Coagulation and fibrinolytic parameters, as well as classical metabolic variables, were measured and compared with 52 age-matched, healthy controls. In MI women we observed elevated tissue type plasminogen activator (t-PA) antigen levels, which correlated significantly with parameters of the plurimetabolic syndrome. In LACI women we found elevated fibrinogen, which correlated with D-dimer, systolic blood pressure, smoking, and sedimentation rate. Prolonged euglobulin clot lysis time, elevated t-PA antigen, PAI-1 antigen and activity, which all correlated with parameters of the plurimetabolic syndrome, were found in women with idiopathic VT, who were also clearly obese but not in women in whom oral contraceptives were the triggering factor for VT. Our results showed not parallel, but different profiles of alterations in fibrinolytic and coagulation parameters in line with the prediction of a vascular bed specific thrombosis process.

Adult↗

PubMed1983

Cerebral venous and arterial thrombosis in pregnancy and puerperium. A study of 135 patients.

Cerebral venous thrombosis occurring in puerperium is about 10 to 12 times more frequent in India than in Western countries. A clinical study of 135 patients with cerebrovascular accidents in early puerperium is reported. Cortical vein thrombosis is common and arterial thrombosis rare (6/135). The illness usually occurs within the first two weeks, after normal delivery at full term, in a multiparous woman, with multi-focal seizures, stupor or coma, regressing focal signs or at times as pseudotumour cerebri. Deep leg vein thrombosis and pelvic sepsis are rare. Mortality has been high reaching 28 to 33 percent in both Indian and Western countries. With the use of anticoagulants in some selected patients and earlier; energetic, supportive and symptomatic measures in others the mortality could be reduced to less than 20 percent. The quality of survival is good since those who survive have only minimal physical disability.

Adult↗

PubMed2000

Fatal cerebral venous sinus thrombosis as major complication of metastatic cervical mass: computed tomography and magnetic resonance findings.

Cerebral venous sinus thrombosis is an uncommon but potentially lethal condition, with mortality between 5.5-30 per cent. It was previously associated with infections of the orbit, mastoid or face, but, after the advent of antibiotics, the most common causes include neoplasms, dehydration, oral contraceptives, coagulopathies, collagen diseases, and pregnancy and the puerperium. We report a case of fatal cerebral venous sinus thrombosis in a 68-year-old patient with a metastatic cervical mass, who developed internal jugular vein thrombosis that progressed cranially to transverse and sagittal sinus thrombosis.

Aged↗

PubMed2001

Coagulation and thrombosis in cardiovascular disease: plausible contributions of infectious agents.

An occlusive thrombus in the coronary arteries is the critical pathological event that immediately precedes most cases of myocardial infarction. Often the thrombus originates with a bleed from a fissured atheroma. Atheroma formation, therefore, creates risk of thrombosis; asymptomatic episodes of thrombosis and healing contribute to the pathogenesis of atherosclerosis and the development of atherosclerotic plaques. Based largely on in vitro and animal model evidence, infectious agents and their products can activate the coagulation cascade enzymatically or by up-regulating tissue factor. By initiating a procoagulant response, infectious agents can indirectly trigger a prothrombotic response. Alternatively, some microbes can directly trigger platelet aggregation in vitro and in animal models, suggesting direct prothrombotic potential in human cardiovascular disease. Activation of coagulation and thrombosis characterizes the pathological response to infectious agents in human disseminated intravascular coagulation and infective endocarditis. Given the underlying biological plausibility, the cumulative lifetime burden of chronic pathogens may be expected to create risk of atherosclerosis and thrombosis, and, indirectly, signs of cardiovascular disease.

Animals↗

PubMed2006

Etiology and consequences of thrombosis in abdominal vessels.

The thrombophilia which can be either congenital or acquired in adult life has major implications in the abdominal vessels. The resulting portal vein thrombosis, Budd-Chiari syndrome and mesenteric vein thrombosis have a variety of consequences ranging from acute abdomen to chronic hepatomegaly and even totally asymptomatic patient in whom the only finding is pancytopenia. The complications like esophageal varices, portal gastropathy, ascites, severe hypersplenism, liver failure requiring liver transplantation are well known. Interesting features of collateral venous circulation showing itself as pseudocholangiocarcinoma sign and its possible clinical reflection as cholestasis are also known from a long time. The management strategies for these complications of intraabdominal vessel thrombosis are not different from their counterpart which is cirrhotic portal hypertension, but the prognosis is unquestionably better in former cases. In this review we presented and discussed the abdominal venous thrombosis, etiology and the resulting clinical pictures. There are controversial issues both in nomenclature, and management including anticoagulation problems and follow up strategies. In light of the current knowledge, we discussed some controversial issues in literature and presented our experience and our proposals about this group of patients.

Abdomen↗

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