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PubMed2002

Fulminate intracardiac thrombosis associated with Budd-Chiari-syndrome and inferior vena cava thrombosis.

The most common cause of edema of the legs and dyspnea is congestive heart failure. Further differential diagnosis such as renal or hepatic failure have to be considered. We report the case of a previous healthy 65-year-old woman who developed dyspnea and massive edema of the legs followed by acute hepatic and renal failure. Imaging studies showed a thrombosis of the inferior vena cava (IVC) caused by a tumor between the right kidney and the IVC. Histological examination revealed a leiomyosarcoma of the IVC. Hepatic failure due to venous outflow obstruction (Budd-Chiari syndrome, BCS) was diagnosed. Coagulation profile showed a complex disorder due to acute hepatic failure. Factor V Leiden and prothrombin gene mutation G20210A could be excluded. The thrombosis extended from the femoral veins up to the right atrium. After 11 days of anticoagulation with heparin platelet counts decreased by more than 50%. Suspecting a heparin-induced thrombocytopenia the patient was placed on recombinant hirudin (lepirudin) for anticoagulation. Hepatic venogram showed a thrombosis of the hepatic vein orifices but not of the hepatic veins. The tumor and the thrombi were removed surgically. When the cardiopulmonary bypass was terminated new intracardiac thrombi occurred. Despite immediate surgical intervention the patient finally died due to right ventricular failure caused by the fulminate intracardiac thrombosis. In conclusion, thrombosis of the IVC may mimic congestive heart failure and may cause BCS. Neoplasms and coagulation disorders may cause thrombosis of the IVC.

Aged↗

PubMed2002

Interleukin 8 and venous thrombosis: evidence for a role of inflammation in thrombosis.

Elevated plasma levels of interleukin 8 (IL-8) were previously shown to be associated with recurrent venous thrombosis. To assess the risk of venous thrombosis, IL-8 plasma concentrations were measured in patients and control subjects of the Leiden Thrombophilia Study (LETS). This population based case-control study included 474 patients with a first deep-vein thrombosis and 474 age- and sex-matched controls. The risk of venous thrombosis for subjects with elevated IL-8 levels (above 90th percentile of controls) compared with subjects with IL-8 levels below the 90th percentile was increased 1.8-fold (95%CI 1.2-2.8). Adjusted for age and sex, the odds ratio was 1.9 (95%CI 1.3-2.8). IL-8 concentrations were weakly correlated with age, male sex, and concentrations of C-reactive protein, factor VIII coagulation activity and homocysteine, but adjustment for these factors did not substantially affect the association between IL-8 and venous thrombosis. Our results suggest that IL-8 is a risk factor for venous thrombosis.

Adolescent↗

PubMed2003

Use of elastic compression stockings after deep venous thrombosis: a comparison of practices and perceptions of thrombosis physicians and patients.

Daily long-term use of elastic compression stockings (ECS) by patients with deep venous thrombosis (DVT) may help to prevent the post-thrombotic syndrome (PTS). However, the effectiveness of ECS in clinical practice is difficult to predict, since the practices and perceptions of patients and thrombosis physicians regarding ECS have not been documented. The objectives were to survey DVT patients and thrombosis physicians on their practices and perceptions regarding use of ECS after DVT, and to evaluate whether physician perceptions are supported by patient responses. Two surveys were conducted. The first was sent to 38 Canadian thrombosis physicians. The second was administered to 80 DVT patients attending Thrombosis Clinic at one of two Canadian university-affiliated hospitals. Most physicians believed that ECS were useful in preventing PTS and in managing venous symptoms. However, there was a lack of consensus regarding the optimal timing of initiation of ECS, duration of therapy, and compression strength, and only one-third routinely prescribed ECS to asymptomatic patients to prevent PTS. Most DVT patients who were prescribed ECS purchased them, 87% wore them daily, and most reported that ECS relieved swelling and symptoms. Physicians underestimated the degree of patient compliance with ECS, but correctly identified the main reasons for non-compliance. There is a lack of consensus among thrombosis physicians regarding ECS use after DVT. Patients with DVT are willing to comply with ECS therapy and most find them to be helpful. Our findings suggest that long-term study of the optimal use of ECS after DVT is both necessary and feasible.

Adult↗

PubMed2001

Long-term clinical course of proximal deep venous thrombosis and detection of recurrent thrombosis.

Symptomatic proximal deep vein thrombosis of lower extremities carries a high risk for recurrent venous thromboembolism that persists for many years. This risk is dependent on readily identifiable risk factors, being low after a trauma or a surgical intervention and higher in all the other patient categories. Moreover, postthrombotic sequelae will develop in one of every three patients, this risk being strongly related to the development of ipsilateral thrombosis. Although the optimal duration of anticoagulation in patients who experience an episode of proximal vein thrombosis is unknown, it seems reasonable to administer a short-term course of coumarin drugs to patients with thrombosis associated with transient risk factors, whereas a longer course (6 to 12 months) should be considered in patients with idiopathic thrombosis and in those with permanent risk factors. Indefinite anticoagulant therapy is a clinical judgement in the individual patient. The management of patients who develop clinical manifestations suggestive of recurrent ipsilateral venous thrombosis still represents a challenge for clinicians. Recent data suggest that these patients can be safely managed with the use of serial compression ultrasonography.

Clinical Trials as Topic↗

PubMed2002

Safety and efficacy of only 2 weeks of ticlopidine therapy in patients at increased risk of coronary stent thrombosis: results from the Antiplatelet Therapy alone versus Lovenox plus Antiplatelet therapy in patients at increased risk of Stent Thrombosis (ATLAST) trial.

BACKGROUND: Controversy exists regarding the frequency of late stent thrombosis among patients treated with intracoronary stents and the most appropriate duration of treatment with a thienopyridine that is required to prevent this complication. METHODS: We analyzed the frequency of stent thrombosis and other ischemic events in the Antiplatelet Therapy alone versus Lovenox plus Antiplatelet therapy in patients at increased risk of Stent Thrombosis (ATLAST) trial. In the ATLAST trial, 1102 patients at increased risk of stent thrombosis (ST-elevation myocardial infarction within 48 hours, diffuse distal disease, a large amount of thrombus, acute closure, residual dissection, etc) were randomly assigned to receive either enoxaparin (40 or 60 mg given every 12 hours for 14 days) or placebo; all patients received aspirin (325 mg daily) and ticlopidine (250 mg twice daily) for only 14 days. RESULTS: The primary end point, the 30-day combined incidence of death, nonfatal myocardial infarction, and urgent revascularization, was reached in 2.3% of patients (1.8% of patients taking enoxaparin vs 2.7% of patients taking placebo; P =.295). However, during the 15th through 30th days, the frequency of ischemic events was only 0.73%, and only 0.27% (3/1102) of patients had possible stent thrombosis (95% CI 0.06, 0.77). CONCLUSION: The frequency of stent thrombosis and other adverse ischemic events in the 15th through 30th days after stent placement in even high-risk stent patients treated with ticlopidine for only 2 weeks is low whether or not enoxaparin is administered.

Coronary Thrombosis↗

PubMed1996

Progression of superficial venous thrombosis to deep vein thrombosis.

PURPOSE: We have evaluated the progression of isolated superficial venous thrombosis to deep vein thrombosis in patients with no initial deep venous involvement. METHODS: Patients with thrombosis isolated to the superficial veins with no evidence of deep venous involvement by duplex ultrasound examination were evaluated by follow-up duplex ultrasonography to determine the incidence of disease progression into the deep veins of the lower extremities. Initial and follow-up duplex scans evaluated the femoropopliteal and deep calf veins in their entirety; follow-up studies were done at an average of 6.3 days, ranging from 2 to 10 days. RESULTS: From January 1992 to January 1996, 263 patients were identified with isolated superficial venous thrombosis. Thirty (11%) patients had documented progression to deep venous involvement. The most common site of deep vein involvement was progression of disease from the greater saphenous vein in the thigh into the common femoral vein (21 patients, 70%), with 18 of these extensions noted to be nonocclusive and 12 having a free-floating component. Three patients had extended above-knee saphenous vein thrombi through thigh perforators to occlude the femoral vein in the thigh, three patients had extended below-knee saphenous disease into the popliteal vein, and three patients had extended below-knee thrombi into the tibioperoneal veins with calf perforators. At the time of the follow-up examination all 30 patients were being treated without anticoagulation. CONCLUSIONS: Proximal saphenous vein thrombosis should be treated with anticoagulation or at least followed by serial duplex ultrasound evaluation so that definitive therapy may be initiated, if progression is noted. More distal superficial venous thrombosis should be carefully followed clinically and repeat duplex ultrasound scans performed, if progression is noted or patient symptoms worsen.

Adult↗

PubMed1998

Proposal of a new nomenclature for Budd-Chiari syndrome: hepatic vein thrombosis versus thrombosis of the inferior vena cava at its hepatic portion.

Budd-Chiari syndrome (BCS) was initially defined as a symptomatic occlusion of the hepatic veins, but subsequent reports on various obliterative changes that occur in the hepatic portion of the inferior vena cava (IVC) and hepatic vein orifices have resulted in a broadened and ambiguous definition. Membranous obstruction of the inferior vena cava has been regarded by many as a congenital vascular malformation, but its relation to the classical BCS has remained obscure. With modern imaging and recent histological study of new cases, membranous obstruction of the IVC is now considered to be a sequela to thrombosis. How to classify various forms of occlusion and stenosis of the IVC and hepatic vein ostia is a major challenge. In this review, we emphasize that primary hepatic vein thrombosis (classical Budd-Chiari) and an obliterative disease predominantly affecting the hepatic portion of the IVC, both of which account for most patients with venous outflow block, are clinically quite different. In the West, the former is more common than the latter, which constitutes the vast majority of cases of outflow block in developing countries such as Nepal, South Africa, China, and India. The latter is frequently complicated by hepatocellular carcinoma (HCC), and primary hepatic vein thrombosis is not. The major cause of thrombosis is a hypercoagulable state in hepatic vein thrombosis, but more of the latter cases are idiopathic. The clinical presentation of the latter is milder, and onset is frequently inapparent, whereas the former is more severe, sometimes causing acute hepatic failure. Markedly enlarged subcutaneous veins over the body trunk characterize the latter. We propose that these two disorders be clinically distinguished with a suggested term "obliterative hepato-cavopathy" for the latter against classical BCS.

Budd-Chiari Syndrome↗

PubMed2000

Sudden infant death syndrome, childhood thrombosis, and presence of genetic risk factors for thrombosis.

Sudden infant death syndrome or "cot death" has until the late eighties been a significant cause of death in children between the ages of 1 month and 1 year. Approximately two per 1000 children born alive dies of sudden infant death syndrome each year in Western Europe, North America, and Australia. The vulnerability of the infant brain stem to ischemia has been suggested to be a conceivable cause of sudden infant death syndrome. This is compatible with a hypothesis that genetic risk factors for cerebral thrombosis could cause microinfarction in the brain stem during the first month of life, affecting vital centers or their blood supply. The presence of three common point mutations seen in families with thrombophilia (1691G-->A in the coagulation factor V gene, 677C-->T in the methylenetetrahydrofolate reductase gene, and the 20210G-->A mutation in the prothrombin gene) could increase the risk for thrombosis in the child. This prompted us to investigate these genetic markers of thromboembolic disease in 121 cases of sudden infant death syndrome and in relevant controls, in the expectation of a more frequent occurrence of these markers if thrombosis is an etiological factor in sudden infant death syndrome. The frequency of homozygous 1691G-->A mutation in SIDS cases was higher than expected (odds ratio: 7.3, 95% confidence interval, 1.2-45.8). The allele frequencies (theta;) in cases of sudden infant death syndrome of the 1691G-->A, 677C-->T, and 20210G-->A alleles was 2.6% (1.0-5.5), 32.6% (26.8-38.9), and 0.9% (0.1-3.4), respectively. None of the allele frequencies found in the background population (3.4% for the 1691G-->A allele, 29% for the 677C-->T allele, and 1% for the 20210G-->A allele) differed significantly from that in cases of sudden infant death syndrome. In 5,251,027 inhabitants in Denmark, the incidence of venous thromboembolism was 0.9 per 1000 per year in the background population, and less than one-thousandth of these were children. Consequently it is not likely that venous thrombosis is a major cause of sudden infant death syndrome. On the other hand, this does not exclude other known or unknown risk factors for thrombosis as possible etiological factors for sudden infant death syndrome. It is likely that we must continuously employ the exclusion principle on possible etiological causes in genetic material from a large group of victims of sudden infant death syndrome if the phenomenon of sudden infant death syndrome is to be ascribed to a specific hereditary disorder.

3' Untranslated Regions↗

PubMed1996

Hepatic artery thrombosis after liver transplantation: temporal accuracy of diagnosis with duplex US and the syndrome of impending thrombosis.

PURPOSE: To determine how the interval between ultrasonography (US) and a definitive diagnosis affects the accuracy of duplex US for the diagnosis of hepatic artery thrombosis after transplantation. MATERIALS AND METHODS: Retrospective chart review was performed in 202 patients with liver transplants. Results of duplex US were compared with those of angiography, surgery, or autopsy. RESULTS: Sensitivity for US was 54% up to 1 month before and 82% on the day of the definitive diagnostic study. Specificity remained relatively constant over time (86%-87%). Accuracy reached 85%, and negative predictive value reached 93%. Qualitative changes on the sonogram enabled prediction of subsequent thrombosis. Rejection, recurrent hepatitis, aberrant anatomy, hypotension, arterial collaterals, and operator error caused false-positive or false-negative results. CONCLUSION: Although duplex US remains a good screen for hepatic artery thrombosis, angiography is strongly recommended. Serial US studies are necessary for diagnosis. Sensitivity improves over time as the clinical picture clarifies. Qualitative changes on the sonogram (the syndrome of impending thrombosis) enable prediction of subsequent hepatic artery thrombosis.

Adult↗

PubMed1988

Experimental study of acute coronary sinus thrombosis--clinical references to coronary sinus thrombosis and coronary venography.

The study was carried out to ascertain the effects caused by thrombosis in the coronary venous system. The coronary sinus (CS) of 21 adult mongrel dogs was abruptly obstructed to produce acute CS thrombosis. These dogs were then tested for serial changes of ECG, coronary arterial blood flow (CBF), left ventricular pressure (LVP), serum enzymes originating from the injured myocardium and histological changes of myocardium. Furthermore, the clinical application of a new coronary venography procedure was investigated. The results obtained in these experiments were as follows; (1) When the CS thrombosis was produced by the abrupt obstruction of the sinus, ECG patterns and serum enzymes originating from the myocardium showed changes similar to those of acute myocardial infarction. (2) The histological examinations showed that the changes in myocardial infarction were characteristically similar to those of hemorrhagic infarction. (3) Despite the complete obstruction of the coronary-venous system by thrombosis, the development of thrombosis or obstruction was not observed on the coronary-arterial side. This phenomenon is probably due to the recirculation of blood flow through the Thebesian vessels. (4) The experiment confirmed that the clear coronary venograms were easily obtained, without any risk, by the fixation of a balloon-tipped catheter inside the CS.

Animals↗

PubMed1992

Hematological causes of venous thrombosis in young people: high incidence of myeloproliferative disorder as underlying disease in patients with splanchnic venous thrombosis.

Thrombotic events occur frequently in myeloproliferative disorders, namely polycythaemia vera and essential thrombocythaemia. Standard diagnostic criteria are designed quite stringent, so that a number of patients could be underdiagnosed. Spontaneous erythroid colonies formation from bone marrow or peripheral blood in the absence of exogenous erythropoietin is considered a reliable index of myeloproliferative disorder even at early stages. Endogenous erythroid colonies (EECs) formation was assessed in 43 patients having recently suffered from venous thrombosis prior to 45 years and without a previous diagnosis of hematological disease favouring thrombosis. A screening for coagulative abnormalities associated with thrombophilia was also carried out: in 5 patients (11.6%) a plasmatic thrombogenic defect was found (quantitative deficiency of antithrombin III, 1 case, protein C, 2 cases, protein S, 1 case, and plasminogen, 1 case). In 10 patients (2 males and 8 females) (23.2%) EECs assay was positive, allowing diagnosis of myeloproliferative disease even though 7 of them did not fulfill standard diagnostic criteria. In the other 3 patients who met the criteria for diagnosis of overt myeloproliferative disease the thrombotic event was the inaugural manifestation. In all these EECs-positive patients thrombosis involved mesenteric and portal veins (n = 4), hepatic veins (n = 3), portal vein (n = 2), mesenteric vein (n = 1). One of them was simultaneously affected from congenital protein C deficiency. Thus latent or atypical forms of myeloproliferative disease as well as the overt stages were the most frequent recognized cause of splanchnic venous thrombosis, accounting for 55% of the cases of our series. On the contrary no EECs-positive subject was found among the 25 patients with other sites of thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2006

Cerebral cortical and deep venous thrombosis without sinus thrombosis: clinical MRI correlates.

BACKGROUND: Cortical and/or deep vein thrombosis (CDVT) without dural sinus involvement is uncommon and presents diagnostic difficulty for many reasons. Our aim is to determine the relationship between magnetic resonance imaging (MRI) findings and clinical findings in patients with CDVT. METHODS: Forty-six patients with venous stroke proved on MRI included in our Registry, corresponding to 0.1% of 4650 patients with stroke, were studied. Magnetic resonance angiography (MRA) was performed in all patients, and 18 of them had follow-up MRA. Outcome was evaluated by using the Glasgow Outcome Scale at the time of discharge and during follow-up. RESULTS: Thirty-two patients presented cortical venous stroke; 21 of them had involvement of the dorsomedial venous system, six had a defect in the posteroinferior venous group, and five had a defect in the anteroinferior venous group. Thirteen patients presented simultaneous involvement of the superficial and deep venous system; seven with a defect in the parietal and internal cerebral veins (three with involvement of vein of Gallen), four with a defect in the temporooccipital (vein of Labbé) and basal vein of Rosenthal, two with a deficit in the anterior frontotemporal and uncal-pterygoid venous system. One patient had deep venous thrombosis primarily localized to the thalami bilaterally and the basal ganglia on the right because of occlusion of the thalamostriate veins. The main presenting symptoms of CDVT were headache, focal neurologic signs, partial complex or secondary generalized seizures, and consciousness disturbances in those with deep venous thrombosis, presented alone or in combination at onset. CDVT was more than twofold more frequent in women than in men. Pregnancy, puerperium, oral contraceptive use, and infections were the most common predisposing factors. CONCLUSION: Computerized tomography, conventional MRI and diffusion-weighted imaging showing ischemic and/or hemorrhagic lesion that does not follow the boundary of classical arterial boundaries without signs of sinus thrombosis, and partial or generalized seizures followed by focal neurologic signs may predict CDVT. The outcome of patients with cortical venous stroke was good, but not in those with cortical plus deep venous infarction.

Adult↗

PubMed2005

Is heparin treatment the optimal management for cerebral venous thrombosis? Effect of abciximab, recombinant tissue plasminogen activator, and enoxaparin in experimentally induced superior sagittal sinus thrombosis.

BACKGROUND: Based on a newly developed model of reversible superior sagittal sinus (SSS) thrombosis in the rat, we investigated the effect of thrombolytic and anticoagulant treatment on recanalization, brain parenchymal changes, and motor deficits. METHODS: Thrombosis of the SSS was induced by topical application of ferric chloride. Occlusion was confirmed by magnetic resonance angiography (MRA). Six hours after operation, single treatment with 10 mg recombinant tissue plasminogen activator (rtPA)/kg and 6 mg abciximab/kg or subcutaneous injection of 450 IU/kg enoxaparin twice daily was started, each group containing 10 rats. Follow-up MRI with T2- and diffusion-weighted images was performed on the first, second, and seventh postoperative day. RESULTS: Control and enoxaparin-treated animals developed diffuse brain edema without infarction or intracerebral bleeding. This was indicated by an increase of T2 relaxation time and a decrease of the apparent diffusion coefficient in the parasagittal and lateral cortex. In these groups, the degree of recanalization after 7 days was comparable (48% versus 52%). Enoxaparin-treated animals showed significant amelioration of functional deficits. Clinical outcome was best in the abciximab-treated group, with a residual sinus occlusion of 36% after 1 week. Highest recanalization was achieved by lysis with rtPA (85%). CONCLUSIONS: Enoxaparin treatment in rats with cerebral venous thrombosis significantly influences clinical outcome. However, it has no effect on recanalization. GPIIb/IIIa antagonists and rtPA accelerate thrombolysis. They may represent an alternative in treatment of cerebral venous thrombosis.

Abciximab↗

PubMed1978

[Coronary atherosclerosis, coronary thrombosis and myocardial infarction in autopsy cases. 9th communication: relationship of coronary thrombosis and myocardial infarction (author's transl)].

The autopsy reports of the Pathological Institute Erfurt of the period from 1.1.1951 until 31.12.1969 were scored for cases of myocardial infarction and coronary thrombosis. Among 2,393 morphologically analysed myocardial infarctions 454 coronary thromboses (18.97 per cent) were found. Males were significantly more affected than females. Fresh infarcts showed significantly more thromboses than callous infarcts. We found fresh and occluding vessel thromboses more frequently in fresh infarctions. The analysis of age distribution yielded an increase of the rate of thrombosis in cases with myocardial infarction. On the other hand, the frequency of infarctions in cases with a coronary thrombosis was decreasing. It is suggested that the risk for infarctions is larger in younger people with coronary thrombosis than in older ones. No infarctions were detected in 165 cases of thrombosis. Preferably this group includes those cases in which the patients deceased within 6 to 8 hours and, therefore, the infarction was not morphologically detectable.

Adult↗

PubMed2003

Deep vein thrombosis followed by internal jugular vein thrombosis as a complication of in vitro fertilization in a woman heterozygous for the prothrombin 3' UTR and factor V Leiden mutations.

Thrombosis of the internal jugular vein is a rare event but one that can have serious consequences. Most cases reported in the literature have occurred in patients with indwelling central venous catheters, in association with head and neck sepsis, or in hypercoagulable states. However, a small number of cases have been associated with in vitro fertilization and more often with the ovarian hyperstimulation syndrome (OHSS). We report the case of a 30-year-old woman heterozygous for both the prothrombin 3' UTR mutation and for the factor V Leiden mutation who presented with a proximal deep vein thrombosis following in vitro fertilization. She subsequently developed an internal jugular vein thrombosis extending into the subclavian and axillary vein despite therapeutic anticoagulation with a low molecular weight heparin. Thromboembolic events can occur in the absence of other clinical features of OHSS, especially in patients with underlying prothrombotic abnormalities. Neck pain and swelling in a pregnant woman, especially one that has undergone in vitro fertilization, should be taken seriously and investigated with duplex scanning and/or MRI. Women with a personal or family history of thrombosis undergoing in vitro fertilization should be made fully aware of the potential thrombotic risks and should be considered for a thrombophilia screen.

3' Untranslated Regions↗

PubMed2002

Selectins influence thrombosis in a mouse model of experimental deep venous thrombosis.

BACKGROUND: This study characterizes venous thrombosis in the mouse and examines the important role that the adhesion molecules P-selectin and E-selectin and the anti-inflammatory cytokine interleukin-10 (IL-10) play in the thrombotic process. MATERIALS AND METHODS: C57BL/6 (wild-type) mice in a natural history protocol (Phase I) and gene-targeted (KO) mice for P-selectin, E-selectin, P/E-selectin, and IL-10 in a follow-up protocol (Phase II) were studied. Inferior vena caval thrombosis was produced by ligation just below the renal veins, and mice were sacrificed and evaluated at various time points up to 12 days later. RESULTS: Phase I: A significant increase in neutrophils on day 2 and in monocytes on day 6 postthrombosis was found in ligated vs sham animals. An associated significant increase in vein wall P-selectin mRNA (6 h, day 2) and an increase in protein (6 h through day 6) were found, while E-selectin mRNA was significantly increased (day 2 through day 6), with a smaller increase in E-selectin protein. IL-10 mRNA increased significantly later (day 2 through day 9), with the values increasing progressively. A positive correlation existed (r = 0.77) between neutrophils and thrombosis at day 2. PHASE II: The E-selectin and P/E-selectin double-KO mice showed the least thrombus at day 2 vs wild-type clotted mice, P < 0.01. Additionally, P/E-KO mice demonstrated the lowest inflammatory cell extravasation into the vein wall at day 2. CONCLUSIONS: This study demonstrates an acute to chronic inflammatory response in the vein wall associated with venous thrombosis. Inhibition of selectins decreased thrombus formation.

Animals↗

PubMed2005

An optimized murine model of ferric chloride-induced arterial thrombosis for thrombosis research.

INTRODUCTION/OBJECTIVES: Animal models are important tools in thrombosis research and preclinical drug development. Ferric chloride has been widely used to induce arterial thrombosis in a variety of species. However, almost all previous reports applied a very high concentration of ferric chloride (10-60%) to induce thrombus formation leading to difficulties in evaluating the efficacy of antithrombotic agents. Thus, the purpose of this study was to refine the ferric-chloride-induced thrombosis model to be better suited for thrombosis research. METHODS AND RESULTS: Dose-dependent study was used to identify a threshold concentration of ferric chloride sufficient for consistent occlusion (as reflected by the Doppler blood flow) of the carotid artery in C57BL/6 mice. Ferric chloride concentration at or about a threshold of 2.5% was found to be sensitive to anticoagulant (e.g., heparin) and antiplatelet (e.g., clopidogrel) agents. In contrast, the vessel rapidly occluded at or above 5% ferric chloride concentration despite pretreatment with the antithrombotic agents, even at doses that exerted maximal prolongation of tail bleeding time. CONCLUSIONS: Our study provides a simple, sensitive and highly controlled method for limiting vessel injury in mice to better detect the efficacy of antithrombotic drugs and/or evaluate therapeutic targets.

Animals↗

PubMed1998

Thrombotic storm: when thrombosis begets thrombosis.

Patients with hypercoagulability may present with a single thrombosis and subsequently develop progressive thromboses at other sites. With inadequate therapy, the thrombotic process may self-perpetuate, leading to multiple thromboses and even death. Six cases are presented demonstrating key features of what may be termed thrombotic storm: (1) an underlying hypercoagulable disorder; (2) a provocation to initiate thrombosis; (3) rapid development of new thromboses; (4) response to prompt use of thrombolytic agent or anticoagulant therapy; and (5) remarkable good long-term prognosis if the cycle of thrombosis is interrupted. Continued activation of coagulation by fresh thrombosis is hypothesized as the cause of the syndrome, which may explain its control by anticoagulants. Whereas these unusual patients' courses most likely represent only an extreme of hypercoagulability and not a new disorder, their characteristic behavior warrants attention.

Adult↗