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PubMed1999

Adenovirus-mediated local expression of human tissue factor pathway inhibitor eliminates shear stress-induced recurrent thrombosis in the injured carotid artery of the rabbit.

The main cause of acute coronary syndrome may be recurrent thrombosis, which is initiated by the activation of the extrinsic coagulation pathway. Tissue factor (TF) pathway inhibitor (TFPI) efficiently inhibits an early step in this pathway by the formation of a complex with factor VIIa, TF, and factor Xa. We determined whether local TFPI gene transfer can inhibit thrombosis in an injured artery without inducing systemic side effects. Balloon-injured rabbit carotid arteries were infected with an adenoviral vector that expressed either human TFPI (AdCATFPI) or bacterial beta-galactosidase (AdCALacZ). Two to 6 days after gene transfer, thrombosis was induced by the production of constant stenosis of the artery, and blood flow was measured continuously with an electromagnetic flow probe. A cyclic flow variation, which is thought to reflect the recurrent formation and dislodgment of mural thrombi, was observed in all AdCALacZ-infected arteries as well as in saline-infused arteries. In contrast, no cyclic flow variation was detectable in AdCATFPI-transfected arteries, even in the presence of epinephrine (1 microg. kg-1. min-1 infusion). Prothrombin time, activated partial thromboplastin time, and the ex vivo platelet aggregation induced by either adenosine diphosphate or collagen were unaltered in AdCATFPI-infected rabbits. We found that in vivo TFPI gene transfer into an injured artery completely inhibits the recurrent thrombosis induced by shear stress even in the presence of catecholamine, without affecting systemic coagulation status. Adenovirus-mediated local expression of TFPI may have the potential for the treatment of human thrombosis.

Adenoviridae↗

PubMed1992

Antithrombotic effects of a platelet fibrinogen receptor antagonist in a canine model of carotid artery thrombosis.

BACKGROUND AND PURPOSE: Platelet-fibrin thrombi in the lumen of atherostenotic carotid arteries may underlie transient ischemic attacks and cerebral infarction. For this reason, we investigated the antiplatelet and antithrombotic effects of a novel and potent platelet fibrinogen receptor (glycoprotein IIb/IIIa) antagonist (SK&F 106760). METHODS: The effects of 0.1-3.0 mg/kg i.v. SK&F 106760 on platelet aggregation were examined ex vivo in canine platelet-rich plasma (n = 20). In addition, the antithrombotic effects of SK&F 106760 were compared with those of aspirin in an acute canine model of extracranial carotid artery thrombosis with high-grade stenosis. Sham-operated (n = 4), vehicle-treated (n = 6), SK&F 106760-treated (n = 8), aspirin-treated (n = 9), and SK&F 106760+aspirin-treated (n = 5) dogs were examined. RESULTS: The intravenous administration of SK&F 106760 caused a dose-related inhibition of ex vivo platelet aggregation. In the carotid artery thrombosis model, an occlusive thrombus formed at stenotic sites in the region of the carotid bifurcation. The thrombogenic process caused a progressive reduction in carotid blood flow and reduced the cortical microvascular perfusion and electroencephalographic power. Based on nuclear magnetic resonance spectroscopy, the occlusive events depleted the stores of high-energy phosphates (adenosine triphosphate and phosphocreatine) and increased the lactate concentration in the forelimb somatosensory area of the parietal cortex. In this model, the administration of 1 mg/kg i.v. SK&F 106760 prevented thrombosis of the stenotic carotid artery. Consequently, neurophysiological, cerebral hemodynamic, and metabolic parameters were all improved significantly in the SK&F 106760-treated group. No dog receiving SK&F 106760 reoccluded during the 1-hour posttreatment observation period. In contrast, thrombosis of the carotid artery was associated with neurophysiological deterioration in six of the nine dogs treated with 5 mg/kg i.v. aspirin. Both spontaneous and evoked (increased carotid stenosis) aspirin-resistant thrombosis were abolished by SK&F 106760 treatment. CONCLUSIONS: These results suggest that antagonism of fibrinogen binding to platelet glycoprotein IIb/IIIa (the final common pathway for aggregation) may represent a new and more effective antithrombotic approach to the treatment of cerebral transient ischemic attacks and infarction associated with extracranial carotid artery disease.

Animals↗

PubMed1992

Serotonin release into plasma during common carotid artery thrombosis in rats.

BACKGROUND AND PURPOSE: We have tested the hypothesis that platelet-derived serotonin is released into the bloodstream during cerebrovascular thrombosis. METHODS: Nonocclusive common carotid artery thrombosis was produced photochemically in 22 anesthetized adult male Wistar rats using the photosensitizing dye rose bengal and irradiation with an argon-pumped dye laser. Plasma serotonin levels were recorded before, during, and after photothrombosis by intra-arterial in vivo microdialysis with the probe placed distal to the site of thrombosis. RESULTS: During and immediately after the common carotid artery thrombosis, serotonin levels increased significantly to a peak value of 781 nmol/l (p less than 0.001 by analysis of variance), representing a 15-fold increase compared with baseline levels. The increased serotonin levels gradually decreased but remained significantly elevated for 90 minutes. Ultrastructural analysis of the carotid thrombi identified a dense mass of aggregated platelets at various stages of degranulation. CONCLUSIONS: These results are the first to demonstrate directly that serotonin accumulation occurs in plasma during and after the acute phase of common carotid artery thrombosis. Increased plasma serotonin levels may play a major role in the cerebral blood flow and blood-brain barrier abnormalities previously documented in this model of large-vessel thrombotic stroke.

Animals↗

PubMed1993

Combined use of aspirin and heparin inhibits in vivo acute carotid thrombosis.

BACKGROUND AND PURPOSE: Carotid atherosclerotic thrombosis is an important cause of ischemic stroke in Western countries. The therapeutic efficacy of either aspirin or heparin alone in this setting is still controversial. Recently we developed a simple model, the "clamp" method, to induce acute carotid mural thrombosis in vivo in guinea pigs. In this study, we used this model to evaluate the antithrombotic effects of aspirin, heparin, and their combination. METHODS: Sixty-four male guinea pigs were divided equally into control, aspirin, heparin, and combined groups. Physiological saline, aspirin (5 mg/kg body wt), heparin (200 units/kg body wt), or a combination of aspirin and heparin, respectively, was injected via the jugular vein before the use of the clamp method. Thirty minutes after the injection of saline or drug(s), Péan's forceps was used to clamp the carotid artery at a tangent angle for 3 minutes. One hour later, the carotid artery was resected and prepared for observation under a scanning electron microscope or light microscope to evaluate the degree of mural thrombosis. RESULTS: The results showed that the combination of aspirin and heparin had an excellent effect in inhibiting in vivo acute carotid thrombosis (p < 0.001) and was significantly better than the effect of aspirin alone (p < 0.01) or heparin alone (p < 0.01). CONCLUSIONS: Our study clearly demonstrated that the combined use of aspirin and heparin produced a much better antithrombotic effect than either agent alone at sites of carotid endothelial injury when given before the injury. This combined regimen may be useful clinically in acute carotid thrombosis secondary to carotid diseases or carotid endarterectomy.

Animals↗

PubMed1995

Superior sagittal sinus thrombosis and thyrotoxicosis. Possible association in two cases.

BACKGROUND: Superior sagittal sinus thrombosis is an uncommon cerebrovascular accident that is frequently associated with diseases that may contribute to the development of thrombosis through hypercoagulability, stasis of the local blood stream, and abnormalities of the vessel wall. In approximately 25% of cases underlying diseases remain unrecognized. CASE DESCRIPTIONS: Two patients with superior sagittal sinus thrombosis during a thyrotoxic phase of Graves' disease are described. Both patients presented with hemiplegia, seizures, and a large goiter. CONCLUSIONS: The development of superior sagittal sinus thrombosis is multifactorial. Patients with thyrotoxicosis and a large goiter may be predisposed to the development of superior sagittal sinus thrombosis through hypercoagulability and stasis of the local venous blood flow.

Adult↗

PubMed1999

Assessment of intracranial venous hemodynamics in normal individuals and patients with cerebral venous thrombosis.

BACKGROUND AND PURPOSE: Despite ongoing improvements in noninvasive imaging techniques, transcranial color-coded duplex sonography (TCCS) has so far been used only on a limited basis in patients with cerebral venous thrombosis. We evaluated the diagnostic value of both noncontrast and contrast-enhanced TCCS by comparing normal volunteers and patients with acute cerebral venous thrombosis. METHODS: In 75 healthy volunteers (aged 45.8+/-17.4 years), normal values for the deep cerebral veins (DCVs) and the posterior fossa sinuses were established by transtemporal insonation. Eight patients with cerebral venous thrombosis were assessed by TCCS, through which the hemodynamics of the DCVs were measured, and the patients were followed-up over a period of between 33 and 387 days after examination. MR angiography served as the "gold standard" technique for confirming the venous status in all 8 patients. RESULTS: No side differences in flow velocities were detected in the paired venous structures in normal volunteers. As indirect signs of (and diagnostic criteria for) cerebral venous thrombosis, pathologically increased flow velocities or significant side differences in the DCVs were registered in 5 of the 8 patients; the other patients showed nonsignificant increases in flow velocity which decreased over time. During follow-up, the status of the posterior fossa sinuses could be diagnosed correctly in seven patients after contrast enhancement when these results were compared with those of venous MR angiography. In 1 patient, a partial recanalization was mistakenly diagnosed as an occlusion. CONCLUSIONS: TCCS allows a reliable evaluation of the major DCVs and posterior fossa sinuses. The anterior and mid portions of the superior sagittal sinus and cortical veins cannot be assessed. Increased venous blood flow velocity can be used as an indirect criterion for indicating a cerebral venous thrombosis. Clinical recovery coincided with decreases in blood flow velocity in the series of patients investigated in this study.

Adult↗

PubMed2002

Association of the platelet glycoprotein Ia C807T/G873A gene polymorphism and thrombosis in Behçet patients.

Thrombosis is a common complication of Behçet disease and the pathogenic mechanism of thrombotic tendency in Behçet disease is not well known. Several platelet membrane glycoprotein gene polymorphisms have been identified as risk factors for thrombosis. This study aimed to evaluate the possible role of the GP Ia C807T/G873A polymorphism as a risk factor for thrombosis in Behçet disease. We determined the prevalence of platelet glycoprotein Ia C807T/G873A gene polymorphism in Behçet patients. Genomic DNA was obtained from 20 patients with Behçet disease and 61 controls. All individuals were of Turkish ancestry and were genotyped for the GP Ia C807T/G873A polymorphism with real-time PCR method by LightCycler system. The 807 CC, CT and TT genotypes corresponded with 873 GG, GA and AA genotypes, respectively. Complete linkage between the 807 and 873 sites was found in all samples. The 807CC(873 GG), 807CT(873GA), 807TT(873AA) genotypes found to be 45.9%, 45.9% and 8.1% in controls and 30.0%, 55.0% and 15.0% in patients with Behçet disease, respectively. The Odds Ratio for BD (OR = 1.97; 95% confidence interval (CI): 0.42-9.13) is high for the 807 TT genotype compared with controls. Thrombosis was found in 7 cases of Behçet disease group: five cases have 807CT, one case has 807TT genotype and one case has 807CC genotype. Our data indicate hat patients with BD are affected by the glycoprotein Ia gene 807TT genotypes and carrying 807T allele. The risk of thrombosis is significantly higher in patients who have 807TT and 807CT genotypes than in patients who have 807CC genotype.

Behcet Syndrome↗

PubMed1991

Active site-blocked factor IXa prevents intravascular thrombus formation in the coronary vasculature without inhibiting extravascular coagulation in a canine thrombosis model.

To assess the contribution of Factor IX/IXa, to intravascular thrombosis, a canine coronary thrombosis model was studied. Thrombus formation was initiated by applying current to a needle in the circumflex coronary artery. When 50% occlusion of the vessel developed, the current was stopped and animals received an intravenous bolus of either saline, bovine glutamyl-glycyl-arginyl-Factor IXa (IXai), a competitive inhibitor of Factor IXa assembly into the intrinsic Factor X activation complex, bovine Factor IX, or heparin. Animals receiving saline or Factor IX developed coronary occlusion due to a fibrin/platelet thrombus in 70 +/- 11 min. In contrast, infusion of IXai prevented thrombus formation completely (greater than 180 min) at doses of 460 and 300 micrograms/kg, and partially blocked thrombus formation at 150 micrograms/kg. IXai attenuated the accumulation of 125I-fibrinogen/fibrin at the site of the thrombus by approximately 67% (P less than 0.001) and resulted in approximately 26% decrease in serotonin release from platelets in coronary sinus (P less than 0.05). Hemostatic variables in animals receiving IXai, remained within normal limits. Animals given heparin in a concentration sufficient to prevent occlusive thrombosis had markedly increased bleeding, whereas heparin levels that maintained extravascular hemostasis did not prevent intracoronary thrombosis. This suggests that Factor IX/IXa can contribute to thrombus formation, and that inhibition of IXa participation in the clotting mechanism blocks intravascular thrombosis without impairing extravascular hemostasis.

Animals↗

PubMed1997

Monocytes and tissue factor promote thrombosis in a murine model of oxygen deprivation.

Clinical conditions associated with local or systemic hypoxemia can lead to prothrombotic diatheses. This study was undertaken to establish a model of whole-animal hypoxia wherein oxygen deprivation by itself would be sufficient to trigger tissue thrombosis. Furthermore, this model was used to test the hypothesis that hypoxia-induced mononuclear phagocyte (MP) recruitment and tissue factor (TF) expression may trigger the local deposition of fibrin which occurs in response to oxygen deprivation. Using an environmental chamber in which inhaled oxygen tension was lowered to 6%, hypoxic induction of thrombosis was demonstrated in murine pulmonary vasculature by 8 h based upon: (a) immunohistologic evidence of fibrin formation in hypoxic lung tissue using an antifibrin antibody, confirmed by 22.5-nm strand periodicity by electron microscopy; (b) immunoblots revealing fibrin gamma-gamma chain dimers in lungs from hypoxic but not normoxic mice or hypoxic mice treated with hirudin; (c) accelerated deposition of 125I-fibrin/fibrinogen and 111In-labeled platelets in the lung tissue of hypoxic compared with normoxic animals; (d) reduction of tissue 125I-fibrin/fibrinogen accumulation in animals which had either been treated with hirudin or depleted of platelets before hypoxic exposure. Because immunohistochemical analysis of hypoxic pulmonary tissue revealed strong MP staining for TF, confirmed by increased TF RNA in hypoxic lungs, and because 111In-labeled murine MPs accumulated in hypoxic pulmonary tissue, we evaluated whether recruited MPs might be responsible for initiation of hypoxia-induced thrombosis. This hypothesis was supported by several lines of evidence: (a) MP depletion before hypoxia reduced thrombosis, as measured by reduced 125I-fibrin/fibrinogen deposition and reduced accumulation of cross-linked fibrin by immunoblot; (b) isolated murine MPs demonstrated increased TF immunostaining when exposed to hypoxia; and (c) administration of an anti-rabbit TF antibody that cross-reacts with murine TF decreased 125I-fibrin/fibrinogen accumulation and cross-linked fibrin accumulation in response to hypoxia in vivo. In summary, these studies using a novel in vivo model suggest that MP accumulation and TF expression may promote hypoxia-induced thrombosis.

Animals↗

PubMedDate not supplied

Bilateral iliac vein thrombosis after seat belt-related trauma revealing hypoplasia of the inferior vena cava--a case report.

Hypoplasia of the inferior vena cava can be revealed by a deep venous thrombosis of the lower limbs. Associated precipitating factors or clotting defects leading to thrombosis are frequently observed. A case of bilateral iliac veins thrombosis occurring after a motor vehicle accident with seat belt injury is reported, revealing hypoplasia of the inferior vena cava. This young man was totally asymptomatic up to the crash, and did not have coagulation abnormalities. The patient had a very good outcome after anticoagulant treatment with complete regression of venous thromboses. Hypoplasia of the inferior vena cava was a predisposing anatomic abnormality that led to thrombosis, but seat belt trauma was probably the precipitating factor. This observation should be kept in mind in the evaluation of a deep venous lower limb thrombosis.

Accidents, Traffic↗

PubMed1980

Prevention of experimental venous thrombosis induced by contrast medium in the rat.

In order to assess experimentally the usefulness of some procedures employed in man to prevent venous thrombosis following phlebography, thrombosis was induced in rats using sodium diatrizoate in a temporarily isolated segment of a jugular vein. The prevention of thrombosis was attempted by washing out the vein with physiologic saline or saline plus heparin or by injecting saline plus heparin in the opposite jugular vein. Thrombosis occurred in all animals in the control group and in the group treated with saline alone. Both treatment schemes with heparin significantly reduced the incidence of thrombosis, the wash out with heparin being more effective than systemic heparin.

Animals↗

PubMedDate not supplied

Effort thrombosis in the elite throwing athlete.

BACKGROUND: Upper extremity vascular injuries are uncommon in the elite throwing athlete. However, the extreme stresses that are placed on the upper extremity of elite baseball players, especially pitchers, puts them at risk for such injuries. One such injury is upper extremity venous thrombosis or "effort thrombosis." PURPOSE: We wanted to review the common initial clinical symptoms and physical examination findings of effort thrombosis in elite baseball players and to review the associated clinical conditions such as hypercoagulable states and pulmonary embolism. STUDY DESIGN: Retrospective review of a series of cases. METHODS: A retrospective review of the medical records of a Major League Baseball organization and a Division I college was performed for the period 1987 to 1997. RESULTS: We located four cases of effort thrombosis involving elite baseball players. Contrast venography was used to confirm the diagnosis in all cases. All patients were successfully treated with transluminal catheter-directed urokinase thrombolysis followed by first rib resection and systemic anticoagulant therapy for up to 3 months. All four players returned to play at or above their previous level of competition with no long-term chronic sequelae. CONCLUSIONS: Prompt clinical recognition, diagnosis, and treatment of effort thrombosis in the elite baseball player provides the player with an excellent prognosis for return to the previous level of play.

Adult↗

PubMedDate not supplied

"Effort" thrombosis of the subclavian vein in a competitive swimmer.

"Effort" thrombosis is a unique form of subclavian and axillary vein thrombosis because it is the result of an unusual variant of the thoracic outlet syndrome. Another cause of subclavian vein thrombosis is local compression from trauma, tumor, or development anomalies; a third is intimal damage from indwelling central venous catheters. This is a case report of "effort" thrombosis of the subclavian vein in a competitive swimmer. A recently developed technique of local infusion of low-dose streptokinase therapy is used for clot lysis. Early diagnosis is essential for effective thrombus dissolution with streptokinase. The rationale, risk, and method of streptokinase administration are discussed. Since "effort" thrombosis is secondary to thoracic outlet syndrome (TOS), decompression of the thoracic outlet by removal of the first rib after clot lysis is recommended.

Adult↗

PubMedDate not supplied

The incidence of deep venous thrombosis after arthroscopic knee surgery.

We retrospectively reviewed the records of 2050 arthroscopic knee surgeries performed at The Orthopedic Specialty Hospital from January 1993 to December 1994. The number of clinically detected deep venous thromboses, with confirmation by duplex ultrasonography, was determined. Prospectively, preoperative and postoperative duplex ultrasonographic images were completed on 239 patients divided into 2 groups: those undergoing nonligament, intraarticular arthroscopic surgery (N = 131) and those undergoing arthroscopically assisted ligament surgery and extraarticular or osteotomy surgery (N = 108). For the retrospective study, the incidence of deep venous thrombosis was 0.24%. Prospectively, seven total deep venous thromboses were identified (rate, 2.9%), with five being identified within 8 days of surgery in asymptomatic patients (rate, 2.1%). There were no statistically significant associations or correlations between the development of deep venous thrombosis and patient personal data or surgical variables, respectively. The difference in the rate of deep venous thrombosis between the two prospective groups was not statistically significant; however, patients who had more invasive surgery tended to be at higher risk for developing deep venous thrombosis. A cost-benefit analysis did not support the routine use of duplex ultrasonography to detect deep venous thrombosis in patients undergoing arthroscopic knee surgery.

Adult↗

PubMed2004

Cerebral sinovenous thrombosis in children: another reason to treat iron deficiency anemia.

Iron deficiency anemia is a rare cause of cerebral sinovenous thrombosis in children. We report three cases of cerebral sinovenous thrombosis and iron deficiency anemia treated at Primary Children's Medical Center in Salt Lake City, Utah, between 1998 and 2001. The children were 9, 19, and 27 months old at the time of admission. Hemoglobin levels ranged from 6.6 to 7.0 g/dL, mean corpuscular volume levels from 45 to 56 fL, and platelet counts from 248,000 to 586,000/microL. Magnetic resonance imaging and magnetic resonance venography revealed thrombosis of the straight sinus and internal cerebral veins in all three children, with the addition of the vein of Galen, left transverse and sigmoid sinuses, and upper left internal jugular vein in one child. Recovery ranged from excellent to poor in 3 months to 3 years of follow-up. Four additional cases, ages 6 to 22 months, were found in the English-language literature. Evaluation for prothrombotic disorders was negative in all children, including the current cases. Treatments have included thrombectomy, corticosteroids, mannitol, heparin, low-molecular-weight heparin, warfarin, aspirin, blood transfusion, and iron supplementation, but there is no consensus regarding therapy, other than to correct the anemia and treat iron deficiency. Iron deficiency anemia, a preventable cause of cerebral sinovenous thrombosis, deserves consideration when cerebral sinovenous thrombosis is detected in young children.

Anemia, Iron-Deficiency↗

PubMed2005

Short-term intellectual outcome after arterial ischemic stroke and sinovenous thrombosis in childhood and infancy.

Arterial ischemic stroke is approximately four times more prevalent than sinovenous thrombosis and has been associated with a worse neurologic outcome than sinovenous thrombosis; however, no data are available comparing intellectual outcome after pediatric arterial ischemic stroke and sinovenous thrombosis. We report the short-term intellectual outcome (mean 5.8 months since stroke) in a sample of 72 children, 47 with arterial ischemic stroke, and 25 with sinovenous thrombosis. Intellectual outcome measures were the Full-Scale IQ of the age-appropriate Wechsler intelligence test for older children and the Mental Developmental Index of the Bayley Scales of Infant Development for younger children. Stroke type did not directly influence intellectual outcome. Intellectual outcome was in the normal range whether the children had suffered an arterial ischemic stroke or a sinovenous thrombosis.

Age Factors↗

PubMed2000

Risk of thrombosis in patients homozygous and heterozygous for factor V Leiden in the East Bohemian region.

A retrospective investigation on the frequency of thrombotic events in 227 heterozygous and 16 homozygous carriers for the factor V R506Q mutation (factor V Leiden) from 102 unrelated families in the East Bohemian region is reported. A majority of 130 of the 227 (57%) heterozygous and a minority of 5 of 16 (31%) homozygous carriers for the factor V R506Q mutation remained asymptomatic. Deep venous thrombosis without pulmonary embolism in a minority was the main and the most frequent clinical manifestation in 97 of 243 carriers for the factor V R506Q mutation. Deep venous thrombosis occurred in 92 of 227 (41%) heterozygous and in 11 of 16 (69%) homozygous carriers of the factor V R506Q. Spontaneous thrombosis prevailed in symptomatic men. Thrombosis in women usually occurs during risk situations well known to elicit venous thrombosis. Oral contraceptives and pregnancy were significantly the most frequent risk factors in female carriers of the factor V R506Q mutation, which in fact can readily explain the lower average age for the first thrombotic event of 30.6 years in women compared to 37.1 years in men.

Adolescent↗

PubMed2004

Effect of age on oral contraceptive-induced venous thrombosis.

This study was undertaken to investigate the effect of age on oral contraceptive-induced venous thrombosis. All women seen in the University of Padua Department of Medical and Surgical Science who had had two courses of oral contraceptive therapy at different ages were included. A total of 28 subjects met these criteria. Fifteen patients had a congenital or acquired prothrombotic condition, whereas 13 women were normal subjects. The mean age at which thrombosis occurred was 33.3 and 36.3 years for women with or without a prothrombotic condition, respectively. The ages during which the women remained asymptomatic were 23.1 and 23.3 years for women with or without a predisposing defect, respectively. Thrombosis occurred, during the second course of oral contraceptive therapy, after the mean duration of 6.5 cycles or 18.4 cycles in women with or without prothrombotic defects, respectively. During the asymptomatic course, approximately the same number of women took old progestins or third-generation compounds. On the contrary, during the second period, 21 of 28 women took progestins with third-generation compounds. Age seems to plays an important role in oral contraceptive-induced venous thrombosis. In normal women, thrombosis occurred after a greater number of oral contraceptive cycles as compared with the women with prothrombotic defects. Because the majority of women took preparations that contained third-generation progestins during the second course of therapy, concomitant contributing effects of these compounds cannot be excluded.

Activated Protein C Resistance↗