Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THROMBOEMBOLISM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources

Local heat shock priming promotes recanalization of thromboembolized microvasculature by upregulation of plasminogen activators.

OBJECTIVE: Thromboembolization and subsequent microvascular perfusion failure is implicated in the pathology of a variety of diseases, including transient ischemic attack (TIA), stroke, and myocardial infarction, and also for the complications after interventional and microsurgical procedures in coronary heart disease and peripheral arterial occlusive disease. In vitro heat shock priming has been suggested to induce plasminogen activators, which are the major upregulators of the fibrinolytic system. Herein, we determined whether local heat shock priming endogenously upregulates plasminogen activators also in vivo, and whether this promotes recanalization of thromboembolized microvasculature. METHODS AND RESULTS: To induce thromboembolization, a suspension of preformed microthrombi (maximum diameter: 40 microm) was injected via the femoral artery into the left hindlimbs of anesthetized rats. Local heat shock priming (42.5 degrees C, 30 minutes) was performed 24 hours before embolization and resulted in a significant increase of endothelium-derived plasminogen activator expression. The study of the microcirculation by intravital microscopy revealed in all tissues analyzed (muscle, periosteum, subcutis, and skin) that heat shock priming significantly (P<0.05) accelerates recanalization of the thromboembolized microvasculature when compared with nonprimed and sham-primed controls. Importantly, the addition of plasminogen activator inhibitor-1 to the microthrombi suspension completely blunted the heat shock-induced acceleration of microvascular recanalization. CONCLUSIONS: Heat shock induces endogenous hyperfibrinolysis by upregulation of plasminogen activators that promote recanalization of thromboembolized microvasculature.

Animals↗

Endogenous nitric oxide and prostaglandins synergistically counteract thromboembolism in arterioles but not in venules.

It has been shown that NO and prostacyclin (prostaglandin I(2)) from cultured endothelium synergistically inhibit blood platelet aggregation in vitro. However, it is unknown whether this synergism is also effective in the inhibition of thromboembolism in vivo and, if it is, whether it differs between vessel types. Therefore, the effect of endogenous NO and prostacyclin, in combination or alone, on thromboembolism was studied in an in vivo model. Thromboembolism was induced by micropipette puncture of rabbit mesenteric arterioles and venules (diameter 18 to 40 micrometer). In addition, the influence of wall shear rate was analyzed. In arterioles, the combined inhibition of NO synthase (N(G)-nitro-L-arginine [L-NA] 0.1 mmol/L; local superfusion) and of cyclooxygenase (aspirin [ASA] 100 mg/kg IV) resulted in a pronounced, significant prolongation of embolization duration (median >600 seconds) compared with control (median 153 seconds) or treatment with either L-NA (234 seconds) or ASA (314 seconds). This combined effect of L-NA+ASA was greater than the sum of the individual effects of L-NA and ASA. In contrast, in venules L-NA+ASA had no additional effect on embolization duration (209 seconds) compared with the effect of L-NA alone (230 seconds); ASA alone had no effect (122 seconds; control 72 seconds). Interestingly, only in the L-NA+ASA arterioles did embolization correlate positively with wall shear rate (r(s)=0.687; P=0.028). In conclusion, this study indicates that in arterioles, but not in venules, endogenous NO and prostaglandins synergistically counteract ongoing thromboembolism after vessel wall injury and that the combination of endogenous NO and prostaglandins appears to protect against enhancement of arteriolar thromboembolism by wall shear rate.

Animals↗

Familial clustering of high factor VIII levels in patients with venous thromboembolism.

High levels of factor VIII (FVIII) but not von Willebrand factor (vWF) are known to increase the risk for venous thromboembolism. Whether high FVIII levels originate from hereditary defects or from acquired conditions remains unanswered. The objective of our study was to investigate whether there is evidence for familial clustering of elevated FVIII levels in families in which >/=1 member has been affected by a thromboembolic event and had reproducibly high FVIII levels. We investigated FVIII levels in 361 patients with previous venous thromboembolism. FVIII levels were measured by a chromogenic assay; the cutoff value was defined as the 98th percentile of FVIII plasma levels of 266 blood donors. vWF levels were determined by an enzyme immunoassay. After exclusion of known causes of FVIII elevation, such as the acute thrombotic event itself; inflammation; malignancy; liver, renal, or vascular disease; surgery; or pregnancy, we included 17 patients with unexplained, reproducibly high FVIII levels. The investigation was also extended to these patients' relatives. Multiple regressive analysis of blood donors and asymptomatic family members showed that the affiliation with a family in which 1 member suffered from venous thromboembolism and had reproducibly high FVIII levels is the second most important predictor for FVIII levels. Familial clustering was analyzed by the Houwing-Duistermaat familial aggregation test. After adjustment for the influence of age, sex, blood group, and vWF, FVIII levels were significantly (P:=0.038) clustered within families. In conclusion, FVIII levels seem to be familially determined in families in which a member showed high FVIII levels after previous venous thromboembolism.

Adult↗

Percutaneous closure of patent foramen ovale in patients with paradoxical embolism: long-term risk of recurrent thromboembolic events.

BACKGROUND: Patients with a patent foramen ovale (PFO) and paradoxical embolism are at risk for recurrent thromboembolic events. This study investigated the long-term risk of recurrent thromboembolic events in patients with PFO and paradoxical embolism after percutaneous PFO closure. METHODS AND RESULTS: Since 1994, a total of 80 patients with PFO and at least 1 paradoxical embolic event (transient ischemic attack [TIA], cerebrovascular accident [CVA], peripheral embolism) have undergone percutaneous PFO closure with 5 different devices. There were 30 women and 50 men, with a mean age of 52+/-12 years. Sixty patients had only a PFO, whereas 20 patients had both a PFO and an atrial septal aneurysm. The implantation procedure was successful in 78 patients (98%). During 5 years of follow-up (mean, 1.6+/-1.4 years; range, 0.1 to 5.0 years), the actuarial annual risk to suffer a recurrent thromboembolic event was 2.5% for TIA, 0% for CVA, 0.9% for peripheral emboli, and 3.4% for the combined end point of TIA, CVA, or peripheral embolism. A postprocedural shunt was a predictor of recurrent paradoxical embolism (RR, 4.2; 95% CI, 1.1 to 17.8; P=0.03). The risk for recurrent thromboembolic events in patients with both atrial septal aneurysm and PFO was not significantly increased compared with patients with only PFO (RR, 1.0; 95% CI, 0.2 to 4.7; P=0.95). CONCLUSIONS: Percutaneous PFO closure appears to be a promising technique in the prevention of recurrent systemic thromboembolism in patients with a PFO after a first event. Prospective studies comparing percutaneous PFO closure with antithrombotic medications or surgery must define its therapeutic value.

Actuarial Analysis↗

Inhibition of factor Xa reduces ischemic brain damage after thromboembolic stroke in rats.

BACKGROUND AND PURPOSE: Factor Xa (FXa) is a key coagulation protease and target for novel antithrombotic agents for prevention and treatment of diverse thromboembolic disorders. In the present study we describe the effect of a novel, potent, and selective FXa inhibitor, DPC602, on brain damage and neurobehavioral consequence in a rat thromboembolic model of stroke. METHODS: Thromboembolic stroke was induced in rats by placement of an autologous clot into the middle cerebral artery. RESULTS: Laser-Doppler monitoring of cerebral blood flow demonstrated that DPC602 (8 mg/kg, single IV/IP bolus pretreatment) markedly improved cerebral blood flow after thromboembolic stroke by 25% to 160% (n=6; P<0.001) at 1 to 6 hours. DPC602 demonstrated concentration- and time-dependent reductions in infarct size, with maximal effect (89% reduction; n=14; P<0.001) at the highest dose over controls. Neurological function was also significantly improved in DPC602-treated rats at days 1, 3, and 7 (n=13; P<0.01). DPC602 treatment did not cause cerebral hemorrhage, assessed by free hemoglobin in the ischemic brain tissues. CONCLUSIONS: These data suggest that anticoagulation with a selective FXa inhibitor might ameliorate the extent of ischemic brain damage and neurological deficits after a thromboembolic event. Enhanced clot dissolution and early reperfusion may account for the cerebrovascular-protective effect of the drug.

Animals↗

Inhibition of factor IX(a) is protective in a rat model of thromboembolic stroke.

BACKGROUND AND PURPOSE: Although used clinically to prevent stroke, there are few examples of anticoagulant investigations in the treatment of acute thromboembolic stroke in animal models. The treatment of thromboembolic stroke in experimental models has been investigated almost exclusively around the use of tissue plasminogen activator (tPA). In this study, using a rat thromboembolic stroke model, we investigated the use of an inhibitory anti-factor IX(a) monoclonal antibody (SB 249417) for the treatment of thromboembolic stroke and compared its efficacy to that of tPA. METHODS: Stroke was initiated by delivering 6 clots into the internal carotid artery. After 2, 4, or 6 hours, rats received either intravenous vehicle, 10.0 mg/kg tPA, or 1.0, 2.0, or 3.0 mg/kg SB 249417. At 24 hours after stroke, infarct volumes and neurological deficits were assessed. RESULTS: Treatment with tPA 2, 4, or 6 hours after stroke reduced infarct volumes by 35% (P=NS), 45%, and 39%, respectively. tPA treatment did not improve neurological deficits at any time point. Treatment with SB 249417 (3.0 mg/kg) 2, 4, or 6 hours after stroke reduced infarct volumes by 44%, 50%, and 13% (P=NS), respectively. Neurological deficits were reduced by 49%, 42%, and 13% (P=NS), respectively. Neither mortality nor hemorrhage was affected by either treatment. CONCLUSIONS: The data indicate that the inhibition of factor IX(a) within 4 hours of thromboembolic stroke produced a more favorable outcome than tPA. When treatment was initiated 6 hours after stroke, the benefits of factor IX(a) inhibition were lost, whereas tPA continued to suppress lesion development, albeit without a corresponding improvement in functional deficits. This study suggests that cerebral ischemia and the resultant perfusion deficit are exacerbated by the activation of blood coagulation and that anticoagulants like SB 249417 may find utility in the treatment of ischemic stroke.

Acute Disease↗

Venous thromboembolic disease in obstetrics and gynaecology: the Scottish experience.

The incidence and pattern of thromboembolic complications in obstetric and gynaecological patients in Scotland between 1981 and 1992 was investigated by analysing ICD coded data retrieved from the SMR1 and SMR2 database. The effect of mode of delivery and maternal age over 35 on risk of thromboembolism in pregnancy was also assessed. 0.076% of gynaecological episodes were subsequently complicated by thromboembolic events. Nineteen percent of those suffering thromboembolic complications within two weeks of discharge were referred back to gynaecology. The incidence of deep venous thrombosis (DVT) in those under 35 years and over 35 years was 0.615/1000 maternities and 1.216/1000 maternities respectively. Respective figures for postnatal DVT were 0.304/1000 and 0.720/1000 and for pulmonary thromboembolism (PTE), 0.108/ 1000 and 0.405/1000. In both age groups, emergency caesarean section was associated with a higher incidence of DVT than elective caesarean section and vaginal delivery.

Adult↗

Enoxaparin: the low-molecular-weight heparin for prevention of postoperative thromboembolic complications.

OBJECTIVE: To introduce readers to a new low-molecular-weight heparin (LMWH) product, enoxaparin. The chemistry, pharmacology, pharmacodynamics, clinical efficacy in thromboembolic prophylaxis following surgery, and adverse effects are reviewed. DATA SOURCES: A MEDLINE search of the English-language literature was used to identify relevant literature. STUDY SELECTION: A focus was placed on human clinical studies with well-accepted measures of antithrombotic efficacy endpoints, i.e., venography and ultrasonography. Emphasis was on pharmacologic and pharmacokinetic studies conducted in humans. DATA EXTRACTION: Most data were extracted from double-blind, controlled clinical studies. Other study designs were accepted if the results were believed to be significant. Pharmacology and pharmacokinetic data were selected from studies with exceptional design conducted in humans. DATA SYNTHESIS: Enoxaparin is a polysaccharide chain produced by the depolymerization of heparin. In comparison with heparin, which has an average molecular weight of 12,000-15,000 daltons, the average molecular weight of enoxaparin is approximately 4500 daltons. Enoxaparin does not form a complex with antithrombin III and thrombin as extensively as does heparin; however, the anti-Xa activity of enoxaparin is similar. The significance of this fact is an enhancement of antithrombotic activity and clinical efficacy. Trials comparing enoxaparin with other thromboembolic prophylaxis techniques are ongoing. CONCLUSIONS: Thromboembolism remains one of the major complications of all surgical procedures. Attempts have been made throughout the last century to develop the most effective means to prevent this complication. Clinical studies performed throughout the world have shown that enoxaparin is superior or equivalent to other antithrombotic agents, including heparin, in preventing the formation of venous thromboembolism. In addition, enoxaparin appears to possess an equivalent or lower incidence of bleeding complications when compared with heparin prophylaxis. Enoxaparin is expected to be joined by other LMWH products in the future. As a result, the methods of providing effective prophylaxis against thromboembolic complications is expected to change in the coming years.

Clinical Trials as Topic↗

Danaparoid in the prevention of thromboembolic complications.

OBJECTIVE: To review the therapies used to prevent postoperative thromboembolic complications with a focus on the role of danaparoid, a new low-molecular-weight glycosaminoglycan. DATA SOURCES: A MEDLINE search was performed to identify pertinent English-language literature including studies, abstracts, and review articles. Key search terms included danaparoid, heparinoid, lomoparin, heparin, prophylaxis, thrombosis, embolism, thromboembolism, and thromboembolic and postoperative complications. The manufacturer of danaparoid was contracted for additional information related to this compound. STUDY SELECTION AND DATA EXTRACTION: All identified articles were reviewed for possible inclusion in this review. Comparisons primarily focused on data obtained from prospective, randomized, controlled, blind clinical trials. Another important consideration was the use of venography to determine the presence of deep venous thrombosis. DATA SYNTHESIS: Various therapies are available for the prevention of postoperative thromboembolic complications. Effective pharmacologic treatments currently available include adjusted-dose heparin, warfarin, aspirin, dextran, and low-molecular-weight heparins (LMWHs). Until recently, warfarin was considered the drug of choice for thromboprophylaxis in high-risk patients, including patients undergoing orthopedic surgical procedures. Because of their comparable efficacy and greater ease of use, LMWHs are gaining favor over warfarin in this patient population. In well-designed clinical trials involving patients undergoing elective total hip replacement or fractured hip surgery, danaparoid has demonstrated greater efficacy than other active treatments, including warfarin, dextran, aspirin, and heparin plus dihydroergotamine. While studies comparing danaparoid with LMWHs have not yet been published, danaparoid may be more useful in patients with heparin-associated thrombocytopenia. CONCLUSIONS: Danaparoid is an antithrombotic agent with characteristics that distinguish it from heparin and LMWHs. Based on the efficacy and safety data reviewed, danaparoid should be considered one of the drugs of choice for the prevention of thromboembolic complications in patients undergoing orthopedic hip procedures and the drug of choice for the management of any patient with heparin-induced thrombocytopenia who requires anticoagulant therapy.

Chondroitin Sulfates↗

Review: intravenous immunoglobulin therapy and thromboembolic complications.

Intravenous immunglobulin (IVIg) is used to treat a number of immune-deficiences and autoimmune diseases. Safety concerns related to a number of reported thromboembolic complications prompted us to review the literature. These complications happened mainly in individuals that had risk factors for thromboembolism, like advanced age, previous thromboembolic diseases, bed-ridden, and in individuals in which high doses or high infusion rates of IVIg were administered. The mechanism responsible for these events seems to be a rise in plasma viscosity that can trigger a thromboembolic event, especially in cases in which there is an underlying circulation impairment. Complications can be minimized by using IVIg only in clear-cut indications, weighting risk versus benefit in patients who are at high risk for thromboembolism and by sticking to carefully monitored slow infusion rates. IVIg for the treatment of autoimmune disorders should be administered as a five-day course of 2 g/kg of body weight. Each daily dose of 400 mg/kg should be given in not less than eight hours.

Autoimmune Diseases↗

Thromboembolic complications after perioperative chemotherapy in women with early breast cancer: a European Organization for Research and Treatment of Cancer Breast Cancer Cooperative Group study.

PURPOSE AND METHODS: Data from a randomized phase III trial in early breast cancer, comparing surgery followed by one short intensive course of perioperative fluorouracil, doxorubicin, and cyclophosphamide (FAC) versus surgery alone, were analyzed for the occurrence of thromboembolic complications within 6 weeks after surgery. RESULTS: Twenty-seven of 1,292 patients assigned to the perioperative chemotherapy treatment arm (2.1%) and 10 of 1,332 patients on observation (0.8%) developed thromboembolic events (P = .004). The frequency of thromboembolic complications was higher among postmenopausal women compared with premenopausal women (2.0% v 0.6%, P = .003). Patients who had mastectomy had a higher frequency of thromboembolic disease than those who had tumorectomy (2.3% v 0.7%, P < .001). Three deaths occurred after pulmonary embolism, all of them in the perioperative chemotherapy treatment arm. CONCLUSION: These results suggest a contributing role of perioperative chemotherapy to thromboembolic disease, especially in postmenopausal women and women undergoing mastectomy. Antithrombosis prophylaxis should be considered in the case of adjuvant perioperative chemotherapy.

Aged↗

Anticoagulant prophylaxis markedly reduces thromboembolic complications in Cushing's syndrome.

A hypercoagulable state and an increased incidence of thromboembolic complications are reported in Cushing's syndrome. The hypercoagulable state is related to an increase in plasma clotting factors, especially Factor VIII and von Willebrand factor complex, and to an impairment of fibrinolytic capacity. Retrospective analysis of postoperative thromboembolic events in a large group of patients with Cushing's syndrome, including 75 patients (group 1) evaluated in the period from 1972-1981 not receiving anticoagulants, and 232 patients (group 2), evaluated in the period from 1982-2000. Patients of group 1 underwent routine hemostatic function, i.e. prothrombin time and activated partial thromboplastine time. Patients of group 2 underwent a thorough investigation as to hemostatic parameters and received prophylactic treatment with heparin and/or warfarin. Patients with Cushing's syndrome showed various abnormalities of hemostatic parameters. A significant correlation between activated partial thromboplastine time and urinary free cortisol was observed. During follow-up, 15 patients (20%; mean follow-up, 9.4 +/- 6.4 yr) of group 1 and 14 (6.0%; mean follow-up, 6.6 +/- 4.2 yr) of group 2 showed thromboembolic complications. Of these patients, eight of group 1 and one of group 2 died. Survival analysis demonstrated a significantly higher morbidity and mortality due to thromboembolic events in group 1, not receiving anticoagulant prevention, than in group 2, treated with anticoagulants in the perioperative period until cure of the disease and normalization of clotting parameters. Cushing's syndrome is associated with a hypercoagulable state. An adequate anticoagulant prophylaxis can reverse this prothrombotic state and avoid postoperative thromboembolic events.

Adolescent↗

Lipoprotein(a), left atrial appendage function and thromboembolic risk in patients with chronic nonvalvular atrial fibrillation.

Lipoprotein(a) (Lp(a)) has a prothrombotic effect by modulating the fibrinolytic system. The purpose of the present study was to determine whether serum Lp(a) levels are associated with an increased risk of thromboembolism in chronic nonvalvular atrial fibrillation (NVAF). Clinical, laboratory and transesophageal echocardiographic data were collected in 172 consecutive, non-anticoagulated patients with chronic NVAF. Thirty-four patients (thromboembolic group) had a recent (<1 month) embolic event and/or a left atrial thrombus on transesophageal echocardiography. The thromboembolic group had a higher frequency of spontaneous echo contrast (94 vs. 58%, p<0.0001), increased concentrations of Lp(a) (median: 31.5 vs. 15.5 mg/dl, p<0.0001) and fibrinogen (median: 352 vs. 314 mg/dl, p = 0.0015), larger left atrial dimensions (median: 5.1 vs. 4.8cm, p = 0.0078), and reduced left atrial appendage (LAA) flow velocities (median: 9.5 vs. 21.2 cm/s, p<0.0001) than the nonthromboembolic group. Multivariate analysis identified 3 independent predictors of thromboembolism: Lp(a) level > or =30 mg/dl (odds ratio (OR) 9.5, 95% confidence interval (CI) 4.4-20.4, p<0.0001), LAA flow velocity of <20 cm/s (OR 8.7, 95% CI 3.3-23.0, p = 0.0003) and a fibrinogen concentration of <377mg/dl (OR 3.2, 95% CI 1.5-6.9, p = 0.0201). The Lp(a) elevations and reduced LAA flow velocities are independently associated with thromboembolism in chronic NVAF.

Aged↗

Role of transesophageal echocardiography in the prediction of thromboembolism in patients with chronic nonvalvular atrial fibrillation.

The purpose of this study was to determine whether parameters derived from transesophageal echocardiography (TEE) could predict thromboembolism in patients with chronic nonvalvular atrial fibrillation (AF). Eighty-nine patients, mean age 66+/-9 years, who underwent TEE in 1996 to 1999 were studied. The clinical endpoint was a thromboembolic event, including transient ischemic attack (TIA). Sixty-seven patients (75%) were anticoagulated with warfarin after TEE. After a follow-up period of 29+/-10 months, 1 patient died suddenly, 4 had a thromboembolism, and 3 had a TIA; the annual embolic event rate was 3.3%. Left atrial appendage (LAA) thrombus (86% vs 17%, p<0.001), LAA dysfunction (LAA velocity <20 cm/s; 71% vs 25%, p=0.009), and severe LA spontaneous echo contrast (29% vs 2%, p=0.002) were more prevalent in patients with an embolic event than in those without. In patients with LAA thrombus, the annual event rate was 11% as compared with 1.2% in those without (p=0.004). On the Cox proportional hazards model analysis, LAA thrombus (chi-square 7.0, p=0.008), severe LA spontaneous echo contrast (chi-square 7.0, p=0.008), and LAA dysfunction (chi-square 5.9, p=0.015) were significantly related to thromboembolism. Multivariate analysis revealed that LAA thrombus (chi-square 5.5, p=0.019) and LAA dysfunction (chi-square 4.0, p=0.045) were the independent predictors. In conclusion, TEE parameters, particularly the presence of LAA thrombus, can be used to assess thromboembolic potential in patients with chronic nonvalvular AF.

Aged↗

Two mechanical devices for prophylaxis of thromboembolism after total knee arthroplasty. A prospective, randomised study.

The optimal characteristics of pneumatic compression for mechanical prophylaxis of thromboembolism after total knee arthroplasty (TKA) are not known. Our study compared two methods of calf compression, with the hypothesis that the device which provided a larger increase in peak venous velocity would produce a lower rate of thromboembolism. We performed a prospective, randomised study on 423 patients (472 knees). Duplex ultrasonography was carried out by experienced technicians who were blinded to the device used. Overall, 206 patients (232 knees) used a rapid inflation, asymmetrical compression (RIAC) device and 217 (240 knees) a sequential circumferential compression device (SCD). The rate of venous thromboembolism was 6.9% with the RIAC device compared with 15% for the SCD device (p = 0.007). The incidence of thrombi with unilateral primary TKA was 8.4% for the RIAC compared with 16.8% for the SCD device (p = 0.03). In 47 patients with a bilateral TKA, the incidence of thrombi was 4% for the RIAC compared with 22.7% for the SCD device (p = 0.05 per knee). There was a low rate of mortality and pulmonary embolism when using mechanical prophylaxis for thromboembolism after TKA. Our findings show that the use of rapid inflation, asymmetrical calf compression gave a significantly lower rate of thromboembolism.

Adult↗

Thromboembolic disease involving the superior vena cava and brachiocephalic veins.

PURPOSE: To evaluate the frequency of diagnosis and the characteristics of brachiocephalic vein and superior vena cava (SVC) thromboembolic disease. BACKGROUND: Thromboembolic disease of the brachiocephalic veins or SVC rarely has been reported. In view of the frequent use of central venous access lines, it would seem that the percentage of hospitalized patients with thromboembolic disease of the brachiocephalic veins or SVC should be higher than is generally recognized. METHODS: A retrospective search for thromboembolic disease involving the brachiocephalic veins and SVC was made of patients who were hospitalized over a 2-year period. RESULTS: Thromboembolic disease of the brachiocephalic veins or SVC was diagnosed in 23 of 34,567 hospitalized adults (0.06%) who were > or = 20 years old. Two of 23 patients (8.7%) had pulmonary embolism. Cancer was present in 17 of 23 patients (74%), and 15 of 23 patients (65%) had central venous access lines. Edema of the arm, face, or neck was present in 21 of 23 patients (91%). Pain or discomfort was present 15 of 23 patients (65%). CONCLUSION: Isolated brachiocephalic vein and SVC thrombosis occur in a sufficient number of hospitalized patients to merit consideration of the diagnosis in patients who have cancer, central venous access lines, or both. The signs and symptoms of brachiocephalic vein thrombosis have features in common with SVC syndrome as well as with upper extremity deep venous thrombosis. In a patient with appropriate clinical findings, venography or other imaging may be indicated.

Adult↗

Use of rheolytic thrombectomy in the treatment of feline distal aortic thromboembolism.

The purpose of this prospective clinical trial was to evaluate the safety and efficacy of a commercially available rheolytic thrombectomy system in the treatment of naturally occurring feline aortic thromboembolic disease. All 6 cats enrolled in the investigation were affected at the level of the distal aorta and had signs of the disease affecting both pelvic limbs. Cats were anesthetized and an arteriotomy was performed on 1 carotid artery to gain access to the arterial system. Selective arterial angiography was used to confirm the presence of thromboembolic disease. The thrombectomy system was advanced to the level of the thrombus using fluoroscopic guidance. Repeat angiography was used intermittently to assess progress of thromboembolus dissolution throughout the procedure. The use of the rheolytic thrombectomy system resulted in successful thrombus dissolution in 5 of 6 cats. Three of 6 cats survived to discharge. Both of these results compare favorably with conventional therapies used in the treatment of this disease. Feline distal aortic thromboembolism is a frustrating disease that warrants a guarded to poor prognosis. Rheolytic thrombectomy may provide veterinarians with an alternative therapy in the treatment of thromboembolic diseases, including feline distal aortic thromboembolism.

Animals↗

Oral contraception and the risk of thromboembolism: what does it mean to clinicians and their patients?

For four decades the oral contraceptive pill has remained popular with young women because of its convenience and effectiveness. There have, however, been continuing concerns about adverse effects. In the 1960s the risk of venous thromboembolism was linked to the dose of estrogen, which was consequently reduced. Later the risks of arterial disease were linked to progestogen dose, which was also reduced. In 1995, three case-control studies linked the risk of venous thromboembolism, not to dose, but to the type of progestogen. Newer 'third-generation' progestogens appeared to carry a higher risk than older formulations. Although the contraceptive pill was already known to increase the risk of venous thromboembolism 3- to 6-fold, and the risks in the three studies were within this range, the public perception was that a new risk had been discovered. In the UK there were two consequences--a rapid change in prescribing patterns and a sharp increase in the abortion rate. Critics suggested that the studies may have been affected by confounding--e.g. by a 'new user' effect and differential prescribing. Views became very polarised. Between 1995 and 2001 second- and third-generation formulations were compared in 16 studies. Thirteen found that third-generation pills carried a higher risk of venous thromboembolism. Editorials and reviews recommended second-generation pills as the first choice for new users but official advice was that third-generation pills could still be prescribed, provided the risks were explained. Rates of thrombosis, per 100,000 women, are five for nonusers, 15 with second-generation pills and 25 for third-generation pills. The increase in mortality rates is around 1 to 2 per million. Drug-industry sponsored studies tended to find lower risks than independent studies and it was assumed that sponsorship produces bias, conscious or unconscious. It is also possible that some 'independent' researchers, motivated by antipathy to multinational pharmaceutical companies, are biased in the opposite way. Compared with the energy put into this debate, other aspects of pill prescribing remain under-researched. For example, doctors on opposite sides of the Atlantic are given different advice about whether gross obesity (a major risk factor for thromboembolism) is a contraindication to oral contraception. Women in developing countries continue to die of pregnancy-related causes and many deaths could be prevented by effective contraception. Rather than bickering, drug manufacturers and academics should be discussing ways of providing the pill to the women who need it most.

Contraceptives, Oral, Hormonal↗