Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with iliofemoral deep venous thrombosis suffer the most severe postthrombotic morbidity. Techniques that effectively remove thrombus from the venous system eliminate venous obstruction and potentially preserve valvular function. This will likely reduce or avoid the postthrombotic syndrome and improve long-term quality of life. To evaluate whether catheter-directed thrombolysis is associated with improved quality of life compared with anticoagulation alone and whether outcome in the thrombolysis group is related to lytic success, 98 patients with iliofemoral deep venous thrombosis who were treated at least 6 months earlier were identified and queried with a validated health-related quality-of-life questionnaire. Sixty-eight patients were identified through the Venous Registry (a national, multicenter venous registry) and were treated with catheter-directed thrombolysis with urokinase, and 30 patients were identified by means of medical record review and were treated with anticoagulation alone. All patients were candidates for thrombolysis; however, the treatment decision was made according to physician preference. The two treatment groups did not differ significantly in average time between the reference hospitalization and first contact. No difference was found in physical functioning and well-being between the groups before the development of deep venous thrombosis. Following treatment, patients receiving catheter-directed thrombolysis reported better overall physical functioning, less stigma, less health distress, and fewer postthrombotic symptoms compared to those patients treated with anticoagulation alone. Within the thrombolysis group, successful lysis correlated with health-related quality of life. Catheter-directed thrombolysis for the management of patients with iliofemoral deep venous thrombosis significantly improves health-related quality of life compared to similar patients treated with anticoagulation alone. Improved quality of life is related to successful thrombolysis. These data offer a compelling argument for a prospective randomized study.
Rev Cardiovasc Med 2002
PMID:Quality-of-life improvement using thrombolytic therapy for iliofemoral deep venous thrombosis. 1255 44

The natural history of pulmonary embolism (PE) is incompletely characterized, because most episodes of PE go undetected, the clinical presentation mimics so many other common and uncommon diseases, the sensitivity and specificity of the diagnostic tests are poorly defined, and even detection at autopsy is difficult and requires close examination of the pulmonary arteries. Yet PE is a significant cause of morbidity and mortality in the hospitalized patient, and one reason for its extremely high incidence is the failure of physicians to provide adequate prophylaxis to patients who are at risk of developing venous thromboembolism. The mortality rate for PE is less than 8% when the condition is recognized and treated correctly but approximately 30% when untreated. Pulmonary arteriography is still the gold standard in diagnosing pulmonary emboli, but several other imaging modalities have been used to diagnose pulmonary emboli in recent years, including transthoracic and transesophageal echocardiography, magnetic resonance angiography, spiral computerized tomography, and ventilation-perfusion lung scanning. The treatment modality chosen depends directly on the clinical presentation of the patient. Low molecular weight heparin may be equal or superior in efficacy to unfractionated heparin for the treatment of deep venous thrombosis and PE. Thrombolytic therapy can be considered for patients with hemodynamic instability, those with right ventricular dysfunction, and young patients with a massive PE despite a normal right ventricle on echocardiography. In those patients who cannot receive anticoagulation therapy or thrombolysis, or who remain at high risk, an inferior vena cava filter should be placed.
Rev Cardiovasc Med 2002
PMID:Pulmonary embolism. 1255 45

Cardiovascular disease is the leading cause of death in women. In pooled analysis, observational studies have shown a 50% reduction in death and myocardial infarction among users of hormone replacement therapy (HRT) for the primary and secondary prevention of cardiovascular disease. The first randomized trial of HRT for secondary prevention of heart disease found no benefit to therapy (Heart and Estrogen/progestin Replacement Study ). Even after 6.8 years of follow-up, there was still no cardiovascular benefit from the use of HRT (HERS II). HRT was associated with a 50% increased risk of heart attacks within the first year as well as an increased risk of deep venous thrombosis (DVT) and pulmonary embolism (PE) (relative risk 2.89) and gallbladder disease (RR 1.38). The Estrogen Replacement and Atherosclerosis trial found no evidence that HRT slowed the progression of subclinical angiographic disease either. This was despite a favorable effect on high-density lipoprotein and low-density lipoprotein. The first randomized trial of HRT for the primary prevention of heart disease found no overall benefit (Women's Health Initiative). The combination of estrogen and progestin resulted in a 29% increase in heart attacks, 41% increase in stroke, a doubling of thrombotic events (DVT and PE), as well as a 26% increase in breast cancer. The risk for thrombotic events was greatest in the first year whereas the risk of breast cancer increased progressively with duration of therapy. HRT is no longer recommended for the primary or secondary prevention of cardiovascular disease or stroke. It may still be considered for short-term relief of menopausal symptoms in women without high-risk conditions, but alternatives exist.
Curr Treat Options Cardiovasc Med 2003 Feb
PMID:Hormone Replacement Therapy for Primary and Secondary Prevention of Heart Disease. 1268 16

Because of its wide range of presentations, its highly variable mode of onset, its numerous causes, and its unpredictable outcome, cerebral venous thrombosis (CVT) remains a diagnostic and therapeutic challenge. Treatment of CVT consists primarily of symptomatic treatment of seizures and intracranial hypertension, antithrombotics, and etiologic treatment whenever possible. Heparin remains the first line of treatment for CVT; although its systematic use remains debated, recent studies have confirmed its safety even in patients with large hemorrhagic infarctions. The addition of local thrombolysis is indicated for patients with clinical worsening related to extension of the venous thrombosis, despite adequate anticoagulation and optimal symptomatic and etiologic treatment. In contrast to arterial stroke, complete recovery of prolonged or severe neurologic deficit is possible, justifying initiation of anticoagulation and eventually thrombolysis, even when the clinical situation seems desperate. New techniques using mechanical devices disrupting the clot may be used in addition to thrombolysis in rare cases. Ventricular drainage is indicated in cases of cerebellar infarction or deep venous thrombosis associated with hydrocephalus. Decompressive craniotomy may be performed acutely in patients with untractable intracranial hypertension and herniation.
Curr Treat Options Cardiovasc Med 2003 Jul
PMID:Cerebral Venous Thrombosis. 1277 96

Enoxaparin (enoxaparin sodium) is a low-molecular-weight heparin that binds to and increases the activity of antithrombin III. The resulting complex inhibits prothrombinase-mediated thrombin generation and direct thrombin generation by binding to factor Xa and thrombin factor IIa. Enoxaparin, used as prophylaxis in medically ill patients at increased risk for thromboembolism, has shown significantly increased efficacy compared with placebo in reducing the incidence of deep vein thrombosis and pulmonary embolism. Indeed, 291 patients receiving subcutaneous enoxaparin 40 mg/day had a frequency of venous thromboembolism of 5.5% during 14 days of treatment, whereas 14.9% of the 288 placebo recipients experienced thromboemboli (p < 0.001). There was no reduction in the incidence of thromboembolism in the 287 recipients of enoxaparin 20 mg/day (15%). In other studies, prophylactic treatment for 7 days with subcutaneous enoxaparin 40 mg/day was at least as effective as unfractionated heparin in reducing the frequency of venous thromboembolism in 959 nonsurgical patients at increased risk for deep vein thrombosis and pulmonary embolism (total incidence = 0.2 and 1.4%, respectively). Moreover, enoxaparin recipients experienced fewer adverse events than did heparin recipients. The most frequent adverse events reported in medically ill and surgical patients receiving enoxaparin 40 mg/day were hemorrhage (17.4 vs 14.3% for placebo), hematoma at injection site, anemia, fever, peripheral edema, nausea, ecchymosis and edema (unspecified site).
Am J Cardiovasc Drugs 2001
PMID:Enoxaparin: in the prevention of venous thromboembolism in medical patients. 1472 9

Venous thromboembolism is a common and potentially fatal disease. If properly used, anticoagulation therapy is effective in preventing recurrence of venous thromboembolism and in improving survival. Symptomatic patients with an objective diagnosis of acute deep vein thrombosis (DVT) or pulmonary embolism (PE) should receive immediate systemic heparin anticoagulation at dosages sufficient to rapidly prolong the activated partial thromboplastin time into the laboratory-specific therapeutic range; this range corresponds to a plasma heparin concentration of 0.2 to 0.4 IU/ml (as measured by protamine sulfate titration), or 0.3 to 0.7 anti-Xa IU/ml. An oral vitamin K antagonist (e.g. warfarin) should be started within 24 hours after starting heparin; the starting dose should be the estimated patient-specific daily dose with no loading dose. Heparin and warfarin anticoagulation should be overlapped for at least 4 to 5 days and until the international normalized ratio (INR) is within the therapeutic range (2.0 to 3.0) on 2 measurements made at least 24 hours apart. The duration of warfarin anticoagulation should be individualized based on the respective risks of venous thromboembolism recurrence and anticoagulant-related bleeding. In general, warfarin should be continued for at least 3 months, and longer for patients with recurrent or idiopathic venous thromboembolism, malignant neoplasm, neurologic disease with extremity paresis, obesity, or laboratory evidence of a lupus anticoagulant/anticardiolipin antibody, homozygous carrier or combined heterozygous carrier for the factor V R506Q (Leiden) and prothrombin G20210A mutations, and possibly deficiency of either antithrombin, protein C, or protein S. Low molecular weight heparin (LMWH) is effective and well tolerated as acute therapy for patients with DVT or stable PE, and does not require laboratory monitoring or dose adjustment. Outpatient LMWH therapy is also well tolerated and cost effective for most patients with DVT, and possibly for selected patients with PE.
Am J Cardiovasc Drugs 2001
PMID:Current management of acute symptomatic deep vein thrombosis. 1472 51

Many cancer patients reportedly are in a hypercoaguable state, with recurrent thrombosis due to the impact of cancer cells and chemotherapy or radiotherapy on the coagulation cascade. Studies have demonstrated that unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) interfere with various processes involved in tumor growth and metastasis. These include fibrin formation, binding of heparin to angiogenic growth factors such as basic fibroblast growth factor and vascular endothelial growth factor, modulation of tissue factor and, perhaps, other more important modulatory mechanisms such as enhanced tissue factor pathway inhibitor (TFPI) release and inhibition of various matrix-degrading enzymes. Clinical trials have suggested a clinically relevant effect of LMWH, compared with UFH on the survival of cancer patients with deep vein thrombosis. Similarly, the impact of warfarin on the survival of cancer patients with thromboembolic disorders was demonstrated. Studies from our laboratory demonstrated a significant role for LMWH, warfarin, anti-VIIa and LMWH-releasable TFPI on the regulation of angiogenesis, tumor growth, and tumor metastasis. Thus, modulation of tissue factor/VIIa noncoagulant activities by LMWH, warfarin, anti-VIIa or TFPI might be a useful therapeutic option for the inhibition of angiogenesis associated with human tumor growth and metastasis.
Expert Rev Cardiovasc Ther 2003 Jul
PMID:Antithrombotics in thrombosis and cancer. 1503 Feb 87

Venous thromboembolism is a major preventable cause of maternal mortality in developed countries. Following objective diagnosis of deep vein thrombosis or pulmonary embolism, appropriate treatment with anticoagulation should be initiated. The therapeutic options in pregnancy are limited to the use of either unfractionated heparin or low molecular weight heparin. Oral anticoagulants, like warfarin, are relatively contraindicated for use during pregnancy for the treatment of venous thromboembolism because they freely cross the placenta and can be associated with adverse fetal effects. The appropriate length of treatment for acute venous thromboembolic disease diagnosed during pregnancy should be at least 3 months and possibly up till 6 weeks after delivery.
Curr Treat Options Cardiovasc Med 2004 Apr
PMID:Treatment of Venous Thromboembolism in Pregnancy. 1506 44

Arterial and venous thromboembolic events, including myocardial infarction, ischemic stroke, peripheral arterial thrombosis, deep venous thrombosis, and pulmonary embolism are common potentially life-, organ-, and limb-threatening vascular diseases. Anticoagulant therapy is recommended in these settings to prevent further thrombosis pending gradual clearance of the thrombotic occlusion by the endogenous fibrinolytic system. Recognition of the importance of the fibrinolytic system in thrombus resolution has resulted in the development of pharmacologic fibrinolytic (thrombolytic) agents to facilitate rapid restoration of vascular patency. Several plasminogen activator (PA) thrombolytic agents with different pharmacokinetic and pharmacodynamic properties have been developed to treat thrombotic disease. Newer PAs have been developed as "fibrin-specific", bolus-administration drugs to primarily treat acute coronary syndromes. Continuous infusions of these fibrin-specific PAs have become popular for the lysis relatively larger peripheral vascular thromboses. Loss infusion of newer tissue-type plasminogen activator-based PAs may result in an increased risk of bleeding, including intracranial hemorrhage. Currently available data fail to provide compelling evidence that newer PAs offer significantly greater efficacy and safety than well-established agents like urokinase when used to treat peripheral vascular thrombosis.
Rev Cardiovasc Med 2002
PMID:Pharmacologic and clinical characteristics of thrombolytic agents. 1511 13

Low-molecular-weight heparins have several important advantages over unfractionated heparin (UFH). Due to a longer plasma half life together with high bioavailability and a linear dose-response relationship, the drugs can be safely and effectively administered in the hospital or ambulatory settings without the need to monitor the anticoagulant effect. Enoxaparin (Lovenox), Aventis Pharma) is a low-molecular-weight heparin which has been studied in a variety of clinical situations. In general surgery the efficacy of enoxaparin to prevent venous thromboembolism is similar to UFH but the tolerability is better. In patients undergoing cancer, orthopedic or vascular surgery the efficacy of enoxaparin is significantly higher with similar rates of bleeding complications. The database for enoxaparin in nonsurgical patients is smaller compared with surgical groups. There is evidence that the efficacy of enoxaparin may be superior to UFH in patients with severe cardiac disease. Efficacy and safety of UFH and enoxaparin are similar for the treatment of deep vein thrombosis. However, enoxaparin can be safely administered by the patients at home which is not possible with UFH. In patients with acute coronary syndromes, enoxaparin has been shown to reduce the rate of deaths and serious cardiac events in comparison with UFH. Furthermore, exonaparin treatment has been shown to be cost-effective, and therefore is the therapy of choice in this setting. In addition, enoxaparin has been shown to be a safe and effective alternative to the combination of UFH and phenprocoumone therapy in patients undergoing electrical cardioversion for atrial fibrillation.
Expert Rev Cardiovasc Ther 2004 May
PMID:Clinical application of enoxaparin. 1515 80


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