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At least 1,063 records · Page 59Linked to original sources
PubMed2005

Antithrombotic therapy practices in US hospitals in an era of practice guidelines.

BACKGROUND: Antithrombotic therapy is efficacious for the prevention of thromboembolic disease, but it necessitates careful risk-benefit assessment. METHODS: Antithrombotic therapy data were retrospectively collected from inpatient medical records at 38 US hospitals. Patients treated for atrial fibrillation, acute myocardial infarction, deep vein thrombosis, or pulmonary embolism and patients given prophylaxis for total knee replacement, total hip replacement, or hip fracture surgery between July 1, 2000, and June 30, 2003, were randomly selected. RESULTS: The medical records of 3778 patients (53.3% men) were included. The mean patient age was 66.1 years. Of patients with atrial fibrillation at high risk for stroke, only 54.7% received warfarin sodium, and 20.6% received neither aspirin nor warfarin. Of patients with acute myocardial infarction, only 75.5% received aspirin on hospital arrival. After orthopedic surgery procedures, only 85.6% of patients received prophylaxis with a parenteral anticoagulant agent or warfarin. In 49.4% of patients with deep vein thrombosis, pulmonary embolism, or both, unfractionated or low-molecular-weight heparin use was discontinued before an international normalized ratio of 2.0 or greater was achieved for 2 consecutive days. Patients with deep vein thrombosis or pulmonary embolism were rarely discharged from the hospital with bridge therapy (an injectable anticoagulant agent plus warfarin), although the length of hospitalization was significantly shorter than if discharged taking warfarin alone (4.0 vs 8.1 days; P < .001). CONCLUSIONS: A significant percentage of hospitalized patients do not receive adequate antithrombotic therapy for the primary and secondary prevention of thromboembolic disease.

Aged↗
PubMed1994

The risk of thromboembolism in asymptomatic patients with protein C and protein S deficiency: a prospective cohort study.

BACKGROUND: Prospective studies on the incidence of thrombosis in asymptomatic individuals with hereditary protein C- or protein S deficiency have not been performed so far. OBJECTIVE: We have carried out a prospective cohort study in 44 asymptomatic protein C- and protein S deficient subjects and in 49 asymptomatic non-deficient relatives (age at study entry > 14 years) of symptomatic deficient patients. METHODS: 20 asymptomatic protein C deficient (median age 20 years) and 24 asymptomatic protein S deficient patients (median age 21.5 years) were prospectively followed and compared with 20 asymptomatic non-deficient relatives (median age 25 years) of protein C- and 29 (median age 27 years) of protein S deficient patients. The total observation period was 118.8 patient years for protein C deficient and 92.8 for protein S deficient patients. Patients were not on anticoagulants except for short duration in case of high risk situations. RESULTS: Eight thromboembolic events (1 pulmonary embolism, 1 deep vein thrombosis + pulmonary embolism, 3 deep vein thrombosis, 1 caval vein thrombosis and 2 superficial vein thrombosis) occurred in 6 deficient patients. The incidence of thromboembolism was 2.5% per patient year for protein C deficient and 3.5% per patient year for protein S deficient patients. 4 events occurred spontaneously, in 2 patients thromboembolic events were triggered by high risk situations (caesarean section, minor trauma). In the controls no thromboembolic events occurred. The probability for thromboembolism was significantly higher in protein C and protein S deficient patients compared to the control group (Wilcoxon test, p = 0.002, log rank test, p = 0.001). One major and 5 minor uneventful surgeries were carried out in the deficient patients using heparin prophylaxis. 1/8 pregnancies was complicated by superficial vein thrombosis during the second trimester despite prophylactic heparin administration. The same pregnancy was complicated by pulmonary embolism 5 weeks after delivery after discontinuation of heparin. CONCLUSIONS: Asymptomatic deficient relatives of symptomatic patients with protein C or protein S deficiency are at an increased risk of thrombosis compared to nondeficient individuals. Prophylactic treatment seems to be highly effective in high risk situations.

Adolescent↗
PubMed1999

Thrombogenicity of prothrombin complex concentrates.

Thrombogenicity of factor IX complex or prothrombin complex concentrates (PCC) is a well-acknowledged problem. The exact incidence is unknown but has decreased with the improvement of the quality of coagulation factor concentrates and a more judicious use of these products. The clinical spectrum of thrombogenicity ranges from superficial thrombophlebitis, deep-vein thrombosis and pulmonary embolism, and arterial thrombosis to disseminated intravascular coagulation. Several risk factors have been identified: (a) predisposing clinical factors (underlying disease and clinical condition), (b) therapy factors (dosing, concomitant therapy and drug interactions), and (c) quality of the PCC used. It is generally assumed that the risk of thromboembolic adverse effects is greater in patients with acquired disorders of hemostasis than in patients with inherited coagulation factor deficiencies. In hemophilia B, clinical conditions with an increased risk include large muscle hematomas, immobilization, surgery (especially orthopedic surgery), and liver disease. In acquired disorders of hemostasis, a prethrombotic state can be assumed in all patients where an indication for PCC concentrates is considered. Liver disease and/ or antithrombin deficiency are considered as major risk factors. Therapy factors with an increased risk include large, repetitive doses of PCC. It is assumed that heparin and, in the case of antithrombin deficiency, antithrombin substitution decrease the incidence of thromboembolic adverse effects. Heparin neutralisation with protamine and aprotinin therapy may be additional risk factors. The declining incidence and the recent cluster of fatal thromboembolic adverse events in Germany with one brand of PCC is strong evidence for the crucial role of the quality of PCC in the occurrence of thromboembolic adverse effects.

Blood Coagulation Factors↗
PubMed1995

Deep venous thrombosis and pulmonary artery embolism in high-grade non Hodgkin's lymphoma: incidence, causes and prognostic relevance.

To analyse incidence, risk factors, causes and prognostic significance of venous thromboembolism (VTE) in high-grade non-Hodgkin's lymphoma (HG-NHL) a prospective clinical trial (N = 593), also undertaken to analyse other aspects of HG-NHL, a study of haemostasis (N = 25) and a post-mortem analysis (N = 70) were performed. Clinical analysis documented a 6.6% incidence of VTE, and 77% of all cases occurred before or within the first 3 months of chemotherapy. Ann Arbor stage IV and B-mediastinal clear cell histology were risk factors for VTE, while rapid changes in tumour load or application of consolidation chemotherapy were not. Vessel compression by HG-NHL was the leading cause of VTE, whereas a significant (paraneoplastic or chemotherapy-induced) thrombophilic state was not disclosed by haemostatic tests. While VTE-related fatality was found to be low in the clinical trial (1.7%) and at necropsy (8.5%), the occurrence of VTE was associated with an unsatisfactory response of HG-NHL to chemotherapy and a high incidence of treatment-related mortality due to diffuse alveolitis. Thus, fatal VTE in HG-NHL is rare, but VTE is associated with an unfavourable clinical course of HG-NHL.

Adolescent↗