[Chronic cor pulmonale as a result of progressive thrombotic occlusion of the pulmonary artery].
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The literature was reviewed in an attempt to determine whether patients with cancer have an increased risk of venous thromboembolism, i.e. deep vein thrombosis and pulmonary embolism. From case reports it was apparent that various thromboembolic or thrombophlebitic manifestations may be found in a small number of patients, although it is possible that not all cases belong to the same clinical or pathogenetic entity. In clinical series it was found that the risk of postoperative venous thromboembolism was increased in cancer patients, but the possibility that this was due to associated risk factors, rather than to the mere presence of a tumour, could not be excluded. Little is known about patients not undergoing surgery. Retrospective postmortem studies have found more thrombi in patients with malignancy, but a prospective study failed to demonstrate an association between malignancy and pulmonary embolism. It is possible that different types of cancer show various degrees of association with venous thromboembolism. We conclude that further studies should be performed to provide a firm clinical and pathoanatomical basis for investigations into the pathogenesis of venous thromboembolism.
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Protein C and antithrombin III represent main inhibitors of the plasmatic coagulation system. Due to the lack of practicable assays the clinical importance of protein C was only established during the last six years. In familial protein C deficiency 77% of patients present with recurrent venous thromboses, half of them below the age of 30. In addition to recurrent superficial thrombophlebitis more serious manifestations like deep vein thrombosis and pulmonary embolism have been described. Mesenteric vein thrombosis has been reported in only 5 cases all of which could be controlled by conservative treatment. In our patient protein C deficiency was discovered 10 years after the angiographic diagnosis of portal and mesenteric vein thrombosis. Thereafter, the patient complained of recurrent abdominal discomfort. Intestinal ischaemia due to mesenteric vein thrombosis required segmental resection twice. Postoperatively the patient was heparinized. After excluding a secondary protein C deficiency due to a lack in vitamin K, hepatic disease, or disseminated intravascular coagulation, long-term anticoagulation by dicumarol was implemented as therapy of first choice.
In 53 patients with recent (< 6 hrs) acute myocardial infarction a study was undertaken to evaluate the safety of conjunctive therapy with streptokinase (1.5 mln U), aspirin (150 mg) and low molecular weight heparin (Fraxiparine). Patients were treated with Fraxiparine 250 U anti-Xa IC/kg/24 hrs iv for 2 days (with bolus 12.5 U anti-Xa IC/kg), and 125 U anti-Xa IC/kg twice a day sc for 5 subsequent days. Clinical course in one-year observation was compared regarding the time the therapy was initiated. In the group undergoing therapy 3-6 hrs after the infarct had occurred 4 (7.5%) patients died (2 during hospitalization, 2 after discharge). In 31 patients treated within 3 hrs of the myocardial infarction there were fewer cases of recurrent myocardial infarction, unstable angina or congestive heart failure necessitating rehospitalization their (9.1%) than in 22 patients included in the treatment regimen between 3 rd and 6th h of the infarction (27.3%). Earlier thrombolysis was also connected with higher left ventricular ejection fraction (55 +/- 8% vs 49 +/- 10%) and more frequent peak CK-MB values 12 hrs after thrombolysis (81% and 68% of patients respectively). Neither symptomatic deep vein thrombosis nor pulmonary embolism was detected. The left ventricular thrombosis was diagnosed by echocardiography in 4 of 20 patients (20%) with the first anterior myocardial infarction. There was neither bleeding requiring blood transfusion nor cerebrovascular stroke. The treatment with Fraxiparine did not induce the prolongation of APTT values. Conjunctive thrombolytic therapy with low molecular weight heparin was safe and followed by a favorable outcome of the acute myocardial infarction, especially if instituted within the first 3 hrs after the onset of infarction.
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Venous thromboembolism (VTE) causes more than 1,000 deaths and leads to the admission to hospital of 11,000 patients each year in Sweden. Prevention of venous thrombosis and pulmonary embolism is therefore of great importance. Diagnosis is difficult as the symptom profile is diffuse and difficult to interpret. Acute treatment and secondary prophylaxis are complicated as the risk of severe bleeding is great. A systematic review was carried out of the literature on prevention, diagnosis and treatment of VTE. Only randomized controlled studies were included and, to assess diagnostic methods, only studies with an independent comparison with a known reference method. Approximately 1,300 scientific studies met the requirements for high scientific quality. The scientific evidence strongly suggests that low molecular weight heparin can replace unfractionated heparin in preventing and treating venous thrombosis and pulmonary embolism. Treatment with a single daily injection, rather than two, of low molecular weight heparin yields equally favorable effects. The risk for hemorrhage is lower with low molecular weight heparin and management is simpler, which facilitates outpatient treatment. Longer-term secondary prophylaxis with warfarin reduces the risk for relapse, but several years of treatment also increases the risk for severe hemorrhage. The presence of treatment-demanding VTE can be excluded in outpatients by combining the assessment of clinical probability, using clinical decision rules, with measurement of D-dimer. Thorough ultrasonic examination of the leg and a CT scan of the pulmonary vessels usually provide sufficient diagnostic reliability, which strongly supports the use of these methods in clinical practice. It is not meaningful to conduct extensive investigations of patients with venous thrombosis to find possible underlying cancer. It is essential to develop more cost-effective methods to investigate genetic predisposition for thrombosis.
Thrombectomy with arteriovenous fistula was performed between 1977 and 1988 in 103 patients (41 females, 62 males, mean age 46.7 years, 114 involved extremities) with embolizing deep-vein thrombosis (DVT). The sole aim of the surgical procedure was prevention of recurrent embolization. On the basis of the proximal extent of the thrombosis the source of embolization was identified as the iliac veins or inferior vena cava in 63% of the patients; 48% presented with a post-phlebitic vein and/or an older thrombosis, and 46% had already had recurrent pulmonary emboli. Unsuccessful aggressive procedures had been carried out previously in 11%. The rate of intraoperative pulmonary embolism (PE) was 3% (one fatal case). The perioperative mortality was 6.8%, but only one death was related to the surgical treatment itself. During follow-up (8-140 months postoperatively, mean 55 +/- 34 months) late recurrent PE was confirmed in two patients (antithrombin III deficiency, contralateral DVT) and was reported as the suspected cause of death in a third (3.6%). Venous thrombectomy with arteriovenous fistula is a reliable and effective procedure for management of embolizing DVT and is indicated especially in young patients. The rates of early- and late-recurrent PE are low, introduction of artificial material into the vein can be avoided, and long-term preservation of valve function is occasionally possible.
As blood clots it goes through predictable stages that reflect the oxygenation state of hemoglobin within the red cells. One of these stages results in the formation of methemoglobin. This substance acts an endogenous contrast agent when imaged using a T1-weighted magnetic resonance sequence (Magnetic Resonance Direct Thrombus Imaging, MRDTI) - appearing as high signal. MRDTI can therefore be used to detect subacute thrombosis. This technique has been applied in a number of clinical settings arising as a result of thrombosis. Deep vein thrombosis and pulmonary embolism are both readily detected using MRDTI, providing a single imaging modality for the detection of venous thromboembolic disease. The technique is also effective in the peripheral arterial tree. Furthermore, thrombosis within vessel wall atherosclerosis is a marker of vulnerable plaque likely to produce symptoms. The MRDTI technique has thus proved useful in identifying complicated plaque in the carotid arteries in the setting of transient and permanent cerebral ischemia. MRDTI therefore holds promise as a technique that is capable of detecting high risk vessel wall disease prior to significant or permanent end organ damage. Because of the non-invasive nature of magnetic resonance imaging (MRI), application of MRDTI in the research setting for the monitoring of therapeutic interventions in a wide number of settings within vascular disease is very appealing.
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Over a 13-year period we studied all patients who underwent major hip and knee surgery and were diagnosed with objectively confirmed symptomatic venous thromboembolism, either deep venous thrombosis or non-fatal pulmonary embolism, within six months after surgery. Low-molecular-weight heparin had been given while the patients were in hospital. There were 5607 patients. The cumulative incidence of symptomatic venous thromboembolism was 2.7% (150 of 5607), of which 1.1% had developed pulmonary embolism, 1.5% had deep venous thrombosis and 0.6% had both. Patients presented with deep venous thrombosis at a median of 24 days and pulmonary embolism at 17 days after surgery for hip fracture. After total hip replacement, deep venous thrombosis and pulmonary embolism occurred at a median of 21 and 34 days respectively. After total knee replacement, the median time to the presentation of deep venous thrombosis and pulmonary embolism was 20 and 12 days respectively. The cumulative risk of venous thromboembolism lasted for up to three months after hip surgery and for one month after total knee replacement. Venous thromboembolism was diagnosed after discharge from hospital in 70% of patients who developed this complication. Despite hospital-based thromboprophylaxis, most cases of clinical venous thromboembolism occur after discharge and at different times according to the operation performed.
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