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

Autologous 111In oxine-labelled platelet scintigraphy was used to detect left ventricular thrombi in 20 patients with anterior and 18 patients with inferior Q wave myocardial infarction within 48-72 h. Left ventricular thrombi were found in 8/20 patients with anterior myocardial infarction and in 1/18 patients with inferior myocardial infarction, giving a total incidence of 24%. Patients with left ventricular thrombi were older (64.3 versus 58.2 years), had higher peak creatinine kinase (CK) levels (4523 versus 2749 IU 1-1), lower ejection fraction (19.5 versus 37.8%, P less than 0.005) and were more likely to have an enlarged left ventricle than those without left ventricular thrombi (87.5 versus 54.5%, P less than 0.001). Left ventricular thrombi were found overlying sites of myocardial infarction in 8 out of 9 patients. Apical left ventricular thrombi were 1.7 times more common than septal left ventricular thrombi. All patients received minidose heparin for prevention of deep venous thrombosis. This technique is complementary to echocardiography and may provide additional information in the difficult cases where the decision about full-dose anticoagulation is in doubt.
 ...
PMID:Early detection of left ventricular mural thrombi after acute Q wave myocardial infarction using 111In oxine-labelled autologous platelets. 212 15

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.
 ...
PMID:[Low molecular weight heparin (Fraxiparine) as adjunctive therapy with thrombolysis for acute myocardial infarction: a pilot study with a one year follow up]. 867 95

We describe the case of an elderly man who was admitted to our hospital with the diagnosis of an acute anterior myocardial infarction, together with an acute bioccipital ischaemic stroke. Coronary angiography revealed embolization of the distal left anterior descendens and the first septal branch. The definite diagnosis of paradoxical embolism was made by means of a transoesophageal echocardiography which demonstrated a large snake-like floating thrombus crossing a patent foramen ovale. This diagnosis was also supported by the presence of deep venous thrombosis as a probable origin of the intra-atrial thrombus and the secondary pulmonary embolism which contributed to the elevated right heart pressure.The patient was treated with full-dose heparin and subsequently oral anticoagulation. After discharge, follow-up by transoesophageal echocardiography was organized and once the intracardiac thrombus had disappeared, elective transcatheter closure of the patent foramen ovale was performed.
 ...
PMID:Thrombus-in-transit causing paradoxical embolism in cerebral and coronary arterial circulation. 1563 54

Although heart failure is a procoagulant state, the incidence of arterial thromboembolism (peripheral arterial emboli and strokes) is relatively low in the outpatient setting and seems to be higher in those with concomitant atrial fibrillation or recent large anterior myocardial infarction, especially in the presence of a dyskinetic apex. Hospitalized heart failure patients, on the other hand, have an extremely high rate of deep venous thrombosis and pulmonary emboli. Outpatients with heart failure should receive anticoagulation only in the presence of atrial fibrillation or if they have experienced a prior embolic event. Patients with recent large anterior infarction or recent infarction with documented thrombus should be treated with anticoagulation for the initial 3 months after the infarct, whereas those with evidence of a mural thrombus should receive anticoagulation at least until the thrombus has resolved. Heart failure patients with ischemic cardiomyopathy should receive antiplatelet agents for the prevention of myocardial infarction, stroke, or death. Antiplatelet agents should not be prescribed for heart failure patients with nonischemic cardiomyopathy or without other evidence of atherosclerotic vascular disease. All hospitalized heart failure patients who are not taking oral anticoagulants should receive prophylaxis with low molecular weight heparins or factor Xa inhibitors.
 ...
PMID:Thromboembolic risk in the patient with heart failure. 1776 Nov 16