Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently new radioimmunoassay methods have been established to measure plasma concentrations of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), platelet release products which are set free when platelets aggregate. Plasma concentrations of beta-TG and PF4 were investigated in disorders with increased thromboembolic risk. Extremely high concentrations of these platelet proteins were found in patients with venous thrombosis, pulmonary embolism, polycythemia vera, and chronic renal failure. Moderately increased beta-TG and PF4 levels were observed in patients with peripheral vascular disease, coronary artery disease, chronic rheumatoid arthritis, multiple myeloma, and diabetes mellitus. These data indicate, that plasma concentrations of beta-TG and PF4 are useful parameters for the evaluation of the "in vivo" platelet activity. By using these new methods for clinical applications special blood sampling conditions have been taken into account; moreover one has to consider that the plasma levels of the platelet "release products" are dependent from renal function.
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PMID:[Clinical significance of the radioimmunological determination of beta-thromboglobulin and platelet factor 4]. 9 43

The relationship between factor VIII (AHF) procoagulant activity and factor VIII-related antigen were examined in patients with disseminated intravascular coagulation (DIC), pulmonary embolism (PE), and coronary artery disease with or without myocardial infarction (MI). It was found that 13 of 13 patients with DIC, 17 of 17 patients with PE, and 10 of 12 patients with MI possessed a significantly elevated factor VIII-related antigen to factor VIII activity ratio (VIII-ratio). The VIII-ratio returned to normal in each of 2 patients with DIC and 1 paitent with PE after treatment with heparin, heparin and alpha-amino-caproic acid, and heparin and coumadin respectively. In contrast, the VIII-ratio was slightly elevated only in 1 of 15 patients with coronary artery insufficiency without MI. In in vitro studies, after treatment of plasma with thrombin or plasmin, factor VIII activity was lost, whereas the amount of factor VIII-related antigen remained the same or was even increased when measured by agarose quantitative immunoelectrophoresis. These observations have led us to conclude that an elevated VIII-ratio is a very sensitive indicator of intravascular coagulation.
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PMID:In vivo and in vitro effects of thrombin and plasmin on human factor VIII (AHF). 13 71

An 86-year-old man with previous normal renal function was hospitalized because of renal insufficiency. He had a long history of atherosclerotic heart disease, mild hypertension and pulmonary embolism, requiring anticoagulant therapy. In view of the normal-sized kidneys and absence of casts in the urinary sediment, a diagnosis of atheroembolic renal disease was made. The patient's renal function deteriorated, but he refused hemodialysis. Death occurred within a few weeks. At autopsy, severe aortic atherosclerosis was observed and atheroembolic renal disease was confirmed as the cause of renal failure. Occasionally, renal failure can be the sole manifestation of spontaneous atheroembolic disease. This possibility should be considered if the physician is called upon to establish the diagnosis when renal insufficiency develops in atherosclerotic patients.
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PMID:"Spontaneous" atheroembolic disease as a cause of renal failure in the elderly. 46 53

The defibrinating agent ancrod has had limited clinical trial, but appears to give no advantages over heparin. Intravenous infusion of dextran, a glucose polymer, has been shown to have an antithrombotic effect in many experimental models of thrombosis. However, the evidence that dextran is a clinically valuable antithrombotic drug is conflicting. A number of controlled randomized studies have shown that dextran can prevent postoperative venous thromboembolism when a large volume of dextran 40 or 70 was infused rapidly during and after surgery. However, blood volume expansion during dextran treatment prohibits its use in patients with reduced cardiac reserve, and infrequent though sometimes severe, allergic reactions have been reported. Evidence that dextran is of value for the treatment of venous or arterial thromboembolism comes from uncontrolled studies and is not convincing. Many compounds have been shown to inhibit platelet function in vitro but only five of these drugs have been extensively evaluated as prophylactic or therapeutic antithrombotic agents in man. These are aspirin, sulphinpyrazone, dipyridamole, hydroxychloroquine and clofibrate. They have been evaluated mainly in patients with cerebral vascular disorders, coronary artery disease, peripheral artery ischaemia, venous thromboembolism, prosthetic heart valves, and in patients with arteriovenous shunts. The evaluation of the clinical effect of the platelet function suppressing drugs is in its early stages, but they appear to differ from each other in the spectrum of their clinical effectiveness, and they may be more effective in arterial than in venous thromboembolic disorders. Their role in the management of cerebral vascular disease and coronary artery disease is still uncertain, and should be clarified by the results of a number of multi-centre, prospective, randomized studies which are currently in progress. Three types of thrombolytic drugs have been evaluated clinically; the plasminogen activators streptokinase and urokinase, proteolytic enzymes such as plasmin, and agents which increase the level of endogenous plasminogen activator (e.g. anabolic steroids). Of these, the plasminogen activators now have a definite place in clinical practice. The plasminogen activators accelerate the lysis of recent venous thrombi and pulmonary emboli, and of arterial thrombi or emboli. Thrombolytic therapy with these agents should be considered particularly in patients with recent major pulmonary embolism, as lysis of recent emboli is rapid and substantial. It should also be considered in patients with recent extensive venous thrombosis, because total lysis of venous thrombi has been reported to result in long-term preservation of valve function, and is likely to prevent postphlebitic syndrome, though this has not been proven. However, plasminogen activator therapy carries a higher risk of bleeding than heparin treatment...
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PMID:Antithrombotic drugs: part II. 78 6

A detailed pathological study was made in 10 patients dying up to 13 months after aortocoronary saphenous vein bypass grafting for coronary atherosclerosis. The coronary arteries and vein grafts were investigated by injection with a radio-opaque mass, radiography, dissection, and histology. The report is to some extent historical since the patients died during a period when the operation was first being introduced into two cardiothoracic hospitals. About 80 operations were performed during the time the 10 deaths occurred, a mortality of 12-5 per cent (including cases followed up to 13 months after operation). Seven of the patients were operated on for intractable angina and 3 with a view to aneurysmectomy. All the patients selected for operation were severely disabled despite medical treatment. The main cause of death was extremely severe coronary artery disease and its effects on the left ventricle; in one case, over two-thirds of the left ventricle had been destroyed by infarction before operation. Other causes or contributing causes of death were pulmonary embolism, myocardial infarction complicating angiography (ostial stenosis), and cerebral damage. Ten of the 14 vein grafts (71%) were patent at necropsy. A free flow of injection medium usually occurred between patent grafts and coronary arteries. Thrombosis of a graft was thought to have contributed to death in 3 patients, but not in a fourth who died of pulmonary embolism. Since thrombosis of grafts was usually secondary to poor run-off blood into severely atheromatous coronary arteries, this was also an indirect effect of the advanced coronary arterial disease. In one case, thrombosis followed severe chronic intimal thickening of a graft in place for 13 months. The study of these deaths emphasizes that in some patients the pathological changes in the coronary arteries and left ventricle are too severe for them to benefit from surgery. Vein grafts cannot be expected to distribute blood effectively through grossly narrowed coronary arteries. In addition, when a large part of the left ventricle is infarcted or scarred, it is almost certain that improving the blood supply by grafting will not result in significant regeneration of cardiac muscle. Since the time when this study was made, there have been few deaths among the many vein graft operations subsequently carried out in the hospitals involved. The two most important factors thought responsible for the improvement are the selection of cases more suitable for surgery by continued improvement of diagnostic techniques, and also the employment of more radical surgical procedures in the form of coronary endarterectomy and the insertion of more grafts per patient.
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PMID:Pathology of hearts after aortocoronary saphenous vein bypass grafting for coronary artery disease, studied by post-mortem coronary angiography. 108 91

Cardiovascular diseases account for approximately 50% of deaths in patients on chronic haemodialysis. Therefore we prospectively studied 54 consecutive patients on dialysis for the presence or absence of ventricular late potentials (LP). LP, i.e. low-amplitude potentials in the terminal part of the QRS complex, have been shown to be highly indicative of life-threatening arrhythmias and sudden death. The results were correlated with echocardiographic studies and the clinical outcome during a follow-up period of 18 months. Fifty patients were suitable for evaluation (29 males, 21 females; mean age 55 years; mean time on dialysis 32 months; coronary artery disease present in 5) Our analysis revealed LP in seven of 50 patients only. Left ventricular hypertrophy, i.e. mean wall diameter > 12 mm, was present in 78%, a compromised left ventricular function, i.e. shortening fraction < 28%, was found in 28% of the patients. With respect to echocardiographic parameters, patients with and without LP were similar. During follow-up, sudden cardiac death was observed in three of 11 patients deceased. LP were detectable in one of the three only. From the remaining six patients with LP, four are still alive, and two patients died due to atherosclerosis and pulmonary embolism. Our data underline the crucial role of sudden cardiac death in dialysis patients. Ventricular late potentials, however, are of no prognostic relevance with respect to identification of dialysis patients at risk of sudden death.
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PMID:Ventricular late potentials in haemodialysis patients and the risk of sudden death. 133 75

To determine the frequency and etiology of elevations of CK-MB in patients with pulmonary emboli, we studied 52 patients with well-documented emboli and the absence of known ischemic heart disease or ECG changes suggestive of acute infarction. All patients were evaluated with serial CK-MB determinations at 8-h intervals. All patients with elevations of CK-MB had noninvasive cardiac evaluations. Four (7.7 percent) of the 52 patients had a rising and falling pattern of CK-MB that satisfied enzyme criteria of acute infarction. Three of these four also manifested classic echocardiographic features of right ventricular infarction. None of the four had evidence of left ventricular regional wall motion abnormalities or dysfunction. Of the 48 patients without elevations of CK-MB, only two had segmental right ventricular dysfunction. These findings suggest that pulmonary emboli can induce right ventricular infarction in some (7.7 percent) patients even when patients with a history of coronary artery disease and/or ECG changes of infarction are excluded. Conversely, the diagnosis of pulmonary embolism should be considered in patients when right ventricular infarction is diagnosed.
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PMID:Elevations of CK-MB following pulmonary embolism. A manifestation of occult right ventricular infarction. 803 80

Over the past decade there has been an increasing use of thrombolytic agents in the treatment of coronary artery disease, pulmonary embolism, and thromboembolic strokes. The use of thrombolytic agents has been most successful in treating acute myocardial infarction. When treatment with intravenous streptokinase or tissue plasminogen activator (tPA) is initiated within the first 3 to 4 hours from the onset of symptoms, the rate of reperfusion ranges from 60% to 90%, as compared to a rate of 13% to 21% for placebo control. Both streptokinase and tPA have been extensively studied as therapies for acute myocardial infarction, and in general, a higher initial rate of reperfusion is achieved in tPA-treated patients than in streptokinase-treated patients, although the final arterial patency rate may not be different in the two groups due to a higher rate of reocclusion in the tPA-treated population. Furthermore, time dependency for efficacy from the onset of symptoms to the initiation of treatment is less for tPA than for streptokinase. However, the role of thrombolytic agents in the treatment of thromboembolic strokes is more experimental than clinical at the present time. Of all agents, tPA is the most promising and the most extensively studied. This paper will review the experimental data on the use of tPA in acute thromboembolic strokes as well as the existing clinical data on stroke reperfusion.
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PMID:The efficacy and safety of tissue plasminogen activator in acute ischemic strokes. 162 47

A 68-year-old man with remote history of previous myocardial infarction presented with a four-week history of intermittent dyspnea. After developing hypotension during an exercise tolerance test, he underwent cardiac catheterization, revealing significant pulmonary hypertension and two-vessel coronary artery disease. Pulmonary angiography confirmed the presence of pulmonary emboli which partially resolved after thrombolytic therapy. Subsequent treadmill testing confirmed the absence of exercise-induced hypotension two months following treatment. This case underscores the importance of considering pulmonary embolism as a potential cause of exercise-induced hypotension, since it can be successfully treated with thrombolytic agents weeks after the initial onset of symptoms.
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PMID:Pulmonary embolism presenting as exercise-induced hypotension. 198 18

The haemostatic balance can basically be described as the equilibrium between fibrin formation (coagulation) and fibrin lysis (fibrinolysis). The status of this balance may therefore be reflected by the products of these two processes. Until recently, the tests for assessment of fibrin(ogen) degradation products were performed in serum since they were based on polyclonal antibodies, which cross-react with fibrinogen. However, the use of serum introduces many artefacts so the utility of these serum tests is limited. New assays have now become available, which can be divided into quantitative enzyme immunoassays (EIAs) and semi-quantitative latex agglutination assays. The new assays can be carried out in plasma since they use highly specific monoclonal antibodies, the majority of which do not cross-react with fibrinogen. This makes it possible to avoid the serum artefacts. Furthermore, these plasma assays can discriminate between degradation products of fibrin and those of fibrinogen (FbDPs and FgDPs, respectively). The possible clinical utility of the new assays is discussed on the basis of literature data on the following clinical states: deep venous thrombosis (DVT) and pulmonary embolism, liver disease and liver transplantation, sickle cell disease, renal diseases, pregnancy and preeclampsia, disseminated intravascular coagulation (DIC), malignancy, coronary artery disease and thrombolytic therapy. Fibrinolysis appears to be accompanied by fibrinogenolysis. Detection of fibrin(ogen) derivatives may be used to rule out DVT and to monitor efficacy of anticoagulant treatment for DVT or DIC, and reflects severity of renal disease but not renal function. High levels of FgDPs were found during orthotopic liver transplantation and thrombolytic therapy. Fibrin(ogen) degradation products cannot be used to predict reperfusion following thrombolytic therapy. The fibrinolytic system remained active during normal and complicated pregnancy and in patients with malignancies. The new assays provide valuable information on fibrin(ogen)olysis in several diseases. More information on the haemostatic balance may be obtained by using these new assays for fibrin(ogen)olysis products in combination with assays for coagulation products.
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PMID:Monoclonal antibody-based plasma assays for fibrin(ogen) and derivatives, and their clinical relevance. 210 91


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