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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibrinolysis treatment with urokinase was successfully undertaken in two patients, aged 71 and 76 years, with phlegmasia coerulea dolens. In the first case, with necrosis in the fore-foot, there was significant regression of the necrotic area, but a later limited amputation was still necessary. In the second, with severe heart failure, recurrent pulmonary emboli and hyperosmolar uncontrolled diabetes mellitus, complete healing was achieved. Venous thrombectomy was not possible in these two patients because of the duration of the thrombosis in the veins of the pelvic region, necrosis had already occurred, and the patients' general condition was so serious. The advanced age and arteriosclerotic changes argued against streptokinase treatment. Mean urokinase maintenance dosage of 1000-1500 IU/kg X h, with simultaneous administration of heparin at about 20 U/kg X h, produced no significant side-effects. Minor gastro-intestinal bleeding did not require stoppage of urokinase administration.
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PMID:[Urokinase treatment of phlegmasia coerulea dolens (author's transl)]. 31 5

Recent trials of myocardial reperfusion using single-agent thrombolytic therapy and sequential cardiac catheterization have supported a conservative approach to the patient with acute myocardial infarction. To evaluate combination thrombolytic therapy and the role of a previously untested strategy for the aggressive use of cardiac catheterization, we performed a multicenter clinical trial with a 3 x 2 factorial design in which 575 patients were randomly allocated to one of three drug regimens--tissue-type plasminogen activator (t-PA) (n = 191), urokinase (n = 190), or both (n = 194) - and one of two catheterization strategies--immediate catheterization with angioplasty for failed thrombolysis (n = 287) or deferred predischarge catheterization on days 5-10 (n = 288). Patients with contraindications to thrombolytic therapy, cardiogenic shock, or age of more than 75 years were excluded. Global left ventricular ejection fraction was well preserved and almost identical at predischarge catheterization (54%), regardless of the catheterization or thrombolytic strategy used (p = 0.98). Combination thrombolytic therapy was associated with a less complicated clinical course, most clearly documented by a lower rate of reocclusion (2%) compared with urokinase (7%) and t-PA (12%) (p = 0.04) and a lower rate of recurrent ischemia (25%) compared with urokinase (35%) and t-PA (31%). When a composite clinical end point (e.g., death, stroke, reinfarction, reocclusion, heart failure, or recurrent ischemia) was examined, combination thrombolytic therapy was associated with greater freedom from any adverse event (68%) compared with either single agent (urokinase, 55%; t-PA, 60%) (p = 0.04) and with a less complicated clinical course when the composite clinical end points were ranked according to clinical severity (p = 0.024). Early patency rates were greater with combination therapy, although predischarge patency rates after considering interventions to maintain patency were similar among drug regimens. No difference in bleeding complication rates was observed with any thrombolytic regimen. The aggressive catheterization strategy led to an overall early patency rate of 96% and a predischarge patency rate of 94% compared with a 90% predischarge patency in the conservative strategy (p = 0.065). The aggressive strategy improved regional wall motion in the infarct region (-2.16 SDs/chord) compared with deferred catheterization (-2.49 SDs/chord) (p = 0.004). More patients treated with the aggressive strategy were free from adverse outcomes (67% versus 55% in the conservative strategy, p = 0.004), and the clinical course was less complicated when the adverse outcomes were ranked according to severity (p = 0.016). No significant increase in use of blood products resulted from the aggressive strategy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evaluation of combination thrombolytic therapy and timing of cardiac catheterization in acute myocardial infarction. Results of thrombolysis and angioplasty in myocardial infarction--phase 5 randomized trial. TAMI Study Group. 202 33

More than 10 years ago, thrombolytic therapy with urokinase and streptokinase for pulmonary embolism was found to have considerable advantages over standard heparin therapy. After the introduction of alteplase, a recombinant tissue plasminogen activator, further studies confirmed this benefit. However, thrombolytic therapy for pulmonary embolism has not gained universal acceptance, even though it now has U.S. Food and Drug Administration approval. Clear advantages of thrombolytic therapy over conventional heparin therapy are improved pulmonary capillary blood volume, accelerated clot lysis and accelerated pulmonary perfusion. Earlier reversal of right-sided heart failure, a lower incidence of recurrent pulmonary embolism, a reduced risk of chronic pulmonary hypertension and reduced mortality have been claimed as advantages, but these have not been adequately proved. A recent survey suggests that about half of all patients with pulmonary embolism are potential candidates for thrombolytic therapy. In a subset of patients with hemodynamic compromise, thrombolysis has definite advantages over heparin therapy.
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PMID:Thrombolysis for pulmonary embolism. 192 47

For decades management of acute myocardial infarction (AMI) consisted of bed rest, oxygen, prevention for thromboembolic complications, and treatment of arrhythmias and heart failure. In the last years a more aggressive treatment of AMI has been developed, based on the following three basic principles: (1) Mortality of patients with AMI is determined by the infarct size and the degree of left ventricular dysfunction. (2) The time interval between the onset of coronary occlusion and any intervention to limit infarct size is brief and takes usually not more than three to four hours. (3) After the acute phase of infarction a lot of patients remain at high risk of fatal coronary events, i.e. reinfarctions. The angiographic findings during the first hours of AMI showed in about 80% of patients an obstructive coronary thrombus and led to efforts to dissolve the offending thrombi. The demonstration that coronary thrombi can be lysed in about 80% of cases within 60 minutes after the intracoronary injection of thrombolytic agents (streptokinase or urokinase) has boosted the reperfusion therapy in AMI in the hope that ischemic myocardium might be salvaged. Intracoronary infusion of thrombolytic agents however, can be applied only in a minority of patients with AMI because coronary angiography and a skilled team of investigators are required, therefore a short-time intravenous high dose streptokinase infusion was developed. In the meantime two large double blind randomized trials (ISAM and GISSI) could demonstrate a reduction in hospital mortality in AMI especially by early treatment with intravenous streptokinase. Conventional thrombolytic agents produce a systemic lytic state with the possibility of hemorrhage, therefore recombinant tissuetype plasminogen activator (rt-PA) and two other drugs, acylated streptokinase and pro-urokinase, were developed with the aim of inducing coronary thrombolysis without severe systemic lytic state, but the efficacy of these new drugs remains to be demonstrated in randomized trials versus conventional thrombolytic agents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The therapy of acute myocardial infarction: current state of the art. 244 99

The records of 5 neonates with systemic arterial thrombosis (aortic in one case, peripheral in four cases) were reviewed. Fibrinolysis was performed with urokinase administered by infusion (1,000 to 4,000 U/kg/h). This treatment was combined with heparin therapy in 4 cases. Thrombosis was due to various causes: umbilical arterial catheter (1 case), disorders of supraventricular rhythm in utero (1 case), aneurysm of the ductus arteriosus with dysplastic aortic arch vessels (2 cases); one of these patients also had myocardiopathy. No cause could be found in a premature child weighing 1,300 g. The presenting symptoms of systemic arterial thrombosis are ischaemia of the extremities and suppression of peripheral pulses; heart failure with arterial hypertension is frequent. In our series the diagnosis was confirmed by doppler-ultrasonography in one case and by angiography in three cases (angiography in the left ventricule with foramen ovale, or umbilical aortography). Treatment with urokinase lasted 1.5 to 7 days. In 2 children the initial dosage had to be increased as there was no clinical improvement. Four children were completely cured; the fifth child, who had left renal thrombosis, shows slight functional impairment of the left kidney. There were no haemorrhagic complications. The fibrinolytic treatment with urokinase of systemic arterial thrombosis in the newborn is effective and has few drawbacks.
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PMID:[Treatment with urokinase of systemic arterial thrombosis in the newborn infant]. 250 Jan 1

Among 263 patients with acute myocardial infarction, 141 were treated with urokinase (UK group) and 122 received no urokinase (conventional group). Urokinase (UK) was administered intracoronarily in 55 cases; intravenously (mainly 1,920,000 units) in 64 cases; and intravenously and intracoronarily in 22 cases. The mortality rates were ascertained three months after admission and during the mean follow-up periods of 17.5 months for the UK group and 24.5 months for the conventional group. The three month mortality was significantly lower in the UK group (10.6%, 15 cases) than in the conventional group (23.8%, 29 cases) (p less than 0.01). The mortality during the entire follow-up period was also lower in the UK group (14.2%, 20 cases) than in the conventional group (26.2%, 32 cases) (p less than 0.05). Fatalities due to cardiac rupture, ventricular fibrillation, cardiac failure, cardiogenic shock and recurrent infarction were uniformly less in the UK group. It was concluded that coronary thrombolysis is an effective means of reducing mortality in acute myocardial infarction.
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PMID:[The effects of coronary thrombolysis on the short- and long-term mortality in acute myocardial infarction]. 281 55

A 6-month-old female infant was seen with heart failure secondary to severe aortic and mitral regurgitation. As a neonate the infant had undergone an aortic valvotomy for congenital aortic stenosis. Subsequently the infant had aortic and mitral regurgitation with an infarcted papillary muscle. Double valve replacement was carried out with the St. Jude valve. The first approach was by the Manouguian procedure with extension of the aortotomy out between the left coronary cusp and the noncoronary cusp. The posterior mitral apparatus was resected, and a 19-mm St. Jude aortic valve was sewn into the mitral position. Because the enlarged aortic valve annulus was still inadequate to accommodate a 19-mm St. Jude valve, a Konno procedure was carried out to enlarge the aortic ring anteriorly. Atrial, septal, and aortic repair and right ventricular outflow tract reconstruction were carried out with bovine pericardium. Bypass was carried out with standard techniques of hypothermia, aortic cross-clamping, and cardioplegia. Postoperative anticoagulation therapy was initially with aspirin and dipyridamole (Persantine); however, clotting of the mitral prosthesis necessitated treatment with urokinase and heparin, which completely resolved the clot. Sodium warfarin (Coumadin) therapy was then begun. One year postoperatively, the child is developing normally.
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PMID:Combined techniques for double valve replacement in the infant. 388 67

Early recanalization of infarct-related coronary arteries has been attempted in 40 patients with acute myocardial infarction (AMI) and angiographically proven total occlusion by brief high dose intravenous streptokinase infusion (IVSK). In 24 patients (60%) recanalization was achieved after 48 +/- 14 min of IVSK at an infusion rate of 30,000 to 40,000 IU/min (group A), in 16 patients there was a late (greater than 2 h) or no recanalization (group B). The total dose of SK was 1.7 +/- 0.48 Mio IU in group A and 1.74 +/- 0.41 Mio IU in group B, the time from the onset of symptoms to peak myocardial enzyme of creatine phosphokinase (CKMB) 11 +/- 3 h in group A and 22 +/- 6 h in group B (p less than 0.001). Biplane left ventricular ejection fraction increased from 55 +/- 9% at the time of acute angiography to 58 +/- 10% after 14 to 24 days in group A (p less than 0.1) and decreased from 49 +/- 11 to 41 +/- 11% in group B (p less than 0.005). There were four reocclusions in group A, two could be reopened by i.v. urokinase (1 Mio IU over 30 min). During a follow-up period of 18 +/- 8 months one patient in group A died from an early ventricular rupture 2 hours after recanalization, and one patient in group B from heart failure 7 months after IVSK. There was no serious bleeding or other complication related to IVSK. We conclude that IVSK is an effective and safe means of early recanalization of coronary thrombosis in AMI, and feasible in the majority of patients with AMI.
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PMID:High dose intravenous streptokinase in acute myocardial infarction. 662 71

Early postinfarction angina implies an unfavorable prognosis. Most published information on this outcome represents data collected in the prethrombolytic era, in which definitions and populations differed considerably. Our purpose was to evaluate the incidence and importance of recurrent ischemia after administration of thrombolytic therapy. We studied patients enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction studies. Patients were enrolled into 5 studies with similar entry criteria; 552 patients were treated with tissue plasminogen activator (t-PA), 293 were treated with urokinase, and 385 received both thrombolytic agents. Recurrent ischemia was defined as symptoms in association with electrocardiographic changes; reinfarction was defined as a reelevation of creatine kinase myocardial band isoenzyme in an appropriate clinical setting. Both recurrent ischemia and reinfarction occurred in 42 patients (3.4%), recurrent ischemia alone occurred in 226 (18%), whereas neither occurred in 964 (78%). Although baseline characteristics were similar among the 3 groups, in-hospital cardiac events (total 73 deaths, 253 heart failure episodes) were not: in-hospital mortality in patients with reinfarction was 21%; with recurrent ischemia, 11%; and with neither event, 4% (p < 0.0001). The in-hospital heart failure rate of patients with reinfarction was 50%; with recurrent ischemia alone, 31%; and with neither event, 17% (p < 0.0001). As expected, median in-hospital costs were highest in patients with reinfarction ($26,802), intermediate for those with recurrent ischemia alone ($18,422), and lowest in patients with neither event ($15,623). Recurrent myocardial ischemia after thrombolytic therapy is a frequent, important, and expensive adverse clinical outcome, making it a critical target for therapeutic intervention.
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PMID:Frequency, significance, and cost of recurrent ischemia after thrombolytic therapy for acute myocardial infarction. TAMI Study Group. 748 52

This study was designed to evaluate major fibrinolytic parameters in relation to parameters of inflammation associated with different kinds of pleural effusion. Sixty patients with pleural effusion were studied. The underlying aetiology was empyema in 10 cases, tuberculosis in 9, cancer in 31, cardiac failure in 7, and undetermined in 3. Plasminogen, plasminogen activator inhibitor 1 (PAI-1) and 2 (PAI-2), tissue type plasminogen activator (t-PA), urokinase (u-PA) and D-dimers (D-D) were quantified in plasma samples and pleural effusion specimens. These data were then correlated with inflammatory or infectious parameters, i.e. fibrinogen, von Willebrand factor (vWF), erythrocyte sedimentation rate (ESR), protein concentration, and white blood cell count. D-D levels were higher in pleural fluid than in plasma. D-D levels were not correlated with either plasminogen activator or plasminogen activator inhibitor levels, suggesting the presence of other fibrinolytic pathways. PAI levels (PAI activity, PAI-1 antigenicity, PAI-2 antigenicity) and vWF levels were significantly higher in patients with tuberculosis and empyema than in patients with cancer or cardiac failure. Regression analysis between inflammatory and fibrinolytic parameters showed that pleural PAI levels were significantly correlated with pleural neutrophil count, vWF levels, and plasma fibrinogen levels. D-D levels were correlated with blood ESR. No significant difference in pleural t-PA, u-PA and D-D levels was observed between aetiologies. The highest pleural t-PA and u-PA values were noted in patients with cancer, especially lymphoma. Plasma t-PA levels were higher inpatients with pleural effusion secondary to congestive heart failure, but this difference did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fibrinolytic and inflammatory processes in pleural effusions. 748 3


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