Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic thrombolytic therapy was performed in 273 patients with large myocardial infarction: 82 on streptokinase, 25 on tissue plasminogen activator, and 166 on streptodecase. The signs of recovered coronary blood flow were observed in 68, 84, and 33% of the patients, respectively. The application of tissue plasminogen activator resulted in the maximum reperfusion. The success of thrombolytic therapy was related to the fibrinolytic system of a patient: reperfusion was achieved in 96% of patients having a high blood fibrinolytic activity and only in 31% with a low one. The clinical effect of reperfusion was most profound in patients with Killip's Class III heart failure. The patients with early recovery of coronary blood flow developed twice more frequently, which was evidenced by a 12-month follow-up. Fifty percent of patients with an ejection fraction of below 40% died within the first year of the follow-up. The authors discuss whether one can use a differential therapy, including surgical tools for myocardial revascularization.
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PMID:[Immediate and long-term results of thrombolytic therapy in patients with myocardial infarct: the necessity of differential treatment]. 140 37

In order to study the effects of chronic venous hypertension due to heart failure on blood fibrinolytic activity, tissue plasminogen activator (t-PA) antigen, plasminogen activator inhibitor 1 (PAI-1) antigen, t-PA activity and PAI activity were measured before and after venous occlusion of the arm for 20 min in 15 patients with right-sided heart failure, 15 patients with left-sided heart failure, and 30 control healthy subjects. Central venous pressure, measured by observing the jugular veins, was above 15 cm of the blood column in all patients with right-sided heart failure, and normal (below 8 cm) in all patients with left-sided heart failure and control subjects. There was no difference in the basal concentrations of t-PA (11.0, 10.2 and 10.8 ng/ml; all values medians) and PAI-1 antigens and their activities between right and left-sided heart failure and the control subjects. After the occlusion, t-PA antigen increased significantly less in right-sided heart failure (28.6 ng/ml) than in left-sided heart failure and the control subjects (54.5 and 45.9 ng/ml, respectively). It was concluded that the poor increase in fibrinolytic activity that had already been reported in patients with heart failure, was due to low t-PA release during occlusion and not to a high basal PAI level. It was limited to the patients with right-sided heart failure and was probably the consequence of chronic systemic venous hypertension.
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PMID:Tissue plasminogen activator release in chronic venous hypertension due to heart failure. 144 Apr 98

Eighty-nine consecutive Chinese patients (69 males, 20 females) with acute myocardial infarction treated by 100 mg recombinant tissue plasminogen activator (7 intracoronarily, 82 intravenously) at 3.7 +/- 1.0 h after onset, and intravenous heparin or dipyridamole therapy started at 3 h, were studied prospectively. Their mean age was 59.6 +/- 10.6 yr. Forty-six patients (51.7%) had anterior and 39 patients (43.8%) had inferior infarcts. Clinical evidence of reperfusion were seen in 63 patients (70.8%), while new complications included hypotension (5.6%), heart failure (6.7%), cardiac arrhythmias (76.4%) majority of which are related to reperfusion and self-remitting, haematoma around vascular access sites (23.6%), melaena (3.3%) and cerebral infarction (2.2%). Maximal changes in coagulation profiles were seen at 3 h, including a decrease in fibrinogen by 64.2% and an increase in fibrin degradation products by 47 times. The changes in haemostatic variables were not related to body weight or bleeding complications. Nine patients (10.1%) had recurrence of angina and 6 patients (6.9%) died due to pump failure and reinfarction. Angiogram at 14 days confirmed TIMI 2 or 3 patency of infarct-related arteries in 63 out of 73 (86.3%) patients, with a mean global ejection fraction of 52.5 +/- 12.4%. Nearly all survivors could maintain class I-II functional status after discharge. The safety and promise of recombinant tissue plasminogen activator for acute myocardial infarction in the Chinese were confirmed.
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PMID:Recombinant tissue plasminogen activator in acute myocardial infarction in the Chinese in Hong Kong. 151 55

In a study of biological risk factors for sudden death in patients with coronary artery disease, 320 patients were, prospectively, recruited and followed-up over two years. None of the patients had heart failure or recent myocardial infarction. The following variables were recorded: previous acute myocardial infarction, hypertension, smoking habits, ventricular arrhythmia; the angiographic variables included: left ventricular ejection fraction, Jenkins' and mean atherosclerotic scores; lipid profile: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoproteins Al and B; hemostatic profile: fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2-antiplasmin, euglobulin clot lysis time and tissue plasminogen activator before and after venous occlusion, tissue plasminogen activator inhibitor, platelet factor 4, beta-thromboglobulin. During the follow-up period, 12 of the patients died suddenly. In these patients, ejection fraction was lower: 49 +/- 16% versus 61 +/- 14% for the other patients (P less than 0.02), fibrinogen higher: 3.9 +/- 0.8 g/l versus 3.5 +/- 0.8 for the living patients (P less than 0.05) and protein C lower: 89 +/- 39% versus 111 +/- 39% (P = 0.06) for the other patients. In multivariate analysis: lower ejection fraction (P less than 0.008), older age (P less than 0.03) and lower protein C (P less than 0.01) were correlated with sudden death. Among the patients with coronary artery disease, the raised fibrinogen and the decreased protein C appeared to be risk factors for sudden cardiac death. These alterations reflected a prothrombotic state which might increase the ischemic risk, due to an acute thrombosis, leading to the fatal ventricular arrhythmia. Determination of these hemostatic variables might be a useful adjunct for assessment of the vital prognosis of patients with coronary artery disease, especially the risk of sudden death in addition to other known clinical, electrocardiographic, hemodynamic risk factors. This would also guide both the instigation of complementary investigations and appropriate therapy in such high risk group of patients.
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PMID:Biological risk factors for sudden death in patients with coronary artery disease and without heart failure. 156 56

Inadequate anticoagulation in patients with mechanical prosthetic heart valves can result in a significant incidence of thromboembolic complications. An even more life-threatening complication is massive thrombosis of the valve itself. Thrombolytic therapy was given to a moribund 22-year-old woman with intractable heart failure caused by a thrombosed St. Jude prosthetic mitral valve (St. Jude Medical, Inc., St. Paul, Minn.). Although this form of therapy has been used before, this is the first report of a case in which transesophageal echocardiography was performed during thrombolytic therapy to continually record successful thrombolysis of the clotted prosthetic valve. Serial imaging during thrombolysis displayed progressive dissolution of the thrombus and progressive improvement in valve function. Transesophageal echocardiography is helpful in the diagnosis of prosthetic valve thrombosis and has the ability to monitor continually the effect of treatment with thrombolysis. Although thrombolytic therapy with recombinant tissue plasminogen activator is effective in treating prosthetic valve thrombosis, it carries a high risk for serious thromboembolic complications and thus should be reserved for critically ill patients who are too sick to undergo immediate surgery.
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PMID:Use of transesophageal echocardiography during thrombolysis with tissue plasminogen activator of a thrombosed prosthetic mitral valve. 157 Nov 69

A 2-year-old boy with cardiomyopathy and clinical signs of cardiac failure presented with an echodense structure in the left ventricle. This structure was seen from different echocardiographic views adjacent to a hypokinetic area of the apex and lateral free wall. It was different in texture and motion from the underlying myocardium and thus met the diagnostic criteria of a left ventricular thrombus. This thrombus protruded into the cavum and was partly mobile. In view of a high embolic risk, thrombolytic therapy with recombinant tissue plasminogen activator was started. The thrombus resolved within 72 h without any embolic or bleeding complications. No recurrence of the thrombus was observed during a 3-month follow up period.
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PMID:Left ventricular thrombus in a 2-year-old boy with cardiomyopathy: lysis with recombinant tissue-type plasminogen activator. 174 12

We examined the acute phase reaction in myocardial infarction after thrombolytic treatment by streptokinase or tissue plasminogen activator. The magnitude of the acute phase reaction as determined by measurements of serum C-reactive protein and amyloid-A protein did not correlate with infarct size (determined by serial measurements of creatine kinase-MB) in this patient population. On the other hand, the development of acute cardiac failure was more closely associated with the magnitude of the acute phase reaction than with infarct size. The peak serum values of C-reactive protein in patients with and without acute cardiac failure were 128 mg/l (95% confidence intervals 85-170) and 60 mg/l (30-89); P less than 0.01 and concentration time integrals 578 mg/l x days (368-787) and 205 mg/l x days (62-350); P less than 0.01. The corresponding creatine kinase-MB values were 310 U/l (191-429) and 207 U/l (125-289) not significant; and 319 U/l x days (201-437) and 204 U/l x days (124-286) not significant; respectively. Patients requiring medication for cardiac failure on discharge from hospital had higher C-reactive protein and serum amyloid A protein values than those who did not, although the difference did not quite reach statistical significance. The infarct sizes were similar whether the patients needed medication for cardiac failure at discharge or not. Subjectively felt morbidity due to myocardial infarction was linearly associated with serum C-reactive protein peak values (P less than 0.05) and concentration time integrals (P less than 0.05), but not with infarct size. We conclude that thrombolytic treatment of myocardial infarction may reduce hospital inpatient morbidity independently of the limitation of infarct size. This diminished morbidity seems to be associated with modest or low acute phase reaction.
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PMID:Acute phase reaction, infarct size and in-hospital morbidity in myocardial infarction patients treated with streptokinase or recombinant tissue type plasminogen activator. 175 22

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

In a randomised, controlled trial 2514 patients with suspected acute myocardial infarction received 100 mg intravenous alteplase (recombinant tissue plasminogen activator [rt-PA]) plus heparin within 5 h of onset of symptoms, and 2499 similar controls received placebo plus heparin. At 1 month the overall mortality rates were 7.2% and 9.8%, respectively, a relative reduction of 26% (95% confidence interval [CI] 11-39%). At 6 months the mortality rates were 10.4% (alteplase) and 13.1% (placebo), a relative reduction of 21% (95% Cl 8%-32%, p = 0.0026). 6-month mortality rates in patients with proven myocardial infarction were 12.6% and 17.1%, respectively (relative reduction 26%; 95% Cl 14-37%); this effect was similar for anterior (15.6% vs 21.2%) and inferior (7.7% vs 12.8%) myocardial infarction. 6-month mortality rates were lower in those treated with alteplase irrespective of other recognised cardiac risk factors. However, treatment with alteplase made no difference to subsequent cardiac events after one month (readmissions, reinfarctions, death) nor to treatment for angina or heart failure. Product limit estimates of one year mortality are 13.2% with alteplase and 15.1% with placebo. The corresponding figures for patients with an index diagnosis of myocardial infarction are 15.7% and 18.9%, a relative reduction of 16.9%.
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PMID:Effects of alteplase in acute myocardial infarction: 6-month results from the ASSET study. Anglo-Scandinavian Study of Early Thrombolysis. 197 42

Six aneurysms in five patients with acute aneurysmal subarachnoid hemorrhages were treated with direct thrombosis using cellulose acetate polymer within 4 hours of rupture. The aneurysms involved the internal carotid and posterior communicating arteries (two patients), the anterior choroidal artery (one patient), the bifurcation of the basilar artery (one patient), and the middle cerebral artery (two patients). Four patients underwent aggressive volume expansion after direct thrombosis with cellulose acetate polymer. The aneurysms remained thrombosed until operations on the necks were performed 2 to 7 weeks after the subarachnoid hemorrhages. Three patients were given intrathecal tissue plasminogen activator. One patient, who remained at neurological Grade V, was not treated surgically and died from cardiac failure. Five aneurysms in the remaining four patients were successfully clipped. These preliminary data suggest that immediate aneurysmal thrombosis, then aggressive preoperative prophylactic volume expansion and/or administration of intrathecal tissue plasminogen activator, can help prevent new bleeding and reduce delayed cerebral ischemia in patients after aneurysmal subarachnoid hemorrhages.
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PMID:Prophylactic thrombosis to prevent new bleeding and to delay aneurysm surgery. 759 94


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