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

There is abundant evidence from angiographic studies that reperfusion and/or patency rates are greater when thrombolysis is initiated earlier. Evidence of a reduction in infarct size has been provided by a number of studies, which have also suggested that earlier therapy preserves left ventricular function. The major intravenous thrombolytic mortality trials appear to confirm the importance of delivering therapy soon after the onset of symptoms e.g. GISSI and ISIS-2. However, the benefit reported in the first hour in GISSI may be questioned. Furthermore, it seems probable that those coming in late to trials are patients who did not have a sudden onset of symptoms, but whose symptoms persisted, perhaps with recurrent pain, or with heart failure symptoms. This may account for the fact that the benefit seen relatively late, particularly in ISIS-2, does not seem to accord with reperfusion, infarct size and LVEF findings. The true benefits of earlier therapy will be established only when patients are randomized to active therapy or placebo at one point in time and then switched to alternative therapy at a specified later time. This has been done in a small trial with alteplase in Belfast. The findings were suggestive but not conclusive of an improvement in LVEF in those treated earlier. The European Myocardial Infarction Project (EMIP) should go far towards answering the question. In most European cities the time between onset of symptoms and the initiation of skilled treatment for myocardial infarction is of the order of 5-6 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Time as a factor in thrombolytic therapy. 222 42

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

To evaluate the effects of the fibrinolytic system on the development of coronary heart disease (CHD), the level of released plasminogen activator was measured by venous occlusion in 60 CHD cases, and 20 healthy subjects. The level of plasma basic plasminogen activator activity, plasminogen, fibrinogen and serum fibrin degradation products (FDP) were determined also. In comparison with control subjects, a lower level of released plasminogen activator was found in all CHD patients, being especially marked in those with unstable angina pectoris and acute myocardial infarction. The levels of plasma plasminogen, fibrinogen and FDP were also significantly changed in these patients. In acute myocardial infarction patients, the level of released plasminogen activator was lower in cases complicated with heart failure than in those without.
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PMID:Fibrinolytic activity in coronary heart disease. 251 77

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

Streptokinase and alteplase are established therapies in acute myocardial infarction. Reteplase is a new thrombolytic agent that can be given as a double bolus. This trial was designed to determine whether the effect of reteplase on survival was at least equivalent (within 1% of fatality rate) to that of a standard streptokinase regimen. Patients from 208 centres in nine countries (n = 6010) with symptoms and electrocardiographic criteria consistent with acute myocardial infarction were randomised to receive double-blind either streptokinase 1.5 MU intravenously over 60 min or reteplase two boluses of 10 MU given 30 min apart. Treatment could be started up to 12 h from onset of symptoms. All patients received intravenous heparin for at least 24 h. The primary endpoint was 35-day outcome. There were 270 deaths (9.02%) in the reteplase and 285 deaths (9.53%) in the streptokinase group, a non-significant difference (95% CI -1.98% to 0.96%). Among patients who received treatment (98.8%) there were 263 deaths (8.90%) in the reteplase compared with 279 deaths (9.43%) in the streptokinase group (a difference of -0.53%). Because the upper limit of the 90% CI for this difference is 0.71%, this result shows that reteplase is at least as effective as streptokinase. In-hospital stroke rates were 1.23% for reteplase and 1.00% for streptokinase. Bleeding events were similar in the two treatment groups (0.7% reteplase, 1.0% streptokinase). The incidence of recurrent myocardial infarction was similar, but there were significantly fewer cases of atrial fibrillation, asystole, cardiac shock, heart failure, and hypotension in the reteplase group. We conclude that reteplase is an effective drug in the treatment of acute myocardial infarction. It is clinically safe, its administration is simple, and it will be a useful addition to the range of thrombolytic agents available.
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PMID:Randomised, double-blind comparison of reteplase double-bolus administration with streptokinase in acute myocardial infarction (INJECT): trial to investigate equivalence. International Joint Efficacy Comparison of Thrombolytics. 1111 34

An acute obstruction is a life-threatening complication of mechanical valve prostheses, and is caused by the formation of fresh clot or fibrous tissue overgrowth, or both. Accurate selection of the most appropriate treatment for a particular patient is mandatory. From January 1991 to July 1992, 28 cases of prosthetic thrombosis were managed. Twenty patients underwent surgical treatment, with one operative death, and 8 patients were treated with thrombolysis using recombinant tissue-type plasminogen activator (rt-PA). The criteria for using thrombolysis were (1) the recent onset of symptoms, (2) transesophageal echocardiographic evidence of clots on the valve or cardiac chambers, and (3) preserved disc excursions. All patients who underwent thrombolysis had mechanical valves (two bileaflets, four tilting discs, and two ball valves); seven valves were in the mitral position and one was in the aortic. Symptoms of obstruction consisted of cardiac failure in 6 cases or thromboembolism in 5, or both. The mean interval between the onset of symptoms and the initiation of thrombolysis was 81 +/- 65 hours. After infusion of the rt-PA, normal valve function was restored in all patients, as documented by transesophageal echocardiography. No deaths or neurologic complications occurred; there was one episode of minor peripheral embolism. Thrombolysis using rt-PA may be the appropriate treatment in patients with primary thrombosis of mechanical valves, thereby avoiding the operation-related risks.
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PMID:Prosthetic valve obstruction: thrombolysis versus operation. 831 97

Besides the thrombolytic therapy several adjuvant therapeutic measures were identified which significantly improve the prognosis of patients with acute myocardial infarction (AMI). These measures include the treatment by means of acetylsalicylic acid (ASA), beta-blockers and ACE inhibitors. Early administration of ASA and beta-blockers are indicated in all patients with AMI who have no contraindications for this therapy. They are especially the patients with manifest heart failure or asymptomatic left ventricular dysfunction who benefit from ACE inhibitors. The effectivity of routine administration of other medicaments such as anticoagulants, nitrates, calcium channel blockers and magnesium, have not been convincingly proved. However, some selected patients with AMI can benefit from these medicaments. Intravenous administration of heparin is unambiguously justified only in thrombolysis with t-PA. Thrombolyses with streptokinase, urokinase, and anistreplase are justified only at high risk of thromboembolic complications. Their prevention and therapy include also the necessity to restrict the administration of pelentan. The use of nitrates is indicated in patients with AMI in case of sustaining stenocardia, arterial hypertension and manifest heart left ventricular failure. Until the definitive standpoint is gained regarding the effect of magnesium in patients with AIM, its administration remains especially indicated in cases of arterial hypertension, tachycardiac disturbances of the heart rhythm and states of assumed or proved hypomagnesiemia. In AMI cases when magnesium is used in order to protect the patient from reperfusion lesion, it must be administered prior to the reperfusion therapy. An intensive research in the field of therapeutical measures in patients with AMI still continues. It is certain that it will soon bring further knowledge which will in turn improve the prognosis and quality of life of patients with AMI. (Tab. 4, Ref. 133.)
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PMID:[Adjuvant therapy in patients with acute myocardial infarct]. 892 11

Thrombotic occlusion of coronary arteries is the reason of most acute coronary syndromes. A significant role in their prevention and therapy is taken by antiplatelet therapy. Acute coronary syndrome justifies also the use of anticoagulation therapy, name by heparin. The adjuvant therapy by means of heparin in thrombolysis seems to be necessary especially when alteplase (t-PA) is used. Peroral anticoagulants represent a further therapeutical procedure in patients with coronary ischaemia. Regarding the increased risk of bleeding, the cost and difficulties coinciding with therapy by cumarine derivates, the antiplatelet therapy is currently preferred. Cumarine derivates, however, should be used in patients with simultaneous atrial fibrillation, venous thromboembolism and it should be considered in patients with heart failure and pre-thrombotic states. Studies aimed at the assessment of the role of low-molecular heparin in acute coronary ischaemia currently take place. Encouraging results are gained from experience with high effective direct inhibitors of thrombin (e.g. hirudin) and antagonists of glycoprotein IIb/IIIa. It seems that they soon will find justification in the therapy of arterial thrombosis. Interesting field of the research is represented by the studies which compare low doses of acetylosalicylic acid with low doses of cumarine derivates. (Ref. 43.)
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PMID:[Antithrombotic therapy in acute myocardial infarct]. 896

In recent years, a prodigious amount of information has been gathered regarding the relationship between vascular biology and the mechanisms underlying cardiovascular disease. Activation of elements of the reninangiotensin system (RAS) appear to play an important role in the development and progression of conditions such as hypertension, coronary artery disease, and heart failure. Indeed, converging lines of evidence indicate that angiotensin-converting enzyme (ACE) regulates a delicate balance among a multitude of factors responsible for vascular tone, cellular growth promotion and inhibition, and pro- and anti-inflammatory effects. Because angiotensin II inhibits fibronectin, stimulates expression of plasminogen activator inhibitors, and degrades bradykinin, thereby impairing production of nitric oxide, ACE and the RAS are also involved in thrombosis and fibrinolysis. The favorable effects of ACE inhibition on endothelial function and, potentially, on cardiovascular morbidity and mortality are believed to result not only from angiotensin II suppression but also its consequent bradykinin preservation and nitric oxide production.
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PMID:The integrated effects of angiotensin II. 912 15


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