Myocardial infarction intravenous

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. 

In a more extensive international trial, 17,187 patients were treated intravenously with streptokinase alone, aspirin alone, a combination of streptokinase and aspirin, or placebo (78). Streptokinase and aspirin were equally effective in treating acute myocardial infarction, each decreasing mortahty by 25% their combination further reduced mortahty by 42%. A significant reduction in mortahty was seen even in those patients treated up to 24 hours after the onset of symptoms. 

Compared to streptokinase, urokinase has been less extensively studied because of its high cost, ie, about 10 times that of a comparable treatment with streptokinase. In addition to the indications described for streptokinase, urokinase is indicated for use in patients with prior streptokinase treatment, or prior Streptococcal infection. Urokinase is commonly used at a loading dose of 4400 units /kg, with a maintenance intravenous infusion dose of 4400 units/kg/h for thromboses other than acute myocardial infarction. In the latter case, a much larger dose, ie, 0.5—2.0 million units/h or a bolus dose of 1.0 million units followed by a 60-min infusion with 1.0 million units, has been found optimal (106). An intracoronary dose of 2000 units/min for two hours was used in one comparative study with intracoronary streptokinase (107). In this study, urokinase exhibited efficacy equivalent to streptokinase with fewer side effects. Other studies with intracoronary urokinase have adrninistered doses ranging from 2,000 to 24,000 units/min with a reperfusion efficacy of 60—89% (108—112). In another urokinase trial, 2.0 million units were adrninistered intravenously, resulting in a thrombolytic efficacy of 60% (113). Effectiveness in terms of reduction in mortaUty rate has not been deterrnined because of the small number of patients studied. 

While epinephrine is usually well tolerated in young and healthy individuals, there may be problems in elderly patients with cardiac arrhythmia or previous myocardial infarction episodes [31-33]. Pharmacological effects of epinephrine include rapid rise in blood pressure, pallor, anxiety, tachycardia, headache and tremor as well as vertigo. Most commonly these effects occur after intravenous injection or after overdosing epinephrine. Cardiac arrhythmia or pulmonary edema may develop in serious cases [33, 34]. 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

A meta-analysis of the collective outcome results from three randomized, controlled intravenous SNP trials suggested that intravenous SNP reduces early mortality by =35% in acute myocardial infarction [78]. Since each of the component trials was... 

Nagays, N., Fujii, T., Iwase, T., et al (2004) Intravenous administration of mesenchymal stem cells improves cardiac function in rats with acute myocardial infarction through angiogenesis and myogenesis. Am J Physiol Heart Circ Physiol 287, H2670-H2676. 

Q86 Patients with a suspected infarction should receive analgesics intravenously as soon as possible. Pain in myocardial infarction may cause adverse haemodynamic effects such as increases in blood pressure and heart rate. 

Meta-analysis is a method often used to determine the effectiveness of a drug but to date it has rarely been used to assess safety. One case illustrates how this technique can help. Six studies examining the use of intravenous lidocaine for acute myocardial infarction did not, on an individual basis, give strong enough evidence to support the hypothesis that this technique could cause excess mortality. The meta-analysis, however, was able to demonstrate this. ... 

Like procainamide, lidocaine is an amide with local anesthetizing action. Lidocaine is usually administered intravenously for short-term therapy of ventricular extrasystole, tachycardia, especially in the severe phase of myocardial infarction, arrhythmia of natural cause, and for arrhythmia that can originate in the heart during surgical manipulations. Synonyms of this drug are lidopen, xylocaine, xylocard, and others. 

Following intravenous injection of Thorotrast, cirrhosis of the liver was the primary systemic effect in humans and animals. Hematological disorders (aplastic anemia, leukemia, myelofibrosis, and splenic cirrhosis), cardiovascular effects (myocardial infarction, severe coronary luminal narrowing and internal alteration of the carotid artery), and Thorotrastoma (localized fibrosis surrounding deposits of Thorotrast) were also found in patients injected with Thorotrast. The effects of Thorotrast were a result of the radiological toxicity of thorium. 

Gruppo Italiano per lo Studio della Streptochinasi nell Infarto Miocardico (GISSI) Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986 1 397-402. 

ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction ISIS-2. Lancet 1988 2 349-360. 

Zijlstra F, de Boer M, Hoomtje J, et al. Comparison of immediate coronary angioplasty with intravenous streptokinase in myocardial infarction. N Eng J Med 1993 328 680-684. 

First International Study of Infarct Survival Collaborative Group. Randomised trial of intravenous atenolol among 16 027 cases of suspected acute myocardial infarction ISIS-1. Lancet 1986 2(8498) 57-66. 

Krumholz HM, Hennen J, Ridker PM, Murillo JE, Wang Y, Vaccarino V et al. Use and effectiveness of intravenous heparin therapy for treatment of acute myocardial infarction in the elderly. J Am Coll Cardiol 1998 31(5) 973-9. 

Marchionni N, Schneeweiss A, Di Bari M, Ferrucci L, Moschi G, Salani B et al. Age-related hemodynamic effects of intravenous nitroglycerin for acnte myocardial infarction and left ventricular failure. Am J Cardiol... 

Tirofiban is a synthetic, nonpeptide inhibitor of glycoprotein-(GP)-receptors. Tirofiban has a rapid onset and short duration of action after intravenous administration. Coagulation parameters turn to normal 4-8 hours after the drug is withdrawn. Tirofiban in combination with heparin and aspirin is indicated in the management of patients with unstable angina or non-Q-wave myocardial infarction. 

In the upper part of Figure 15.2 we see a funnel plot of trials evaluating the effect of intravenous magnesium in the treatment of myocardial infarction. Note the absence of small trials with odds ratios greater than one (which would indicate a lack of benefit for intravenous magnesium) this... 

E. Therapeutic response In human studies, eptifibatide inhibited ex vivo platelet aggregation induced by adenosine diphosphate (ADP) and other agonists in a dose- and concentration-dependent manner. The effect of eptifibatide was observed immediately after administration of a 180pg/kg intravenous bolus. In a placebo-controlled study of patients with acute coronary syndrome, Integrilin reduced the occurrence of death from any cause or new myocardial infarction. Similar benefits were observed in patients undergoing coronary angioplasty. 

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