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Myocardial infarction, acute, therapy with

Clinical use Acetylsalicylic acid is the prototype of a nonsteroidal anti-inflammatory drug and is used in a large number of inflammatory and pain indications including musculoskeletal, soft tissue and joint disorders, headache, dysmenorrhoea and fever (Symposium on new perspectives on aspirin therapy 1983, various authors). Furthermore, acetylsalicylic acid is used as an antiplatelet drug in the acute treatment of myocardial infarction in combination with thrombolytics and for the prevention of myocardial infarction and stroke (Patrono, 1994). [Pg.44]

Alexander KP, Newby LK, Hellkamp AS, Harrington RA, Peterson ED, Kopecky S, Langer A, O Gara P, O Connor CM, Daly RN, Califf RM, Khan S, Fuster V. Initiation of hormone replacement therapy after acute myocardial infarction is associated with more cardiac events during follow-up. J Am Coll Cardiol 2001 38(l) l-7. [Pg.280]

Zeymer U, von Essen R, Tebbe U, et al, Frequency of optimal anticoagulation for acute myocardial infarction after thrombolysis with front-loaded recombinant tissue-type plasminogen activator and conjunctive therapy with recombinant hirudin (HBW 023). ALKK Study Group. Am J Cardiol 1995 76 997-1001. [Pg.106]

Patients with acute coronary syndromes such as acute myocardial infarction and unstable angina remain at risk for recurrent myocardial ischemia despite therapy with antiplatelet agents and heparin. Although first clinical trials indicate a possible use of oral direct TIs for the prevention of cardiovascular events in patients after acute myocardial infarction, the presently available data are still limited and it has not... [Pg.115]

N. A. Ruocco, B. A. Bergelson, A. K. Jacobs, M. M. Frederick, D. P. Faxon, T. J. Ryan, Invasive versus conservative strategy after thrombolytic therapy for acute myocardial infarction in patients with antecedent angina. A report from Thrombolysis in Myocardial Infarction phase II study (TIMI II), J Am Coll Cardiol 20,1445—1551 (1992). [Pg.185]

Gryzbowski M, Clements FA, Parsons L, et al. Mortality benefit of immediate revascularization of acute ST-segment-elevation myocardial infarction in patients with contraindications to thrombolytic therapy A propensity analysis. JAMA 2003 290 1891-1898. [Pg.316]

Mehta RH, Criger DA, Granger CB, Pieper KK, Califf RM, Topol EJ, Bates ER. Patient outcomes after fibrinolytic therapy for acute myocardial infarction at hospitals with and without coronary revascularization capability. J Am Coll Cardiol 2002 40 1034-1040. [Pg.30]

A considerable body of evidence has accumulated about the benefits of antiplatelet therapy, in most cases aspirin, in patients with a previous cardiovascular event (previous myocardial infarction, acute... [Pg.211]

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. [Pg.309]

Krumholz HM, Pasternak RC, Weinstein MC, et al. Cost effectiveness of thrombolytic therapy with streptokinase in elderly patients with suspected acute myocardial infarction. N Engl J Med 1992 327 7-13. [Pg.589]

Alteplase has proven effective in the early treatment of patients with acute myocardial infarction (i.e. those treated within 12 h after the first symptoms occur). Significantly increased rates of patient survival (as measured 1 day and 30 days after the initial event) are noted when tPA is administered in favour of streptokinase, a standard therapy (see later). tPA has thus established itself as a first-line option in the management of acute myocardial infarction. A therapeutic dose of 90-100 mg (often administered by infusion over 90 min) results in a steady-state alteplase concentration of 3-4 mg l 1 during that period. However, the product is cleared rapidly by the liver, displaying a serum half-life of approximately 3 min. As is the case for most thrombolytic agents, the most significant risk associated with tPA administration is the possible induction of severe haemorrhage. [Pg.348]

The Defibrillator in Acute Myocardial Infarction Trial (DINAMIT) enrolled nearly 700 patients with recent MI, ranging from 6 to 40 days (median 7 days), EF < 36%, and reduced heart rate variability but without NYHA class IV symptoms, sustained VT within 48 h of MI, or surgical or percutaneous 3-vessel revascularization [34]. Patients were randomized to ICD therapy versus conventional therapy and at 1 year, there was no difference in total mortality with more arrhythmic deaths in the control arm and more nonarrhythmic deaths in the ICD arm. Thus, there appears to be no benefit to ICD therapy in the immediate post-MI period. An interpretation of the negative result of both of these trials is that significant recovery of LV function may have occurred in the... [Pg.43]

Conduction system abnormalities are common in chronic heart failure, occurring in 15-30% of the population with low left ventricular ejection fraction (LVEF) [1-3]. The prevalence in ischemic heart disease is roughly similar to that seen in other forms of dilated cardiomyopathy. Conduction system disease can occur both at the time of an acute myocardial infarction as well as slowly progressing in chronic ischemic heart disease. Intraventricular conduction delays are associated with a poor prognosis in heart failure, with up to a 70% increase in the risk of death, and are also more prevalent in patients with advanced symptoms [2,4]. In ischemic heart disease, all components of the conduction system are at risk of ischemic injury, from the sinoatrial node to the His-Pukinje system. These conduction system abnormalities have the potential to impair cardiac function by a number of mechanisms. Since conduction abnormalities impair cardiac function, it is logical that pacing therapies to correct or improve these conduction abnormalities may improve cardiac function. [Pg.49]

Franzosi MG, Santoro E, De Vita C, et al. Ten-year follow-up of the first megatrial testing thrombolytic therapy in patients with acute myocardial infarction results of the Gruppo Italiano per lo Studio della Sopravvivenza nellTnfarto-l study. The GISSI Investigators. Circulation 1998 98 2659-2665. [Pg.82]

Grines CL, Browne KF, Oneil W, et al., for the Primary Angioplasty in Myocardial Infarction study group. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. N Engl J Med 1993 328 673-679. [Pg.82]

Table 7.2 Trials of intracoronary cell therapy in patients with acute myocardial infarction... Table 7.2 Trials of intracoronary cell therapy in patients with acute myocardial infarction...
Murad-Netto S, Moura R, Romeo LJ, Manoel Neto A, Duarte N, Barreto F, Jensen A, Vina RE, Vraslovik F, Oberdan A, Benetti F, Saslavsky J, Vina ME, Amino JG. Stem cell therapy with retrograde coronary perfusion in acute myocardial infarction. A new technique. Arq Bras Cardiol 2004 S3 352-254 349-351. [Pg.125]

Miller CD, Roe MT, Mulgund J, Hoekstra JW, Santos R, Pollack CV et al. Impact of acute beta-blocker therapy for patients with non-ST-segment elevation myocardial infarction. Am J Med 2007 120(8) 685-92. [Pg.591]


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Acute myocardial infarction

Acute therapy

Infarct

Infarct, myocardial

Infarction

Myocardial infarction

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