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Myocardial infarction indicators

Long-term follow-up of survivors of acute myocardial infarction indicates that electrophysiology testing has low positive predictive value for the induction of sustained ventricular tachycardia (21%) and ventricular fibrillation (12%) (74). Electrophysiology testing has a low specificity and low positive predictive accuracy even in this setting (65,75). [Pg.501]

There is a close correlation between myocardial infarctions and tachyarrhythmias, illustrated by the presence of complex ventricular arrhythmias among heart attack victims which are estimated to affect one-third of the survivors each year. Frequendy, the immediate cause of sudden death is ventricular fibrillation, an extreme arrhythmia that is difficult to detect or treat. In the majority of cases, victims have no prior indication of coronary heart disease. [Pg.180]

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). [Pg.110]

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]

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. [Pg.310]

Fondaparinux, the factor Xa-binding pentasaccharide (Arixtra, MW 1,728 Da), is prepared synthetically, unlike UFH, LMWH and danaparoid, which are obtained from animal sources. Despite only inactivating free factor Xa, clinical trials indicate that fondaparinux is an effective antithrombotic agent, both for venous thromboembolism prophylaxis and treatment, as well as for acute coronary syndrome and ST elevation myocardial infarction [4]. [Pg.110]

Wagner et. al (46) studied 376 patients to evaluate the importance of identification of the myocardial-specific MB isoenzyme in the diagnosis of acute myocardial infarction. An attempt was made to determine the incidence of falsely positive (mb). No acute infarction was diagnosed in all patients in whom neither total CK nor the isoenzymes of LD indicated myocardial necrosis. Incidence of falsely negative (MB) was zero in 33 patients. They concluded that determination of the isoenzymes of CK provides both a sensitive and specific indication of acute myocardial infarction. [Pg.200]

In rodent stroke models, statin pretreatment has been shown to reduce infarct volumes and improve outcomes. Similarly, several clinical studies have shown that prior statin use reduced the severity of acute ischemic stroke and myocardial infarction. Recent studies indicate that beneftt can be achieved even when treatment is initiated after the onset of symptoms. In rodents, atorvastatin and simvastatin have been shown to reduce the growth of ischemic lesions, enhance functional outcome, and induce brain plasticity when administered after stroke onset. A retrospective analysis of the population-based Northern Manhattan Stroke Study (NOMASS) showed that patients using lipid-lowering agents at the time of ischemic stroke have a lower incidence of in-hospital stroke progression and reduced 90-day mortality rates. Retrospective analysis of data of the phase III citicoline trial showed... [Pg.101]

P-Blockers and ACE inhibitors are also indicated for post-myocardial infarction for the reduction of cardiovascular morbidity and mortality, as are aldosterone antagonists, in post-myocardial infarction patients with reduced left ventricular systolic function and diabetes or signs and symptoms of heart failure.2,48... [Pg.27]

List the quality indicators of care for myocardial infarction and explain the rationale behind each indicator. [Pg.83]

Aspirin decreases the risk of death, recurrent infarction, and stroke following myocardial infarction. Aspirin prescription at hospital discharge is a quality care indicator in MI patients.3 All patients should receive aspirin indefinitely those patients with a contraindication to aspirin should receive clopidogrel.2,3... [Pg.101]

In March of 2007, the FDA announced that tegaserod maleate would be voluntarily withdrawn from the market because of information indicating an increased risk of serious cardiovascular events (myocardial infarction, unstable angina, and stroke). [Pg.320]

C = Chest pain. The presence of chest pain may indicate pulmonary embolism, angina, or myocardial infarction. [Pg.750]

ST-segment elevation A type of myocardial infarction (MI) that typically results in an injury that transects the thickness of the myocardial wall. Following an ST-elevation MI, pathologic Q waves are frequently seen on the electrocardiogram, indicating transmural myocardial infarction. [Pg.1577]

There have been many sporadic reports that lipo-PGEj is effective in fulminant hepatitis, neuralgia associated with herpes zoster, multiple spinal canal stenosis, cerebral infarction, myocardial infarction, chronic renal failure, and bed sores as well as for its registered indications. [Pg.267]

This is not the only example. Recently, polymorphisms in the G protein p3-subunit gene have been shown to predict response to hydrochlorothiazide (Turner et al., 2001). Psaty et al. identified a subset of patients with a variant of the a-adducin gene that were associated with a lower risk of myocardial infarction and cerebral hemorrhage with diuretic therapy (Psaty et al., 2002). In addition, Genaissance has indicated that it has identified markers that predict the response to the statins, a class of drugs used to lower cholesterol. [Pg.97]

In conclusion, we have shown that successful treatment of MI and I/R AKI with MSC holds substantial promise for the development of novel, MSC-based interventions that can improve the treatment of severe, and still largely therapy-resistant, clinical ischemic myocardial infarction as well as ARF that results from I/R injury. Pluripotent MSC, because of their versatility and the ease with which they can be harvested from the bone marrow, culture expanded, and engineered, appear to be a particularly well-suited stem cell type for these clinical indications. [Pg.119]

Indications for colon-irritant purgatives are the prevention of straining at stool following surgery, myocardial infarction, or stroke and provision of relief in painful diseases of the anus, e.g., fissure, hemorrhoids. [Pg.174]

Therapeutic indications for benzodiazepines include anxiety states associated with neurotic, phobic, and depressive disorders, or myocardial infarction (decrease in cardiac stimulation due to anxiety) insomnia preanesthetic (preoperative) medication epileptic seizures and hypertonia of skeletal musculature (spasticity, rigidity). [Pg.226]

Hindman MC, Wagner GS, JaRo M, et al. The clinical significance of bundle branch block complicating acute myocardial infarction. 2. Indications for temporary and permanent pacemaker insertion. Circulation... [Pg.62]


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See also in sourсe #XX -- [ Pg.189 , Pg.193 ]




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Myocardial infarction

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