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Myocardial infarction prior

Left ventricular hypertrophy Angina or prior myocardial infarction Prior coronary revascularization Heart failure... [Pg.572]

E. The data do not permit any conclusion concerning myocardial infarction prior to, or after, admission to the hospital. [Pg.68]

Heart (left ventricular hypertrophy, angina or prior myocardial infarction, prior coronary revascularization, heart failure)... [Pg.191]

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]

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]

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]

Prior to myocardial infarction, coronary artery bypass graft (CABG), peripheral artery disease, cerebrovascular accident, or aspirin use... [Pg.22]

Prior sensitivity to any tricyclic drug. Not recommended for use during the acute recovery phase following myocardial infarction. Concomitant use of monoamine oxidase inhibitors (MAOIs) is generally contraindicated. [Pg.1038]

Although much of the data regarding the frequency of conduction abnormalities during acute myocardial infarction were derived from studies prior to the era of rapid reperfusion [14 17], data from more recent trials suggest that the incidence of intraventricular conduction defects has changed very little. [Pg.50]

Atrial fibrillation is commonly associated with heart failure, and the prevalence of atrial fibrillation is related to the severity of heart failure, with less than 5% affected with very mild heart failure to nearly 50% affected with advanced heart failure [66]. Heart failure and atrial fibrillation are both common cardiovascular disorders and share the same demographic risk factors, including age, history of hypertension, prior myocardial infarction, and valvular heart disease [67, 68]. Further, the incidence of heart failure increases dramatically after the diagnosis of atrial fibrillation [69]. Progression of LV dysfunction can clearly be associated with rapid ventricular rates [70-76]. Conversely, conversion to normal sinus rhythm or control of ventricular response in atrial fibrillation can improve LV function [71-74, 77]. Accordingly, rate control becomes very important in patients with heart failure and dilated cardiomyopathy, and likely even more so when ischemia from rapid rates complicate the patient s course. [Pg.53]

Highly recommended are jS-blockers for those who have a prior MI event. They showed a significant effect on death. Recent studies suggest that patients who have coronary artery disease without acute myocardial infarction and/or congestive heart failure have approximately the same protective benefit against death. [Pg.588]

Drugs that markedly slow conduction, such as flecainide, or high concentrations of quinidine, can result in an increased frequency of reentry arrhythmias, notably ventricular tachycardia in patients with prior myocardial infarction in whom a potential reentry circuit may be present. Treatment here consists of recognition, withdrawal of the offending agent, and intravenous sodium. [Pg.294]

Abacavir NRTT1 300 mg bid Testing to rule out the presence of the HI A-B 5701 allele is recommended prior to the initiation of therapy Rash, hypersensitivity reaction, nausea. Possible increase in myocardial infarction Avoid alcohol... [Pg.1074]

A. The patient had a myocardial infarction 48 to 64 hours prior to admission. [Pg.68]

However, in a second study, data on 1857 women from the Coumadin Aspirin Reinfarction Study were used to assess the incidence of cardiac deaths or unstable angina as related to the use of HRT. Of the population studied, 524 (28%) had used HRT at some point and 111 of the latter (21%) had started HRT after suffering a myocardial infarct ( new users ). Women who began HRT after their first myocardial infarct had a significantly higher subsequent incidence of unstable angina than women who had never used hormones (39 versus 20%) however, these new hormone users suffered death or recurrence of myocardial infarct at a much lower rate than never-users (4 versus 15%). These differences are striking. Prior/current users had no excess risk of the composite end-point after... [Pg.276]

Celik T, Kursaklioglu H, lyisoy A, et al. The effects of prior use of atorvastatin on coronary blood flow after primary percutaneous coronary intervention in patients presenting with acute myocardial infarction. Coron Artery Dis 2005 16 321-326. [Pg.169]

The mean age of the patients was 61 12 years. A total of 21 patients (70%) were males. Systemic hypertension was the most frequent coronary risk factor, involving 15 patients (49%), followed by smoking in 10 patients (33%), and dyslipi-demia in 8 (27%), whereas only three patients (10%) were diabetics. Eleven patients (37%) had a prior history of myocardial infarction (Ml). The procedure was successful in all patients. There were no in-hospital events and no elevation... [Pg.349]

Haffner SM, Lehto S, Ronnemaa T et al. (1998) Mortality from coronary heart disease subjects with type 2 diabetes and in non-diabetic subjects with and without prior myocardial infarction. New England Journal of Medicine 339 229-234. [Pg.32]

A healthy 33-year-old man with prior cocaine use had a small myocardial infarction and, 36 hours later, having inhaled cocaine, developed a dissection of the left main coronary artery, extending distally to the left anterior descending and circumflex arteries. There was marked anterolateral and apical hypokinesis. [Pg.495]


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See also in sourсe #XX -- [ Pg.156 ]




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